Clinical manual and review of transesophageal echocardiography [Third ed.] 9780071830232, 0071830235

Table of contents :
Clinical Manual and Review of Transesophageal Echocardiography, 3e
Title Page
Copyright
Contents
Dedication
Contributors
Preface
1 Fundamentals of Echocardiography
Chapter 1 Physics of Two-Dimensional and Doppler Imaging
Chapter 2 The TEE Probe
Chapter 3 Understanding Ultrasound System Controls
Chapter 4 Transesophageal Tomographic Views
Chapter 5 Quantitative Echocardiography
Chapter 6 Anatomical Variants and Ultrasound Artifacts
2 Assessment of Cardiac Structure and Function
Chapter 7 Assessment of Left Ventricular Systolic Function
Chapter 8 Left Ventricular Diastolic Function
Chapter 9 Right Ventricular Function
Chapter 10 Mitral Valve
Chapter 11 Aortic Valve
Chapter 12 Tricuspid and Pulmonic Valves
Chapter 13 Epicardial Echocardiography and Epiaortic Ultrasonography
3 Clinical Echocardiography
Chapter 14 Mitral Valve Repair
Chapter 15 Prosthetic Valves
Chapter 16 Aortic Surgery and Atheroma Assessment
Chapter 17 Assessment of Mechanical Circulatory Support Devices
Chapter 18 Thoracic Transplantation
Chapter 19 Transesophageal Echocardiography for Congenital Heart Disease
Chapter 20 Cardiac Masses and Pericardial Pathology
Chapter 21 Ventricular Diseases
Chapter 22 Noncardiac Surgery
4 Special Topics
Chapter 23 Three-Dimensional Echocardiography
Chapter 24 Strain and Strain Rate Imaging
Chapter 25 Training and Certification in Perioperative Transesophageal Echocardiography
Chapter 26 Establishing and Maintaining a Quality Perioperative TEE Service
5 Appendices
Appendix A: Normal Chamber Dimensions
Appendix B: Wall Motion and Coronary Perfusion
Appendix C: Diastolic Function
Appendix D: Native Valve Areas, Velocities, and Gradients
Appendix E: Measurements and Calculations
Appendix F: Miscellaneous
Answers
Index

Citation preview

CLINICAL MANUAL AND REVIEW OF TRANSESOPHAGEAL ECHOCARDIOGRAPHY Third Edition Edited by

Joseph P. Mathew, MD, MHSc, MBA Jerry Reves Professor of Anesthesiology Chairman, Department of Anesthesiology

Alina Nicoara, MD, FASE Associate Professor of Anesthesiology Director, Perioperative Echocardiography Department of Anesthesiology Duke University Medical Center

Duke University Medical Center Durham, North Carolina

Durham, North Carolina

Chakib M. Ayoub, MD, MBA Professor of Anesthesiology

Madhav Swaminathan, MD, FASE, FAHA

Department of Anesthesiology Duke University Medical Center Durham, North Carolina

Professor of Anesthesiology Vice-Chair, Faculty Development Department of Anesthesiology Duke University Medical Center Durham, North Carolina

New York I Chicago I San Francisco I Athens I London I Madrid I Mexico City Milan I New Delhi I Singapore I Sydney /Toronto

Copyright © 2020 by McGraw-Hill Education. All rights reserved. Except as pemritted under the United States Copyright Act of 1976, no part of this publication may be reproduced or distributed in any form or by any means, or stored in a database or retrieval system, without the prior written permission of the publisher. ISBN: 978-1-26-046982-0 MHID: 1-26-046982-4 The material in this eBook also appears in the print version of this title: ISBN: 978-0-07-183023-2, MHID: 0-07-183023-5. eBook conversion by codeMantra Version 1.0 All trademarks are trademarks of their respective owners. Rather than put a trademark symbol after every occurrence of a trademarked name, we use names in an editorial fashion only, and to the benefit ofthe trademark own.er, with no intention of infringement of the trademark. Where such designations appear in this book, they have been printed with initial caps. McGraw-Hill Education eBooks are available at special quantity discounts to use as premiums and sales promotions or for use in corporate training programs. To contact a representative, please visit the Contact Us page at www.mhprofessional.com. Notice Medicine is an ever-changing science. As new research and clinical experience broaden our knowledge, changes in treatment and drug therapy are required. The editors and the publisher ofthis work have checked with sources believed to be reliable in their efforts to provide information that is complete and generally in accord with the standards accepted at the time ofpublication. However, in view of the possibility of human error or changes in medical sciences, neither the editors nor the publisher nor any other party who has been involved in the preparation or publication of this work warrants that the information contained herein is in every respect accurate or complete, and they disclaim all responsibility for any errors or omissions or for the results obtained from use of the information contained in this work. Readers are encouraged to confirm the information contained herein with other sources. For example and in particular, readers are advised to check the product information sheet included in the package of each drug they plan to administer to be certain that the information contained in this work is accurate and that changes have not been made in the recommended dose or in the contraindications for administration. This recommendation is of particular importance in connection with new or infrequently used drugs. TERMSOFUSE This is a copyrighted work and McGraw-Hill Education and its licensors reserve all rights in and to the work. Use of this work is subject to these terms. Except as pemritted under the Copyright Act ofl 976 and the right to store and retrieve one copy of the work, you may not decompile, disassemble, reverse engineer, reproduce, modify, create derivative works based upon, transmit, distribute, disseminate, sell, publish or sublicense the work or any part of it without McGraw-Hill Education's prior consent. You may use the work for your own noncommercial and personal use; any other use of the work is strictly prohibited. Your right to use the work may be terminated if you fail to comply with these terms. THE WORK IS PROVIDED "AS IS." McGRAW-HILL EDUCATION AND ITS LICENSORS MAKE NO GUARANTEES OR WARRANTIES AS TO THE ACCURACY, ADEQUACY OR COMPLETENESS OF OR RESULTS TO BE OBTAINED FROM USING THE WORK, INCLUDING ANY INFORMATION THAT CAN BE ACCESSED THROUGH THE WORK VIA HYPERLINK OR OTHERWISE, AND EXPRESSLY DISCLAIM ANY WARRANTY, EXPRESS OR IMPLIED, INCLUDING BUT NOT LIMITED TO IMPLIED WARRANTIES OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE. McGraw-Hill Education and its licensors do not warrant or guarantee that the functions contained in the work will meet your requirements or that its operation will be uninterrupted or error free. Neither McGraw-Hill Education nor its licensors shall be liable to you or anyone else for any inaccuracy, error or omission, regardless of cause, in the work or for any damages resulting therefrom. McGraw-Hill Education has no responsibility for the content of any information accessed through the work. Under no circumstances shall McGraw-Hill Education and/or its licensors be liable for any indirect, incidental, special, punitive, consequential or similar damages that result from the use of or inability to use the work, even if any of them has been advised of the possibility of such damages. This limitation ofliability shall apply to any claim or cause whatsoever whether such claim or cause arises in contract, tort or otherwise.

Contents Contributors Foreword

ix xiii

Preface

xv

1.

FUNDAMENTALS OF ECHOCARDIOGRAPHY

Chapter 1

PHYSICS OF TWO-DIMENSIONAL AND DOPPLER IMAGING

3

Brian P. Barrick, Mihai V. Podgoreanu, and Edward K. Prokop

Chapter 2

THETEE PROBE

18

Joseph A. Sivak, Jose Rivera, and Zainab Samad

Chapter 3

UNDERSTANDING ULTRASOUND SYSTEM CONTROLS

30

Hillary B. Hrabak, Ashlee Davis, and David B. Adams

Chapter4

TRANSESOPHAGEAL TOMOGRAPHIC VIEWS

50

Ryan E. Lauer andJoseph P. Mathew

Chapter 5

QUANTITATIVE ECHOCARDIOGRAPHY

98

Feroze Mahmood, Rajiv Juneja, and Khurram Owais

Chapter 6

ANATOMICAL VARIANTS AND ULTRASOUND ARTIFACTS

125

Katherine Grichnik, Wendy L. Pabich, and AtifY. Raja

2.

AsSESSMENT OF CARDIAC STRUCTURE AND FUNCTION

Chapter 7

ASSESSMENT OF LEFT VENTRICULAR SYSTOLIC FUNCTION

159

Undo D. Gillam, Konstantinos P. Koulogiannis, and Leo Marcoff

Chapter 8

LEFTVENTRICULAR DIASTOLIC FUNCTION

176

Alina Nicoara and Wanda M. Popescu

Chapter 9

RIGHT VENTRICULAR FUNCTION

214

Timothy M. Maus, Dalia A. Banks, Rebecca A. Schroeder, and Jonathan B. Mark

Chapter 10

MITRAL VALVE Johannes van der Westhuizen andJustiaan Swanevelder

237

iv I Contents Chapter 11

AORTIC VALVE

264

Mark A. Taylor, Saket Singh, and Christopher A. Troianos

Chapter 12

TRICUSPID AND PULMONIC VALVES

304

George II. Moukarbel Antoine B. Abchee, and Chakib M. Ayoub

Chapter 13

EPICARDIAL ECHOCARDIOGRAPHY AND EPIAORTIC ULTRASONOGRAPHY

327

Stanton K. Sheman and Kathryn E. Glas

3.

CLINICAL ECHOCARDIOGRAPHY

Chapter 14

MITRAL VALVE REPAIR

341

Ghassan Sleilaty, lssam El-Rossi and Victor Jebara

Chapter 15

PROSTHETIC VALVES

365

Brandi A. Bottiger, Blaine A. Kent, Joseph P. Mathew, and Madhav Swaminathan

Chapter 16

AORTIC SURGERY AND ATHEROMA ASSESSMENT

413

Madhav Swaminathan andJoseph P. Mathew

Chapter 17

ASSESSMENT OF MECHANICAL CIRCULATORY SUPPORT DEVICES

435

J. Mauricio Del Rio, Carmelo A. Milano, and Alina Nicoara

Chapter 18

THORACIC TRANSPLANTATION

466

Sharon McCartney. Susan M. Martinelli, and Priya A. Kumar

Chapter 19

TRANSESOPHAGEAL ECHOCARDIOGRAPHY FOR CONGENITAL HEART DISEASE

486

Stephanie S. F. Fischer and Mathew II. Patteril

Chapter 20

CARDIAC MASSES AND PERICARDIAL PATHOLOGY

527

Nikolaos I. Skubas, Anne D. Cherry, and Manuel L Fontes

Chapter 21

VENTRICULAR DISEASES

548

Mahesh Prabhu, Chandrika Roysam, and Stanton K. Sheman

Chapter 22

NONCARDIAC SURGERY

578

Stefaan Bouchez, Svati H. Shah, and Patrick Wouters

4.

SPECIAL TOPICS

Chapter 23

THREE-DIMENSIONAL ECHOCARDIOGRAPHY Alina Nicoara, Renata G. Ferreira, and G. Burkhard Mackensen

611

Contents I v

Chapter24

STRAIN AND STRAIN RATE IMAGING

649

Kimberly J. Howard-Quijano and Aman Mahajan

Chapter 25

TRAINING AND CERTIFICATION IN PERIOPERATIVE TRANSESOPHAGEAL ECHOCARDIOGRAPHY

669

Madhav Swaminathan

Chapter 26

ESTABLISHING AND MAINTAINING A QUALITY PERIOPERATIVE TEE SERVICE

678

Christopher A. Troianos, Bryan P. Noorda, Shahar Bar-Yosef, Rebecca A. Schroeder, and Jonathan B. Marl
.-1.2 mls. (e.g., regurgitant jets, stenotic valves).

Color Flow Doppler Color flow Doppler is a pulsed US technique that color-codes Doppler information and superimposes it on a 2D image, providing information on the direction of flow and semiquantitative information on the mean velocities of flow. It has the characteristics of pulsed wave Doppler (range discrimination and aliasing). Color flow Doppler uses packets of multi· ple pulses (3 to 20 per scan line), and therefore has a low temporal resolution (Fig. 1-9). It then employs

spectral analysis methods to estimate the mean vdocity at each depth. The information on the direction

FIGURE 1-9. Characteristics of color flow Doppler.

PHYSICS OF TWO-DIMENSIONAL AND DOPPLER IMAGING I 11

. . .-... t

_;

velocity

Nodopplershlft _____.

(Nyquist limit)

··--1

-

'\,.

\.

FIGURE 1-10. Characteristics of color flow maps.

of flow and the magnitude of the Doppler shift are displayed as color maps, which can be ve/Qdty maps or varilln" maps (Fig. 1·10). A variance map contains information on the quality of flow (i.e., laminar vs. turbulent); however, turbulent flow and signal aliasing will result in an apparent wide range of vdocities. Also, in the case of color Bow Doppler, aliasing may introduce confusion as to the direction of flow. Color flow and spectral Doppler are set as a high-pass filter to eliminate tissue motion artifacts. A typical (but not uniform) convention for color Doppler velocity maps is for red to indicate flow toward the probe and fur blue to indicate flow away from the probe (BART= Blue Away, Red Toward). A region that is black on color flow Doppler imaging represents an area where there is no measured Doppler shift.

BIOEFFECTS US bioeffect:s include thmnal 4/'tcts and cavitation. In addition, mechanical effects (Vibration) may be of concern. Thermal bwtjftas consist of a temperature elevation resulting from the absorption and scatter· ing of US by biologic tissue and is related to beam intensity (tbe spatial peak and temporal average [SP'TA] intensity). The SPTA limits are 100 mW/cm2 fur unfocused beams and 1000 mW/cm2 fur fucwed beams. Cavittllirm resulu from the interaction of US with microscopic gag bubbles. Stable cavitation refer& to forces that cause the bubbles to contract and expand. Transient cavitation results in breaking the bubbles and releasing energy, producing perhaps more pronounced c£rccts on tissues at tbe microscopic level. The mechanical irulex (Ml), a calculated and unitless number, is used to convey the likelihood of bioef.. fects from cavitation. At low MI ( 1) sound beams result in bubble disruption (extreme nonlinear behavior). The U.S. Food and Drug Administration (FDA) limits the maximum intensity output of cardiac ultrasound systems to less than 720 W/cm2 due to con~ cerns of possible tissue and neurological dam.age from mechanical injury.

REVIEW QUESTIONS1-3,s

Basics of Ultrasound Select the one best answer for each item. 1. Which of the following is not an acoustic variable? a. Pressure b. Density c. Distance d. Intensity 2. Which of tbe following sound wave frequencies is ultrasonic? a. lOHz b. lOMHz c. lOkHz d. 10,000 Hz

3. An increase in tbe strength of tbe US pulse will increase: a. Frequency b. Intensity c. Pulse duration d. Pulse repetition &cquenc:y 4. If imaging depth decrease&, pulse repetition frequency: a. Decreases b. Does not change c. Increases d. Varies

12 I CHAPTER 1 5. An example of a Rayleigh scatterer is the: a. Red blood cell

b. Kidney c. Mitral valve d. Pericardium 6. If the frequency is doubled, the period: a. Increases two-fold b. Decreases c. Does not change d. Increases ten-fold 7. The wavelength in soft tissue of sound with a frequency of 2 MHz is: a. 6.16mm b. 3.08mm c. 1.54 mm d. 0.77mm 8. The speed of sound is slowest in: a. Air b. Fat c. Soft tissue d. Bone 9. Which of the following parameters of sound are determined by the sound source and the medium? a. Frequency b. Wavelength c. Amplitude d. Propagation speed 10. Reflection occurs when the two media at the boundary have: a. Identical acoustic impedances b. Different acoustic impedances c. Identical densities and propagation speeds d. Different temperatures 11. All of the following are true of refraction except. a. Is a change in direction of wave propagation when traveling from one medium to another b. Occurs when there are different propagation speeds and oblique incidence c. Is described by Snell's law d. Occurs with different propagation speeds and normal incidence 12. A sound beam strikes the boundary between two media at an incident angle of 45 degrees and is partly reflected and transmitted. If medium A has an impedance of 1.25 MRayls and a propagation speed of 1540 m/s and medium B has an impedance of 1.85 MRayls and a propagation speed of 2.54 km/s, what is the angle of reflection? a. 4 5 degrees b. 30 degrees

c. 60 degrees d. 15 degrees 13. A sound beam strikes the boundary between two media at an incident angle of 45 degrees and is partly reflected and transmitted. If the propagation speed of the second medium is slower than the propagation speed of the first medium, then the transmission angle is: a. Equal to the incident angle b. Greater than the incident angle c. Less than the incident angle d. Cannot be determined 14. A sound wave leaves its source and travels through a liquid. If the speed of sound through that liquid is 600 m/s and the echo returns to the source 1 second later, at what distance is the source from the reflector? a. 1540 m

b. 770 m c. 600 m d. 300m 15. The amplitude of a wave is: a. The difference between the average and maximum (or minimum) values of an acoustic variable b. Determined initially by the medium c. Altered by the sonographer d. Twice the average amplitude 16. Intensity is inversely proportional to: a. Beam area b. Power c. Amplitude d. Amplitude squared 17. The speed of sound in a medium increases when: a. Elasticity of the medium increases b. Density of the medium increases c. Stiffness of the medium decreases d. Stiffness of the medium increases 18. Increasing the frequency of a transducer: a. Increases wavelength b. Improves axial resolution c. Increases depth of penetration d. Increases pulse duration 19. Propagation speed: a. Can be changed by the sonographer b. Is an average of 1540 km/sin soft tissue c. Is slower in a liquid than in a solid d. Is determined by the sound source 20. Attenuation of an ultrasound beam results from: a. Absorption b. Reflection

PHYSICS OF TWO-DIMENSIONAL AND DOPPLER IMAGING I 13 c. Scattering d. All of the above 21. Compared with backscatter, specular reflections are: a. Diffuse b. Random c. Well seen when sound strikes the reflector at 90 degrees d. Occur when the wavelength is larger than the irregularities in the boundary 22. Pulsed ultrasound is described by: a. Duty factor b. Repetition frequency c. Spatial length d. All of the above 23. Pulse repetition frequency: a. Is determined by the sound source and the medium b. Can be changed by the sonographer c. Increases as imaging depth increases d. Is directly proportional to the pulse repetition period 24. When a sound beam strikes a reflector at 90 degrees incidence, it is considered: a. Obtuse b. Oblique c. Normal d. Acute 25. Sound waves can be characterized as: a. Electrical b. Transverse c. Longitudinal d. Spectral

Ultrasound Transducers Select the one best answer for each item. 1. Which piezoelectric effect does an US transducer use during the transmission phase? a. Doppler effect b. Reverse piezoelectric effect c. Direct piezoelectric effect d. Indirect piezoelectric effect 2. The most common piezoelectric material currently used includes all of the following except: a. Lead

b. Zirconate c. Titanate d. Tourmaline 3. The optimal thickness for the matching layer as a fraction of the wavelength is:

a. 1/8 b. 114

c. 1/2 d. 3/4 4. All of the following are true of linear switched or sequential arrays except: a. Produces a rectangular image display b. Defective crystal creates a line of dropout from top to bottom c. Has a fixed transmit focus d. Elements are fired in a sequence to create an image 5. In a phased array transducer, beam steering and focusing are produced by: a. Manually rotating the transducer b. Mechanically rotating the transducer c. Changing the timing of pulses to the piezoelectric elements d. Changing the resonant frequency of the piezoelectric elements 6. In an M-mode tracing, the x-axis represents: a. Depth b. Time c. Amplitude d. Frequency 7. The damping material in an ultrasound transducer increases the following: a. Pulse duration b. Spatial pulse length c. Duty factor d. Bandwidth 8. The region or zone between the transducer and the focal point is known as the: a. Farzone b. Fresnel zone c. Fraunhofer zone d. Focal zone 9. At the focus, the beam diameter is: a. One-fourth the transducer diameter b. Half the transducer diameter c. Double the transducer diameter d. Equal to the transducer diameter 10. In a linear phased array transducer: a. Image shape is a blunted sector b. Steering is mechanical c. Focusing is electronic d. A crystal defect produces a vertical line dropout 11. All of the following statements are true regarding the advantages of the backing material except: a. It decreases the Q factor b. It increases the spatial pulse length

14 I CHAPTER 1 c. It improves axial resolution d. The backing material decreases the transducer's sensitivity to reflected echoes 12. The quality factor {Q factor) is defined as: a. Bandwidth I Resonant frequency b. Bandwidth I Nyquist limit c. Nyquist limit I Resonant frequency d. Resonant frequency I Bandwidth

Instrumentation Select the one best answer for each item. 1. The US modality providing the best temporal resolution is: a. Amode b. B mode c. Three dimensional d. M mode 2. Increasing transducer output: a. Creates identical changes in the image as an increase in overall gain b. Cannot be controlled by the sonographer c. Causes no change in the brightness of the image d. Decreases the energy output of the transducer 3. Which of the following is used to create an image of uniform brightness from top to bottom? a. Compression b. Time gain compensation c. Demodulation d. Overall gain 4. The ability to distinguish two objects that are parallel to the US beam's main axis is called: a. Axial resolution b. Lateral resolution c. Transverse resolution d. Azimuth resolution S. If the US image shows no weak reflectors on the image, the best corrective action is to: a. Increase overall gain b. Increase the transducer output power c. Decrease the reject level d. Use a high-frequency transducer 6. The principal display modes for ultrasound include: a. Mmode b. Amode c. B mode d. All of the above 7. Temporal resolution can be improved by: a. Using multifucus b. Using a wide sector

c. Minimizing line density d. Maximizing depth of view 8. Components of an US system include: a. Pulser b. Receiver c. Master synchronizer d. All of the above 9. Lateral resolution can be increased by: a. Increasing beam diameter b. Decreasing transducer frequency c. Focusing d. Increasing gain

Principles of Doppler Ultrasound Select the one best answer for each item. 1. The difference between the transmitted and reflected frequencies is known as the: a. Bernoulli equation b. Doppler principle c. Doppler shift d. Gorlin equation 2. Velocity is defined by: a. Magnitude b. Direction c. Neither d. Both 3. When the angle between the sound beam and the direction of motion is 90 degrees, the measured velocity is equal to: a. True velocity b. Zero c. 20% of true velocity d. 50% of true velocity 4. Current spectral analysis is achieved by: a. Fast Fourier transfurm b. Multifllter analysis c. Zero-crossing detector d. Time interval histogram S. Modal velocity represents: a. Average Doppler velocity b. Greatest amplitude of returned Doppler shift c. Maximum Doppler velocity d. None of the above 6. Wall motion-induced frequency shifts are: a. High amplitude, low velocity, low frequency b. Low amplitude, low velocity, low frequency c. High amplitude, high velocity, high frequency d. High amplitude, low velocity, high frequency

PHYSICS OF TWO-DIMENSIONAL AND DOPPLER IMAGING I 15

7. Doppler wall motion fdters are: a. Lowpass b. High pass c. Zero pass d. Onepass 8. The maximal detectable freque.acy shift. or one-half of the PRF, is known as: a. Doppler effect b. Propagation speed c. Nyquist limit d. Peak Doppler shift 9. The following pulsed Doppler spectral display demonstrates:

.=·-z-~ ...:•:

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a. Normal map b. Velocity map c. Variance map d. Aliased map

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12. The color map shown here is a:

13. The color map shown here is a:

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i~

Ee~·;

a. Reverberation b. .Aliasing c. Mirroring d. Side lobe

10. Color flow Doppler measw:es the: a. Peak velocity b. Mean velocity c. Modal velocity d. Instant2neous velocity 11. When color flow Doppler is used, the number of US pulses per scan line is called: a. Line density b. Fwnerate c. Nyquist limit d. Packet size

a. b. c. d.

Normal map Velocity map Variance map Aliased map

16 I CHAPTER 1

14. In the figure, the anow points

to

a region (black)

wbcrc:

a. There is no flow b. There is no Doppler shift c. There is turbulent ffow d. There is laminar flow

15. A color Doppler examination is performed with the color map shown. If a red blood cell is traveling perpendicular to the direction of the sound beam, the color tha.t will appear on the image for tbia red blood ccll is:

16. If the alWing velocity of the color scale shown here is 40 emfs, laminar flow toward the probe at 50 cm/a would appear:

a. Red

b. Blue c. Yellow

d. Green 17. When a Doppler shift ia displayed above the zero basdine: a. Reflected frequency .is less than the transmitted frequency b. Red blood cclls arc moving away from the transducer c. The sound source and reflector are approaching

each other

d. It .i5 called a negative Doppler shift 18. Continuous wave Doppler: a. Cannot mcaswe very high velocities b. Transmits and tcccives Uiuasound constantly c. Is prone to aliasing a.rtifu:t d. Is character.iud u a wid~bandwidth tranaducer 19. The Doppler spccttal display gt'2phically demon-

strates: a. Direction of blood flow b. Vdocity of blood flow c. Duration of blood flow d. All of the above a. Red

b. Orange c. Black

d. Yellow

20. A 5-MHz transducer with a pulae repetition fre.. quency of 5600 Hz is imaging to a depth of 5.6 cm. The Nyquist frequency .is: a. 2.8MHz b. 2.8 dB

PHYSICS OF TWO-DIMENSIONAL AND DOPPLER IMAGING I 17 c. 2.8kHz

d.. 2500 Hz 21. Compared with pulsed imaging (2D), pulsed wave Doppler: a. Causes less acoustic exposure b. Has tower output power c. Use& shoner pulse repetition periods d.. Uses shoner pulse lengths 22. Color Doppler: a. Report& average vdocities

b. Use& continuous wave US c. Does not provide range resolution d. Is not subject to aliasing 23. The following principle is true of color Doppler imaging: a. Rtd always represents flow toward the transducer b. Turbulent flow is indicated as black c. Blue always .indicates flow away from the transducer d. Color Doppler examinations tend to have lower temporal resolution 24. Blood flow .in the imaged vessd is moving (as labeled on the image) from: a. Right to left b. Right to left and then left to right c. Left to right d. Left to right and then right to left

c. Spatial average temporal peak (SATP) d. Spatial average temporal average (SATA)

2. Which of the following modalities has the lowest intensity value? a. Pulsed wave Doppler b. Continuous wave Doppler c. M rn.ode/B mode d. All of the above have the same intensity 3. C.Ontraction and ei;pans.ion ofgas bubbles is known as: a. Transient cavitation b. Stable cavitation c. Attenuation d. Panide motion 4. US bioeffects can be cawed by all of the following except: a. Thermal effects b. Mechanical effects c. Scan conversion d. Cavitation 5. A number developed to predict the likd.ihood of cavitation-induced bioeffccts is called: a. Duty factor b. Mechanical index c. Pulsatility .index d. Resistivity index 6. Acoustic exposure to the patient is increased by: a. Incn:ase .in receiver gain b. Dec.rease in pulse repetition frequency c. Application of reject d. Increase .in examination time

REFERENCES I. Edelman SK. Untinndrulint Ulmtmnul Phpif:t. 3rd ed. Wood· lands, TX: Education for die Sonographlc Profcaslo11ial, Inc.; 2004. 2. Edelman SK. U"""'11unJ Physia ltnd IMnRnnlt41io11. Woodlancl.. TX: Educ;adon lOr die Sonographlc Profuulonal, Inc.; 2007.

Bioaffects

Select the one but answer for each item. 1. The most relevant intensity heating is:

with respect

a. Spatial peak temporal average (SPTA) b. Spatial peak temporal peak (SPTP)

to

tissue

3. Weyman AE. Princi/la aNl Prtzai&e of&hot4rrli"f!t1Pby. Philadelphia, PA: Lea&: Pebigcr, 1993. 4. Jungwinh B, M~ GB. R.eal·tlme 3-dlmenslo11al edio· carcl.iography l.n the operating room. Smt/11 O.wlillthtJrt1e V.An.mh. 2008;12(4):248-264. 5. Salgo IS. T~111io11al cchocanliographic tt.chnology. CttnlWI Ciin. 2007;25(2):231-239. 6. Ca!dahl K. Kart.am E, IJclbctg J, et al. New concept In cchocardiography: harmonic imaging of tissue without the usc of conuast agent. Lwwer. 1'98;352(9136):1264-1270.

The TEE Probe Joseph A. Sivak, Jose Rivera, and Zainab Samad

STRUCTURE AND DESIGN Transesophageal echocardiogtaphy (TEE) presents a uni'lue opportunity to overcome the limitations posed by chest wall acoustic windows while allowing visualization of cardiac structures with greater spatial ~lution. Since its first reported use to evaluate intracardiac flow in 1971 and to visualize cardiac structures in 1976, the TEE probe has undergone remarkable technological advancement in terms of imaging capability and probe structure and design. l.2 The TEE probe used by Frazin et al1 consisted of an M-mode transducer attached to a coaxial cable. Souquet et al3 then rcponed suc:ccssful use of a phased array transducer attached to the end of a gastroscope, which, in addition to producing tw diagnose traumatic disruption of the aorta, including intimal flaps, pseudoancurysms, dissections, and ini:raluminal or e:x:tralwninal bematonw, and gross dis&ec:tions with identification of false and true lumens. However, the sensitivity and specificity of TEE were lower than those of aortography. most likely due to the inability of TEE to inlage the ug~ third of the ascending aorta and the aonic arch. · 9 Even though some forms of aortic pathology arc not compleu:ly assessed with TEE, this technique is very valuable in ruling out aonic dis.section. Yalcin and coworkers reported TEE to be 98% sensitive and 99% specific fur detection of aonic dissection, and a 2006 meta-analysis of 10 studies ~ortcd similar results (98% sensitive, 95% specific). 1 In addition, of significant importance is the fact that TEE is often safer than other inlaging modalities in hemodynamically unstable patients, as it can be performed at the bedside. Overall, despite its known deficiencies, TEE remains the first-line test fur evaluation of the aorta due to its portability. low cost, low level of invasiveness, rapidity, and low complication rate. In the presence of a negative study, however, it is often necessary

to proceed to further radiological imaging if the clinical suspicion of aortic pathology remains high.18,21-23

Risks of the TEE Procedure TEE is generally a well-tolerated and safe procedure. However, because of its semi-invasive nature, "blind intubation," and the need fur concomiwit sedation, the potential fur serious complications exists. It is crucial fur the procedure team to know potential complications of TEE so that the risks and benefits of the procedure can be discussed and the patient assessed fur any preexisting conditions that may increase the risk of the procedure. Figure 2-3 highlights the anatomical locations where reported injuries associated with TEE occur. In ambulatory, nonoperatlve settings, reported rates of major complications ofTEE range from 0.2% to 0.5%. In one European multicenter survey of 10,419 TEE e:wninations, 90 examinatioru (0.88%) had to be interrupted due to patient intolerance of the probe (65 cases) or because of pulmonary (8 cases), cardiac (8 cases), bleeding complications (2 cases), and 7 other causes. One of the bleeding complications was related to csop~cal infiltration of a lung tumor and proved to be f.u:af (mortality rate 0.0098%). Of note,

l.Myngnl:

·vocal cord trauma ·airway comprl!!ulon

• tradleal intubation

1E111apln19•I: - lacer.rtfon ·perforation ·false passage (dlvertkulum)

GMtrlc: • lflCel'ltfon ·perforation ·bleeding

FIGURE 2-3. Sites of potential injury.

22 I CHAPTER 2

Tonslllarfauces

._-I-m

lEE probe lodged In

Pifif'orm fOSSll

probe lodged In

left plrlform fossa

Demi I glnglval

Esophagus

FIGURE 2-f.. Probe malposltfon examples.

a majority of the cases in this survey were outpatients who did not receive intravenous sedation for the TEE procedw:e.24 In the operative setting, manipulation of a TEE probe in an inrubated patient under general ancsthcsia carries additional risk, but rcponcd rates of major complications are similar to nonsurgical patients and range from 0.2% to 1.2%.25 Several fu.ctors may inacase risk, including the inability of the patient to swallow in order to fa.Cilitate probe insertion and the patient's inability to alert the operator to uncomfortable, possibly injurious probe manipulations. The most dreaded complication of TEE is upper gutrointestinal (GI) tract perforation, which has a reported incidence ofabout 2 per 10,000 paticnts26 and is associated with scvcrc morbidity and mortility.27 It has been reported that 20% of pcrfurations occur during insertion in the hypoph.arynx, and an understanding of the anatomy of the hypoplwynx and potential

pitfalls during insettion is crucial to limit risk of injury (Fig. 2-4). If the probe is not centered during insertion, it can become lodged in one of the pyriform sinuses. where further advancement of the probe could lead to injury to dtis area. or can cause severe flexion of the probe, which could lead co injury during removal The upper esophagus at the 1.cvcl of the aic:opharynx is also susceptible to injury due to the potential for spasm or hyperttophy of the aicoplwyngeal muscle and narrowing of the space secondary to cervical spine disease.25 Manipulation of the probe during the study also carries a small but real risk of injury. One area of the upper GI tract that is particularly vulnerable to injury is the gutrocsophageal (GE) junction. When performing transgutric views, it is important to make sure that the probe tip is past the GI junction into the gastrum. Significant flexion of the probe at the GE junction can cause mucosa! disruption or Mallory-Weias tears.28 The

THE TEE PROBE I 23 risk of upper GI perforation is increased in patients with GE pathology, such as a Zenker diverticulum, esophageal strictures or webs, esop~tis, esophageal mass, or other anatomical anomalies.2 Often the only indication of a potential problem is a history of dysphagia or odynophagia. If the patient has a history of significant gastritis or gastric ulcers, transgastric views should be obtained with caution. In perioperative procedures where the TEE probe sits in the esophagus for prolonged periods, it is important to freeze imaging and release flexion on the probe tip when images are not being acquired to avoid thermal injury or pressure ulceration of the esophagus.

Assessment of the Patient The contraindications for performing a TEE are based on the risk of respiratory compromise, esophageal injury, and bleeding. Given that the probe is typically advanced blindly, due diligence must be performed to ensure that the patient is not at a higher-than-normal risk for any of these complications. Absolute and rdative contraindications to TEE are outlined in Table 2-2. A comprehensive preprocedural assessment should include (1) the assessment of the patient by a physician; (2) ensuring that the patient has not taken any solids or liquids by mouth for 6 to 8 hours prior to the planned procedure; (3) documentation of an informed consent; (4) review of pertinent laboratory data, including coagulation and platelet studies; (S) review of medication and allergies; and (6) review of conditions that might increase procedural risk, including but not limited to history of sleep apnea, unexplained dysphagia, history of chest irradiation, esophageal tumors, varices, strictures or past surgeries, chest radiation, dysphagia, and other esophageal abnormalities. PROBE INSERTION

Insertion of the 1EE Probe in Patients Under General Anesthesia. In patients who undergo TEE as part of their operative procedure, the TEE probe should be introduced into the esophagus after the induction of general anesthesia and tracheal intubation. After the position of the endotracheal tube has been confirmed and the tube secured, a mouth guard should be placed between the patient's teeth. The probe tip can then be lubricated with ultrasound gel and while holding it like a pencil, the probe can be inserted into the oropharynx through the mouth guard. An initial mild resistance may be encountered by the cricopharyngeus muscle, but this should be easily overcome. If there is further resistance, the probe should be withdrawn, centered, and reintroduced. If probe insertion is unsuccessful after two or three attempts, direction laryngoscopy should be employed to aid esophageal

Table 2-2. Contraindications to TEE Absolute

RelMive

Contraindications

Contraindications

Perforated viscous

Restricted cervical mobility (severe arthritis or atlantoaxial joint disease) History of significant radiation to neck and chest

Esophageal pathology (stricture, trauma, tumor, scleroderma, MalloryWeiss tear, diverticulum) Active upper GI bleeding Recent upper GI surgery Esophagectomy, esophagogastrectomy Lack of informed consent

History of GI surgery Esophagitis History of dysphagia Bleeding diathesis (coagulopathy, thrombocytopenla) Barrett's esophagus or peptic ulcer disease Symptomatic hiatal hernia Esophageal varices

Adapted with permission from Hilberath JN, Oakes DA, Sheman SK: Safety of transesophageal echocardlography, J Am Sac Echocardiogr. 201 ONov;23(11):1115-1127.

intubation. Although the use of direct laryngoscopy is not usually necessary for probe placement, one study did show that its use results in successful placement with fewer attempts and reduces complications like odynophagia and minor oropharyngeal injuries.29

Insertion of the TEE Probe Without General Anesthesia. Before starting the procedure, careful preparation is necessary to ensure patient safety. The necessary items include a functioning suction apparatus, oxygen with tubing and facemasks, emergency medications, access to a defibrillator, and continuous electrocardiogram (ECG) monitoring. Peripheral intravenous access is also necessary before starting the procedure. The mouth should be examined for loose teeth, and dentures should be removed. Although it is possible to perform a TEE on an unanesthetized, cooperative patient, use of light-to-moderate sedation with agents such as midazolam, fentanyl, or propofol improve comfort. Prior to administration of sedation, the mouth and oropharynx are anesthetized using liquid viscous lidocaine and lidocaine spray. Because lidocaine dulls the gag reflex and impairs swallowing, the patient should not eat or drink for 2 hours after the procedure. The patient can be positioned in the supine or the left lateral decubitus position. It is preferred to have the patient lie on their left side, with the lower (left) hand rested under a pillow or the patient's head and the upper (right) hand resting on the patient's side. The bed should

24 I CHAPTER 2 be typically at a 10% to 20% incline, with the legs in a comfurtable position and the neck slightly flexed. Befure administering sedation, a mouth guard is placed in the patient's mouth, as the jaw tends to become rigid and difficult to manipulate once the patient is sedated. Befure inserting the probe, it is important to inspect it for damage, making sure there are no sharp edges, checking that the controls properly flex and angle the tip, and that an image is displayed as the probe tip touches ultrasound gel. Prior to insertion, the probe should be straightened, with the control wheels unlocked. The end of the probe is coated with a thin layer of sterile ultrasound jelly, which serves to both facilitate insertion of the probe and improve contact with the esophagus. To facilitate probe insertion, the index finger of the left hand should be inserted into the oropharynx (outside the mouth guard) and the posterior pharynx palpated to ensure there are no deviations from normal anatomy. The index finger can also be used to push the posterior aspect of the tongue and epiglottis forward. At the same time, the TEE probe is inserted into the oropharynx with the left finger helping to keep the probe centercd and guiding it into the esophagus. Often some resistance is encountered as the probe passes through the hypopharynx, caused by the cricopharyngeus muscle. If this occurs, gentle forward pressure should be applied to the probe while the patient is asked to swallow. For many patients, this verbal instruction is all that is requiredswallowing will close the vocal cords and relax the cricopharyngeus muscle. Flexing the patient's neck or slight flexion of the probe tip may also assist its passage past the base of the tongue. Neck flexion also prevents stretching of the esophagus, a condition that might increase the risk of a mucosa! tear or perforation. It may also be helpful to hold the small wheel on the housing at a neutral position to avoid undesirable lateral bending during probe insertion. The large wheel, controlling flexion/extension, should never be locked. If there are feeding or nasogastric tubes in place, the TEE probe can usually be placed alongside these devices, but often they must be removed to allow adequate imaging. If further resistance is encountered, the probe should be withdrawn, centered, and reintroduced into the esophagus. It should be kept in mind that unsuspected pathology may impede advancement of the probe. Any unusual resistance to probe insertion should prompt abandonment of the procedure. Failure to place the probe is rare. Chee et al found a 1.2% rate of failure among 901 TEE exams. 30 In another review, 98.5% of failures were due to lack of cooperation or lack of operator experience, whereas only 1.5% were due to anatomical abnormalities.2'' Other authors have identified prominent vertebral spurs associated with cervical spondylosis as a common cause (16 of 40) of failure of probe placement.3l In intubated patients,

briefly deflating the endotrachca.l tube cuff should be considered, as this may ease passage of the probe tip.32 When unusual resistance is encountered during attempts to advance or withdraw the probe, the physician should consider that the tip may have "folded" 180 defrees onto itself, so-called "buckling" of the probe.3 This mechanical problem should be suspected when probe movement is difficult, image quality is very poor, and the control wheels are bound and difficult to move. If the physician believes this has occurred, the probe should be advanced gently into the stomach, the tip straightened, and the probe removed and inspected. Under the rare circumstance that the TEE probe cannot be moved without exerting undue force, a radiograph may help determine the probe position and guide the next intervention. In very unusual circumstances, if the deflector mechanism is completely jammed inside the patient and all efforts to release it have failed, the probe should be removed from the unit, and the entire probe shaft should be cut with heavy-duty pliers or other suitable tool. This will release the deflecting mechanism, allow the tip to straighten, and facilitate probe removal.

CARE/STORAGE Proper care, disinfection, and storage of the TEE probe is essential for patient safety, as well as to extend the life of the probe. Modern TEE probes cost anywhere from $30,000 to $60,000, and a simple careless mistake such as submerging the multipin connector in cleaning solution can cost over $10,000.

Proper Cleaning Technique Because TEE is a semi-invasive procedure and the probes are reusable, there is a real potential for transmission of infection (Table 2-3). Although there are

Table 2-3. Infectious risks Closs-infection from patient to patient and patient to staff

Bacteria-Helicobacter pyfori, Pseudomonas oeruginoso, Salmonella species, Mycobacterium species Viruses-Hepatitis Band C, human immunodeficiency virus Prions-Creutzfeldt-Jakob disease

Contamlnlltion of patients from the decontamlnldlon

procedure Bacteria-Pseudomonas aeruginosa, J.egionella pneumophila, Mycobacterium species Reproduced with permission from Kanagala P, Bradley(, Hoffman P, et al: Guidelines for transoesophageal echocardiographic probe cleaning and disinfection from the British Society of Echocardiography, Eur J Echocardiogr 2011 Oct;l 2(1O):il7-i23.

THE TEE PROBE I 25

no concrete data for infection rates with TEE procedwe&, it i& piuwned that the infection rates and implicated infectious organisms associated with TEE would be comparable to upper GI endoscopy or bronchoscopy (1 in 1.8 million studies).33 Proper deaning and disinfection of the TEE probe after each procedure is thus essential to preventing transmissible disease from the procedure. Sterilization of the TEE probe is impractical and not warranted because the TEE probe does not penetrate sterile areas of the body. Cleaning and disinfection of the probe is a multistep pro~ (Fig. 2-5) that starts at the patient's

bedside aa soon as the procedure is over. The probe tip and shaft should be wiped sequentially starting from the leading end, while being introduced into a biohazard bag, with a single-use sponge presoaked in a detergent solution to remove gross contamination. A similar second wipe should be used to wipe off the remaining parts of the probe, including the handle and controls, cord, and the nonimmersible connector.33 The second wipe disinfects contamination from the operator's hand. The probe should then be covered and transferred to the designated decontamination room where it should be visually inspected for any damage.

A

B

C

D

FIGURE 2-5. Probe disinfection process. (A} Protective attire. (8) Pre-soak wipe of handle and pin connector. Note that pin connector has protective cover in place. (C) Dilute detergent in basin per manufacturer's instructions. (D) Immerse 'TEE probe, but not the connector, in detergent solution for the specified time period (typically 3 to S minutes). (E) Post-immersion rinse and {F} dry. (G) Automated endoscope reprocessor for further disinfection. (H) Protective covering applied to probe and stored in clean 'TEE closet

26 I CHAPTER 2

E

F

G

H

FIGURE 2-5. (Continued) Decontamination rooms should have demarcated "dirty" and "clean" areas so that nondecontaminated "dirty" probes are not inadvertently confused with decontaminated "clean" probes. The "dirty" probe should be immersed in a wash bin utilizing a detergent made up to the dilution and contact times recommended by the manufacturer. The choice of a detergent solution is guided by its microbicidal. activity and compatibility with the TEE probe materials. Ca.re should be tahn to prevent the pin connector from becoming immersed with the probe. After this initial decontamination step, probe disinfection is then pcrfurmed via an automated endoscope reprocessor (AER). In addition to deaning and disinfection, the Intersodetal Accreditation Commission for echocardiography recommends that the structural and electrical integrity of the probe be checked between each use, using an ult.rasowtd transducer leakage tester.~ Following disinfection,

the probe tip and shaft are placed in a diaposable protective sheath.

Proper Care and Storage Guideline documents advise against storing TEE probes in their delivery cases. This is because a suboptimally deaned probe, if placed in the delivery case, will contaminate the case, which might then become the nidus for cross-contamination of subsequent probes. In addition, a failure to fully suaighten the probe between studies may result in distortion of the probe shaft. Manufacturers typically recommend that the probes be stored fully straight, which can be achieved by hanging them in a locked cupboard. There is no time limit to storage of a clean probe with this type of setup. Table 2~4 presents general rules that should be followed to improve probe longevity.

THE TEE PROBE I 27

Table 2-4. Recommendations to promote probe longevity Inspect probe before each use • Integrity of seal connecting probe tip to shaft • Scratches or damage to probe tip and lens • Cracks. holes, or bite marks in bending rubber around shaft • Lost or damaged controls on TEE handle • Damage to cable or pin connector Routine maintenance • Proper cleaning and storage of probe between each use • Probe testing every six months to test each crystal within the array • Recoat and relabel TEE probe markers showing signs of fading During the procedure • Use of bite guards during procedures • Use of approved ultrasound gel • Freeze image or tum off transducer before connection or removal

REVIEW QUESTIONS 1. An adult TEE probe tip is approximately _ _ wide a. 10 mm b. 15 mm c. 20 mm d. 25 mm 2. The first docwnented use ofTEE was in: a. 1965

b. 1971 c. 1980

d. 1984 3. In general, TEE probes are capable of_ degrees of anteflexion and _ degrees of retroflexion a. 120, 60 b. 60, 120 c. 90, 45 d. 45, 90 4. Which of the following indications received an appropriateness score of 9 (most appropriate) in the 2011 appropriate use guidelines? a. Use of TEE as initial test when there is a high likelihood of a nondiagnostic TIE due to patient characteristics or inadequate visualization of relevant structures b. Evaluation for cardiovascular embolic source with no identified noncardiac source c. To diagnose endocarditis with a moderate pretest probability

d. Routine assessment of pulmonary veins in an asymptomatic patient status post pulmonary vein isolation S. Which of the following is the most common reason for performing a TTE in the surgical ICU? a. Refractory or unexplained hypotension b. Suspected endocarditis c. Evaluation ofventricular function d. Evaluation of pulmonary edema of uncertain etiology

6. The reported rate of upper GI tract perforation caused by the TEE procedure is: a. 1in1000 b. 1 in 100,000 c. 1 in 50,000 d. 1 in 5000

7. The

is located laterally to the pharynx and is a potential space for the probe to become lodged during insertion. a. Tonsillar fossa b. Piriform fossa c. Laryngeal fossa d. Epiglottic fossa

8. The rate of complications from the TEE procedure in the ambulatory setting is estimated to be: a. 1 in SOO

b. 1in1000 c. 1in2000 d. 1 in 5000 9. Which of the following is considered an absolute contraindication to performing a TEE? a. Atlantoaxial disease b. History of dysphagia c. Recent upper GI bleed d. Recent upper GI surgery 10. What percentage of GI tract perforations occur at the hypopharynx? a. 5% b. 20% c. 40% d. 60% 11. Which location in the GI tract is most susceptible to Mallory-Weiss tears from flexion of the probe? a. GE junction b. Gastric fundus c. Mid-esophagus d. Gastric body 12. Dysphagia can be a potential sign of which of the following GI tract abnormalities? a. Zenker diverticulum b. Esophageal strictures or webs

28 I CHAPTER 2 c. Esophagitis d. All of the above

13. How long should a patient be NPO prior to a TEE? a. b. c. d.

2hours 6hours 10 hours 16 hours

14. The muscle in the posterior pharynx that can cause some normal resistance when inserting the probe is the: a. Cricopharyngeus muscle b. Hyoglossus muscle c. Zygomaticus muscle d. Digastric muscle 15. Which of the following is recommended to be available at the time of the TEE procedure in a nonanesthetized patient? a. Peripheral N access b. Supplemental oxygen and suction devices c. Defibrillator d. All of the above 16. The oral use of benzocaine as a local anesthetic has been found to be a cause of: a. Methemoglobinemia b. Anaphylaxis c. Loss of taste d. All of the above 17. It is recommended that patients not eat or drink for _ hours after local anesthesia of the pharynx with topical lidocaine. a. 2

b. 4 c. 6 d. 8 18. Which of the following patient positions is preferred for intubation in an unanesthetized patient? a. Supine b. Prone c. Left lateral decubitus d. Right lateral decubitus 19. A modern TEE probe costs approximately: a. $10,000 b. $50,000 c. $100,000 d. $150,000 20. Which of the following pathogens can be spread from patient to patient if the TEE probe is not adequately cleaned? a. Pseudomonas aeruginosa b. Prions

c. Helicobacter pylori d. All of the above

21. Care must be taken to not allow which component of the TEE probe to be submerged during the disinfecting process? a. Probe tip b. Probe shaft c. Probe handle d. Pin connector 22. The proper dilution of detergent during the immersion portion of the disinfecting procedure is: a. 10 parts to 1 part water to detergent b. 100 parts to 1 part water to detergent c. 1OOO parts to 1 part water to detergent d. Specified by the detergent manufacturer 23. What is the longest a TEE probe can be properly stored before the disinfecting procedure needs to be repeated? a. 1 month b. 3 months c. 1 year d. There is no limit

True or False 24. The TEE probe should be sterili7.ed between each use. 25. The TEE probe transducer works at a higher sound wave frequency than standard chest wall transducers. 26. History of radiation to the neck and/or mediastinum is a risk factor for esophageal injury during TEE. 27. It is appropriate to use TEE to rule out left atrial appendage clot in a patient with atrial fibrillation who is not undergoing electrical or chemical cardioversion. 28. TEE probes should be disposed of when distance markers become faded. 29. TEE probes are capable of a higher degree of anteroflcxion compared to retroflex.ion. 30. All components of the TEE probe are fully waterproo£

REFERENCES 1. Fruin L, Talano JV, Stephanidcs L, et al. Esophagcal echocardiography. Circula#on. 1976;54:102-108. 2. Side CD, Gosling RG. Non-surgical assessment of cardiac function. Nil~. 1971;232:335-336. 3. Souquet J, Hanrath P, Zitclli L, et al. Transesophagcal phased array for imaging the heart. IEEE TrtZns BiD1md Eng. 1982;29:707-712. 4. Roclandt JR. Thomson IR, Vlertcr WB, et al. Multiplane uansesophageal echocardiography: latest evolution in an imaging rcvolution.]ASE. 1992;5:361-367. 5. Sengupta PP, Khandhcria BK. Transocsophageal echocardiography. Heart. 2005;91:541-547. 6. Fddman T, Wasserman HS, Herrmann HC, et al. Percutaneous mitral valve repair wing the edge-to-edge technique: &ix-month

THE TEE PROBE I 29

7.

8.

9.

10.

l 1.

12.

13.

14.

15.

16. 17.

18.

19.

results of the EVERESf Phase I Oinical Trial. JAm Co/i Omliol 2005;46:2134-2140. American College of Cardiology Foundation Appropriate Use Criteria Task F, American Society ofE, American Heart A, et al. ACCF/ASEJAIWASNC/HFSAJHRS/SCAI/SCCM/SCCT/ SCMR 2011 Appropriate Use Criteria fur Echocardiography. A report of the American College of Cardiology Foundation Appropriate Use Criteria Task Force, American Society of Echocardiography, American Heart Association, American Society of Nuclear Cardiology, Heart Failure Society of America, Heart Rhythm Society, Society fur Cardiovascular Angiography and Interventions, Society of Critical Care Medicine, Society of Cardiovascular Computed Tomography, Society fur Cardiovascular Magnetic Resonance American College of Chest Physicians.]ASE. 2011;24:229-267. American Society ofAnesthesiologists, Society of Cardiovascular Anesthesiologists Task Force on Transesophageal Echocardiography. Practice guidelines for perioperative transesophageal echocardiography. An updated report by the American Society of Anesthesiologists and the Society of Cardiovascular Anesthesiologists Task Force on Transesophageal Echocardiography. &mhesioloa. 2010;112:1084-1096. Mishra M, Chauhan R, Sharma KK, et al. Real-time intraopcrative tran.sc.sophagcal cchocardiography--how useful? Expericncc of 5,016 cascs.JCVA. 1998;12:625-632. Cicck S, Demirilic U, Kuralay E, et al. Transesophageal echocardiography in cardiac surgical emergencies. j Card Surg. 1995;10:236-244. Schulmeycr MC, Santdices E, Vega R, et al. Impact of intraoperative transesophageal echocardiography during noncardiac surgery. JCVA. 2006;20:768-771. Suriani RJ, Ncustein S, Shorc-Lesscrson L, et al. lntraopcrativc transesophageal echocardiography during noncardiac surgery. ]CVA. 1998;12:274-280. Feierman D. Case presentation: transesophagcal echocardiography during orthotopic liver transplantation-not only a different diagnosis, but different management. Livn' Tnuupl Surg. 1999;5:340-341. Brandt RR. Oh JK, Abel MD, et al. Role of emergency intraopcrative transcsophageal echocardiography. JASE. 1998;11:972-977. Colreavy FB, Donovan K, Lee KY, et al. Transesophageal echocardiography in critically ill patients. Crit Caw Metl. 2002;30:989-996. Heidenreich PA. Transesophageal cchocardiography (fEE) in the critical care patient. Cardiol Clin. 2000;18:789-805, ix. Skiles JA, Griffin BP. Transesophageal echocardiographic (TEE) evaluation of ventricular function. Carriiol C'lin. 2000;18:681-697, vii. Evangelista A, Avegliano G, Elorz C, et al. Transesophageal echocardiography in the diagnosis of acute aortic syndrome. ]CtJTtJSurg. 2002;17:95-106. Minard G, Schurr MJ, Croce MA, et al. A prospective analysis of transesophageal echocardiography in the diagnosis of traumatic disruption of the aorta.. f Trauma. l 996;40:225-230.

20. Shiga T, Wajima Z, Apfel CC, et al. Diagnostic accuracy of transesophageal echocardiography, helical computed tomography, and magnetic resonance imaging fur suspected thoracic aortic dissection: systematic review and meta-analysis. Arch Inurn Metl. 2006;166:1350-1356. 21. Yalcin F, Thomas JD, Homa D, et al. Transesophageal cchocardiography: first-line imaging fur aortic diseases. CCJM. 2000;67:21-28, 417-418. 22. Gendreau MA, Triner WR, Bartfleld J. Complications of transesophageal echocardiography in the ED. Am J Emerg Metl. 1999;17:248-251. 23. Stoddard MF, Longaker RA. The safety of transesophagcal echocardiography in the elderly. Am Heart]. 1993;125:13581362. 24. Daniel WG, Erbe! R, Kasper W, et al. Safety of transesophagcal echocardiography. A multiccnter survey of 10,419 examinations. Circu/4#on. 1991;83:817-821. 25. H.ilberath JN, Oakes DA, Shernan SK, et al. Safety of trans· esophagcal echocardiography.JASE. 2010;23:1115-1127; quiz 220-221. 26. Min JK, Spencer KT, Furlong KT, et al. Clinical features of complications from transcsophageal cchocardiography: a single-center case series of 10,000 consecutive examinations. ]ASE. 2005;18:925-929. 27. Dubost C, Kaswin D, Durantcau A, et al. Esophageal perforation during attempted endouacheal inrubation. J ThOTllC CanJjOVllSc Surg. 1979;78:44-51. 28. Dewhirst WE, Stragand JJ, Fleming BM. Mallory-Weiss tear complicating intraopcrative transesophageal echocardiography in a patient undergoing aortic valve replacement. Anesthesiology. 1990;73:777-778. 29. Na S, Kim CS, Kim JY, et al. Rigid laryngoscope-usisted in&ertion of transesophageal echocard.iography probe reduces oropharyngeal mueo&al injury in anestheti7.ed patients. AnestiMsroloa. 2009;110:38-40. 30. Chee TS, Quck SS, Ding ZP, et al. Clinical utility, safety, acceptability and complications of transoesophagcal cchocardiography (fEE) in 901 patients. Singt1pow Med f. 1995; 36:479-483. 31. Tam Jw. Burwash IG, Ascah KJ, et al. Feasibility and complications of single-plane and biplane vel'llus multiplane transesophageal imaging: a review of 2947 consecutive studies. Can J CardioL 1997;13:81-84. 32. Cote G, Denault A. Transesophagcal echocardiography-relatcd complications. Can]Anesthesiol. 2008;55:622-647. 33. Kanagala P, Bradley C, Hoffman P, et al. Guidelines for transoesophageal echocardiographic probe cleaning and disinfection from the British Society of Echocardiography. Eur J EchoctZrdiogr. 2011;12:il7-i23. 34. IAC Standards and Guidelines for Adult Echocardiography Accreditation. 2017. Available at http://www.intersocietal.org/ echo/standards!IACAdultEchocardiographyStandards2017. pdf.AcccssedJune 24, 2017.

Understanding Ultrasound System Controls Hillary B. Hrabakl Ashlee Davis, and David B. Adams

It is crucial for clinicians performing transesophageal echocardiographic (TEE) examinations to understand how the controls on an ultrasound machine alter the display. Without this knowledge, it is impossible to consistently optimize images, and unskilled manipulations may misrepresent diagnostic information and result in missed diagnoses. This chapter describes the controls found on most ultrasound machines, how they affect the image, and how they are used to optimize the ultrasound image. Table 3-1 presents the most commonly used controls for two-dimensional (2D) imaging.

PREPARING THE MACHINE After providing power to the machine itself, a TEE probe must be connected to the machine, register as compatible with the machine, and be selected from other possible transducer options. The basic parameters for the ultrasound examination may be defined by choosing an appropriate TEE preset. The preset provides a starting point for basic machine settings such as depth, gain, and image processing settings. The operator can adjust all the machine's variables from the initially fixed settings as needed. Adjustments to the preset can be saved permanently under a different name when desired. Patient identification (name and medical record number) and any other relevant information should be entered into the machine before beginning an exam. This includes date of birth, sex, the name of the person performing the examination, location, and a number of other qualifiers. The five most common modes used during TEE examinations are 2D gray-scale imaging, color Doppler, pulsed-wave (PW) Doppler, continuouswave (CW) Doppler, and three-dimensional {3D) imaging. The usual buttons to enable these modes are 2D, Co/or, PW, CW, and 3D, respectively. Other scanning modes, such as M-mode and angio, are often available but are minimally important in comparison. Fig. 3-1 is an example of two common ultrasound control panels. Although the number and layout of buttons and controls are different, there are many similarities. This chapter focuses on controls

that affect 2D imaging, color Doppler, pulsed-wave Doppler, and continuous-wave Doppler. Threedimensional imaging has become a fundamental addition to TEE, especially for the evaluation of the mitral valve. Basic controls and image display will be briefly discussed at the end of this chapter, and more indepth clinical examples will be discussed in Chapter 23. Research in two-dimensional speckle tracking echocardiography {STE) has been ongoing for many years and finally is finding clinical utility, especially in global longitudinal strain (GLS) assessment. GLS and other strain imaging techniques will he discussed in more detail in Chapter 24.

TWO-DIMENSIONAL IMAGING AND BASIC IMAGE MANIPULATION Two-dimensional gray-scale imaging is a type of B-mode imaging (B is for brightness) in which the various amplitudes of returning ultrasound signals are displayed in multiple shades of gray. Higheramplitude signals are closer to white, whereas loweramplitude signals are displayed closer to black. The many different shades of gray form an image or representative picture of the patient's cardiac anatomy. TEE probes generate a sector or pie-shaped display of gray-scale images, with the top portion of the sector showing the tissue closest to the transducer. Of the five modes, the 2D display mode is most commonly used and manipulated during a TEE examination. Two-dimensional imaging also provides a reference point from which to activate all three forms of Doppler {color, PW, and CW).

GAIN Overall gain or amplification is the first postprocessing function performed by the receiver and is the most important variable to adjust during a study. Overall gain controls the degree of amplification that returning signals undergo before display. By increasing gain, small voltages are changed into larger voltages by an operator-specified level of amplification. Gain is also the one control that is misused most often, with the

UNDERSTANDING ULTRASOUND SYSTEM CONTROLS I 31

Tobie 3-1. Commonly used controls for 20 Imaging

Amplifies retuming signals before display Selectively amplifies returning signals before display (horizontally) Selectively ampllfles returning signals before display (venlcally) Compression Changes the difference between the highest and lowest 7'celved amplitudes (shades of gray) Power Power(dB} Controls rate at which energy is propagated into an imaged medium Frequency Dependent on probe Detennines number of times/second a sound wave completes a cycle Alters the placement of the narrowed region that designates an area Focal zone Focal zone of Improved resolution Depth Depth Selects how shallow or deep an area Is Imaged Size, trackball Narrows or widens the image sector Sector size Magnifies a particular area of interest within the sector Zoom Zoom Stops or starts live imaging Freeze Freeze Freeze, callper, trace, enter, erase Quantifies features of a20 Image Measurement Harmonics Harmonics Uses frequencies created by the tissues, rather than the fundamental frequency, to create an Image Annotation Annotation Adds text or picture to image Abbreviations: 2D, two-dlmenslona~ dB, der the ccbocatdiographcr. The valve an roughly be divided into 1upporting structures (annulus. papillary muscles, and chordac tendineae) and leaflets (anterior and posterior). The mittal annulus is a saddle-shaped structure with two axes. The longer axis parallels the line of coaptation in the lower portion of the "saddle· and runs in a mostly mcd.ial-co-lateral orientation. The shorter axis, perpcndiculat to the line of coaptation, ruw between the high poinu of the "saddle" in a mostly anterior-to-posterior orientation. As seen in Fig. 4-17C, the anterior portion of the mitral annulus is continuous with the aortic valve annulus. The annulus is strongest here, where it has structural suppon from the fibrous skeleton of the heart. and is weakest posteriorly, where the fibrous tissue is less dense. The papillaty muscles and chordac tcndineae form the rest of the supporting structure of the mitral valve. The papillary muscles originate from the anterolateral and p0$tcromcdial portions of the w:ntricular walls and are named as such. The anterolateral papillary muscle is supplied by branches from the left anterior descending coronary anery and from the marginal branches of the left cin:umflcx artery. In 71 % of patients .ti,rcsenting fur coronary surgery, the anteJt>. lateral papillary muscle had a dual-ves.scl supply and 29% had a singl~vessd supply.6 The po.steromcdial papillary mwde receive. a variable &upply from the left circumflex artery and branches of the right coronary

TRANSESOPHAGEAL TOMOGRAPHIC VIEWS I 65 artery, but in 63% of patients, it was perfused by a single vessel, commonly the right coronary artery.6 The anatomy of the mitral leaflets has been described most commonly using terminology developed by Carpentier, thus allowing standardized communication between physicians on leaflet pathology. The crescent-shaped posterior mitral leaflet has three scallops, which in Carpentier's terminology arc known as P 1, P2, and P3, with P 1 being the most anterior, P2 in the middle, and P3 the most posterior. The anterior leaflet attaches to the same fibrous skeleton of the heart as the left and noncoronary cusps of the aortic valve. It is not scalloped, but the portions coapting with the posterior leaflet are termed Al, A2, and A3, from anterior to posterior. The anterolateral and posteromedial commissures are associated with their respective papillary muscles, and each is attached to portions of both mitral leaflets. Thus, the chordae originating from the anterolateral papillary muscle support the anterolateral commissure and the adjoining halves of the anterior and posterior leaflets (Al, PI, and part of A2 and P2), and the posteromediaJ papillary muscle's chordae support the posteromediaJ commissure and the adjoining halves of the anterior and osterior leaflets (A3 and P3 and part of A2 and P2). The orientation of the mitral valve as seen in the basal short-axis image and in Fig. 4-17A and B does not correspond to the orientation of the valve as seen by the operating surgeon, who sees the anterior leaflet above the posterior leaflet as represented by the en face 3D view (see Fig. 4-l?C). A systematic examination of the mitral valve begins with optimization of the ultrasound image. The depth of view should be decreased so as to only view the mitral valve leaflets and subvalvular apparatus. This enlarges the areas of interest and increases the frame rate (temporal resolution). The overall gain should be adjusted down until the blood pool just turns black, thereby decreasing the likelihood that the leaflets will artifactually appear thickened. Increasing the transducer frequency will also improve leaflet resolution. In each of following views the valve should fust be examined in two dimensions (2D) and then with a color flow Doppler sector that includes the left atrial portion to assess the regurgitant jet and the LV aspect of the valve to assess flow convergence. Examination of the mitral valve frequently includes five mid-esophageal views, two transgastric views, and 3D views. The mid-esophageal four-chamber view is a frequent starting place as it provides an overall sense of the valve function or pathology. The imaging plane (20 to 30 degrees) transects the mitral valve in an oblique plane relative to the valve commissures, thus showing the A3 segment of the anterior leaflet to the left of the display and the Pl scallop of the

f

posterior leaflet to the right of the display (see Fig. 4-7, Video 1). By slightly withdrawing or anteflexing the probe, the tomographic plane will transect the valve closer to the anterolateral commi~ure, bringing the left ventricular outflow tract into view, whereas slightly advancing or retroflexing the probe transects the valve more toward the posteromedial commissure. Next, the mid-esophageal mitral valve commissural view is obtained by rotating the multiplane angle forward to about 60 degrees (Fig. 4-18, Video 8). In this view, three parts to the mitral leaflets are visible, as the posterior leaflet is captured at the posteromedial (P3 to the left of the display) and anterolateral (P 1 to the right of the display) portions, with the anterior leaflet (A2) appearing in between. Imaging with color flow Doppler in this view can help to determine the origin of a regurgitant jet and localize it to either commissure. The long axis of the mitral annulus can be measured in this view as well. Rotating the multiplane angle forward to approximately 90 degrees creates the mid-esophageal twochamber view. P3 is always seen on the left of the image, and Al and A2 are typically seen on the right of the image (see Fig. 4-8, Video 2). By turning the probe to the left, more of the posterior leaflet (P2, P1) is visualized on the right, while turning the probe to the right visualizes more of the anterior leaflet (A2, A3) on the right. Finally, the multiplane angle is rotated forward (between 120 and 150 degrees) until both the mitral valve and aortic valve are seen but neither papillary muscle is in view (mid-esophageal long-axis view). In this view, A2 is typically seen on the right with P2 on the left (see Fig. 4-9, Video 3). As the image plane cuts perpendicularly through the line of coaptation, all segments of both leaflets can be assessed by simply turning the probe (left for Al/Pl and right for A3/P3). The short axis of the mitral annulus can be measured here, and it is the best imaging plane for measurement of vena contracta. An additional imaging plane for the assessment of the mitral valve is the five-chamber view, which is obtained by withdrawing the probe slightly from the four-chamber view to also visualize the left ventricular outflow tract and the aortic valve (Fig. 4-19, Video 9). In this view, Al and A2 are seen on the left of the display and P 1 and P2 on the right. Before leaving the mid-esophageal views, two pulsed Doppler flow profiles should be examined: (1) a mitral inflow flow profile that provides information about the diastolic function of the LV (see Chapter 8) and is used for evaluating mitral stenosis by the pressure half-time method (see Chapter 10) and (2) pulmonary vein flow, used in the evaluation of LV diastolic function and severity of mitral insufficiency (see Chapter 10).

66 I CHAPTER 4 ME two-chamber view MEmltral commlssural view view

Posterior

Medial~ {"Lateral A

Antl!flor

8 FIGURE 4-17. (A) Anatomy of the mitral valve. The three scallops of the posterior mitral leaflet {P1, Pl, and P3) and their corresponding antertor segments (A1, A2, and A3) are shown schematlcally (A) and In a 30 Image (B), Illustrating how the valve Is transected by the mld-esophageal (ME) views. (CJ Three-dlmenslonal view of the mltral valve from the atria! perspective with the Image rotated to match the surgeon's orientation to the mltral valve while standing on the patient's right side. The relatlonshlp of the mltral and aortic valves (AOV) Is also seen In this Image, with the anterior portion of the mltral annulus In continuity with the aortic annulus.

TRANSESOPHAGEAL TOMOGRAPHICVIEWS I 61

c FIGURE 4-77. (Continued)

For the uansgastric views, the probe is withdrawn and anteflexed from the mid-papillary short-axis view, as necessary. to bring the mittal valve clearly into view (see Fig. 4-10, Video 4). The image then corresponds to the anatomical orientation shown in Fig. 4-17A, with the posteromedial commissurc in the upper left of the disylay and the anterolateral commissure to the lower right. This imaging plane (see Fig. 4-10) some.times can be helpful with color flow Doppler to find tbe origin of a regurgitant jet. The ttarugastric tw~ chamber view (see Fig. 4-14, Video 7) is often very good for displaying the papillary muscles and chotdae tendineae (subvalvular appararus). The chordae to the postcromcdial papillary muscle are seen at the top of tbe display. and those to the antcromedial papillary muscle an: at the bottom. Real-time 3D TEE adds significantly to the routine evaluation of the mitral valve and is described in greater detail in Chapter 23. Three-dimensional imaging is most commonly used to acquire tbe so-called m f«e or "surgeon's" view that displays the anterior mitral lca:flet above the posterior leaflet and the aortic valve at about 12 o'clock (sec Fig. 4-17C). Once acquired, the mittal valve can be viewed ttom the left atrium or be easily manipulated to view the ventricular surfu.ce.

•Views

Mld-e.sophageal aortic short and long axis Transgastric long axis and deep transgastric flve-chamber • Assessment Valve and annular morphology LVOT, annular, slnotubular junction, and aortic mot dimensions Stenosls: valvular, subvalvular, supravalvular Regurgitation LVOT and tiansvalvular flow

The four views listed here allow examination of the aortic annulus, the aortic cusps, tbe sinuses of Valsalva, the sinotubular junction, the origins of the right and left main coronaries, the proximal ascending

68 I CHAPTER 4

8 FIGURE 4-18. Anatomical (A) and ultrasound (8) lllustratlon of the Imaging plane as It cuts through the heart for the mid·esophageal mitral commissural view. In this view, P3 is seen to the left of the display, P1 to the right of the display, and A2. appears in between. LA, left atrium; LV, left ventricle.

aorta, and the LVOT. The LVOT i& of particular interest for the occasional subvalvular membrane mimicking true aortic valve stenosis, for ventricular scptal defects, and for the detection of outflow tract obstruction that may occur with LV septal hypertrophy (e.g., hypcnrophic obstructive cardiomyopathy; see Chapter 21) or after mittal valve repair (systolic anterior motion; see Chapter 14). The mid~phageal aortic valve short-axis view is obtained by placing the aortic valve in the center

of the screen, usually with a depth of neld of 10 to 12 cm, and then rotating the angle forward to 30 to 60 degrees to display the iluee cusps of the aortic valve as the "Mercedes-Benz" sign (Fig. 4-20, Video 10). Minimal anteflexion also may be necessary to optimize the view. The noncoronary, right and left cusps should be specifically identified (sec Fig. 4-20); the thickness and mobility of the leaflets should be noted, and the addition of color will reveal the origin of n:gurgitant jets. This view is also used to measure

TRANSESOPHAGEAL TOMOGRAPHICVIEWS I 69

A

8

FIGURE 4- 79. Anatomical (A) and ultrasound (B) Illustration of the Imaging plane as It cuts through the heart for the mld-esophageal five-chamber view. A11ow Is positioned In the left ventricular outflow tract and points to the aortic valve. RA, right atTlum; RV, right ventricle; I.A, left atrium; LV, left ventricle.

the valve onncc by planimctty. Forward rotation of the angle from this point to about 120 degrees brings the mid-esophagcal aortic valve long-axis plane into view. However, to carefully examine the aortic valve in the long axis, the depth of fidd should be

adjwted to 10 to 12 cm, and the angle may need to be rotated forward to 120 to 160 degrees to visualize as much of the LVOT, aortic valve, and ascending aorta as possible (Fig. 4-21, Video 11). This imaging plane permits further assessment of leaflet mobility and

70 I CHAPTER 4

B FIGURE 4-20. Anatomical (A) and ultrasound (8) lllustratlon of the Imaging plane as It cuts through the heart for the mld-esophageal aortic valve short-axis view. RA, right atrium; LA, left atrium; RVOT, right ventTlcular outflow tract L, left coronary cusp; N, noncoronary cusp; R, right coronary cusp.

morphology. as well as measurement of the sinotubular junction, proximal ascending aorta, LVOT, and aortic valve annulus, idcntiDcd as the points of attachment of the valve cusps to the aortic wall The aortic valve cusp at the bottom of the display is the right coronary cusp, but the other cusp can be the left or noncoronary cusp, depending on the imaging plane. Aortic regurgitation is best assessed with color flow

Doppler from tlris view. The transgastric long-axis view is developed from the trarugastric short-axis view by rotating the angle forward to 90 to 120 degree& and often twning the probe slightly to the right (Fig. 4-22, Video 12). To obtain the deep tra.nsgastric five-chamber view, the tip of the TEE probe first must be adwnced deep into the stomach and positioned adjacent to the LY apex:. At this point,

TRANSESOPHAGEAL TOMOGRAPHIC VIEWS I 71

8

FIGURE 4-21. Anatomical (A) and ultrasound (8) illustration of the imaging plane as it cuts through the heart for the mid-esophageal aortic valve lon~axis view. 'The aortic valve cusp at the bottom of the display is the right coronary cusp, but the other cusp may be the left or noncoronary cusp, depending on the imaging plane. LA, left atrium; LV, left ventricle; RV, right ventricle; MV, mitral valve; ASC AQ ascending aorta.

72 I CHAPTER 4

A

8

FIGURE 4-22. Anatomical (A) and ultrasound (I) Illustration of the Imaging plane as It cuts through the heart for the transgastrlc long-axis view. LV, left ventricle; ASCAO, ascending aorta.

the probe is anteflexed and slowly withdrawn until contact with the stomach is again achieved, thus creating an imaging plane originating at the apex (Fig. 4-23, Video 13). Occasionally, lateral flexion of

the probe tip to the left can be helpful. The trarugasttic long-axis and deep ttansgastric five-chamber views put the aortic valve in the far field, so these views are not helpful for closely assessing valve anatomy.

TRANSESOPHAGEAL TOMOGRAPHICVIEWS I 73

8

FIGURE 4-23. Anatomical (A) and ultrasound (8) illustration of the imaging plane as it cuts through the heart for the deep transgastric five-chamber view. MV, mitral valve; Ao!/, aortic valve; ASC AO, ascending aorta.

However, if a prosthetic mit.ral valve cases an acoustic shadow on the aortic valve in the mid-esopbageal window, then these views will minimize the effect of shadowing and permit at least a cursory color flow Doppler examination of the aortic valve. The real

value of these views is for measwing the blood flow velocity through the LVOT and the aortic valve with pulsed· or continuous--wave Doppler, because the blood flow stream is better aligned (more paralld) with the Doppler beam (Fig. 4·24).

74 I CHAPTER4

FIGURE ~24. Transgastric long-axis and deep transgastric five-chamber views demonstrate that the blood flow stream is more parallel with the Doppler beam in these views.

• Views

Mld-esophageal four chamber, two chamber, pulmonary vein, and left atr!al appendage Mld-esophageal blcaval Upper esophageal right and left pulmonary vein • Assessment Atria! dimensions Atria! masses (appendage thrombus and tumors) Pulmonary venous flow Atrial septa! defects Coronary sinus dimensions and catneter placement Vena caval dimensions and catheter placement

To evaluate the left atriwu. the depth of field first should be reduced to 10 cm in the mid-c&0pbageal four-chamber view to enlarge the left atrium on the display screen. Advancing and withdrawing the probe allow for the complete examination of the left atrium from its superior to its inferior margins. However, because the probe is situated immediately posterior to the left atrium, the exact superior margin is often difficult to quantify. The left atrial appendage is best examined in the mid-esopbageal left attial appendage view, which can be obtained from the mid-esophageal cwo-cham.ber view by withdrawing slightly and rotating the probe to the left (Fig. 4-25, Video 14). The appendage arises from the superior part of the left atrium, appearing on the right side of the display screen as a triangular structure. Imaging the appendage through additional planes and with 30 is often useful in identifying pathology (see Chapte.r 23). It is sepuatcd from the left superior pulmonary vein by a ridge of tissue (ligament of Marshall) that has been mistaken for a mass or thrombus and is therefore popularly

For shunts occurring through a patent ductus arteriosus:

Conservation of Flow Assuming a constant flow of fluid through a conduit at a certain velocity, if there is a stenosis in the conduit, the velocity of fluid will increase at the site of stenosis to conserve flow. This concept is known as the continuity offlow and sometimes as the conserva-

tion offlow:

Flowt.orvercom1u1t = FlowStenmis

I 06 I CHAPTER 5 Prlnctples of Continuity of Flow

ume 8 SuokeVol...,. C

Siroka Volume A

Stroke Volume A= Stroke Volume B =Stroke Volume C

FIGURE 5- 73. Prtnclples of the continuity equation. sv, stroke volume; CSA, cross-sectlonal area; PWD, pulsedwave Doppler; CWD,. continuous-wave Doppler; V11, velocity-time Integral.

As de.scribed earlier, constant £low (cm.3/s) in a conduit is the product of cross-sectional area (CSA) of the conduit (cm2) and the ave.rage vdocity of the fluid (cm/s). Thus, CSA...,._.c.nc1ut • Velocity1.1-cancM1 =CSA-.· Velodty-11111

When three wriahles arc known, the fourth is easily determined with this equation, commonly known as the continuity eq""1ion. In aortic stenosis, flow across the aortic valve is equal to the flow across the LVOT (Fig. 5-13) and in. order to determine the stenotic area. the continuity equation can be reordered. as: CSA1.alll -

VTiu1ur)

SVL'fCR -

(CSAMlnl.

SVL\OT

sv...... VIM

vn,..,>

Regurgitant Fraction...(96) Regurgitant Volumev...,. . 100 Stroke Volumew.. Effective Regurgitant Orifice Area (EROA) Regurgitant Volumev.i.. VTl~11W.1et

Thus, in aortic: stenosis: Aortic Valve Area=

MitraI Valve Area =

CS~·

VTI

VTI

_.,.....

i.wr

Mitra! valve area can also be similarly calculated, but it must be remembered that the transmittal flow must be the same as left ventricular SY, a condition that is met only in the absenc:e of ventricular shunts and mitral and aortic regurgitation.

Veloclty Acceleration When blood Bows towud a small orifice, as in stenotic and regurgiwu l.e&ions, its velocity increases, forming concentric, roughly hemispheric shdls of increasing velocity and decreasing surface area. The velocity over the surfu:e of a hemisphere is c:onsid· crcd to be the same (isovdocity), and because the

QUANTITATIVE ECHOCAROIOGRAPHY I I 07

A

B

FIGURE 5-14. Color flow Doppler examination of transmit.Tai flow in mitral stenosis. (A) Velocity acceleration as flow approaches the stenotlc or1ftce Is demonstrated by allaslng of color flow, which shows a shell ofthe proximal lsovelodty surface area. The edge of the proximal lsoveloclty surface area Is defined by the transition from blue to red. In this case, the aliasing velocity Is 23 cm/sand r represents the radius of the lsoveloclty shell. (B) The angle (Q) subtended by the mttral leaflets Is shown.

hemisphere is proximal to the orifice, the surface area is known as proximal istwelodty surface area (PISA). The product of the (iso)velocity (cm/s) and the sur· fue area of the hemispherical velocity profile (cm2) yields the Bow (cm3):

By the principle of conservation of flow, the flow through an oriflc:c is the same as the flow where the PISA is located:

PISA· VelocltyMesq= CSAO!lke. PeakVelocltyQ1tloe

Flow= PISA· Velocity_....,..... ~

If the flow approaching the orifice is e:wnined with color flow Doppler, with the color scale set so that the accelerated velocity e:xceeds the Nyquist limit. aliasing will • place and a semicircular shell of a contrast· ing color will ~pear to cap the orifice (Fig. 5·14). To obtain this shell, the baseline for the color scale should be shifted in the direction of the jet of intetest (e.g., mward the ttansesophagcal ediocardiography [TEE] tr.wducer fur mitral regurgitation). The semicircular shell is in fut a hemisphere in three dimensions, and iu sw.fu:e area can be calculated as that ofa hemisphere: Surface Area of a Sphere = 4ir · r2, where r Is the radius of the hemisphere Surface Area of a Hemisphere (PISA) = (41r. r 2)/2 =21r·

,2

The velocity at the surf.tee of the hemispherical vdocity profile is the Nyquist limit (aliasing velocity) on the color flow Doppler scale. Thus, Flow= PISA. VelocityAlm~

In the setting of stcnosis, the valve area can be calculated by .r:cordering the equation a&: CSA ~Odb

= _Pl_SA_·_Vi_el_oc_lty_Alimv__..._ Peak Velocltys-ucOlttloe

For a regurgitant lesion, the calculation of the effective regurgitant orifice area (EROA) employs the peak velocity of the regurgitant jet so that: CSA

1119•.PntDrttb

=

PISA· VelocltyM.,..H ----....,..--,-----=-·Peak Velocity111gu..-.J•

The PISA radius should be measured at the same time as the peak velocity of the jet, and this can be more readily accomplished using color M·mode imaging. PISA bas been validated for mitral valve assessment, and it is not commonly applied to TEE assessment of the aortic valve. PISA is performed in diastole and on the left atrial side fur assessment of mittal ste.n.osis severity, and during systole and on the left ventricular side for calculation of the EROA

I 08 I CHAPTER 5 PISA for Mltnil Stllnoll1

PISA for Mltral Rllgurgltatfon

1. Measured during diastole 2. Left atrial side of the mitral valve

1. Measured during systole 2. Left ventricular side of tne mitral valve

3. Stroke volume at point A 4. Stroke volume at point B s. Equation solved for mitral valve area A

3. Stroke volume at point A 4. Stroke volume at point 8 S. Equation solved for EROA B

FIGURE 5- 7S. Application of the PISA prlnclple for assessment of mltral stenosls {A) and mltral regurgitation (B). PISA, proximal lsoveloclty surface area.

CWDofMRjtt

Ewiwe

FIGURE 5- 7f. PISA for mltral stenosls. PISA, proximal FIGURE 5-77. PISA for mltral regurgitation. MR, mttral regurgitation; CWD, continuous-wave Doppler;

lsoveloclty surface area. (Fig. 5-15). Summarizing, the assessment of the mitral valve (Figs. 5-16 and 5-17): 2

_ 21'1' • VelocityAl•llV MttralValveArea- P kV ea e1oc1ty,...._11n1

(FtgureS-16)

PISA, proxlmal lsoveloclty surface area.

True hemispheric shells require a ftat valve surface area, and because the miual valve surface area is not flat, an angle correction term is sometimes used to increase the accuracy of volumetric flow assessment:

PISA= 211.. r2 · c:r/180

where a is the angle subtended by the mitral lea£lets 2

EROA =

21R' • Velocity1.11as1ng (Figure 5-17) Peak VelocltyM1ttalRepi91aot.1+ pJ:~ ds + R(µ,v) 1

P1 - P2 = Pressure difference betwt:en the two locations p = Mass density of blood (gm/cm3) V1 =Velocity proximal to stenosis (m/s) V2 =Velocity at vena contracta (m/s) dv/dt =Acceleration s = Distance over which flow accderates R = Viscous resistance

Bamoulll aqumtlon I

I I

'

Increase In velocity I

Significant error can be introduced into the calculation in specific situations when the assumptions inherent in simplifying the equation are violated. For example, flow acceleration (inertial force) can become significant with some prosthetic valves, where a greater-than-normal force is required to open the valve. Similarly, the presence of viscous friction is negligible with laminar flow, but should be accounted for in lesions with tubular obstructions greater than 4 cm in length and orifices less than 0.1 cm2 • The simplified Bernoulli equation also ignores the proximal vdocity (V1}, but in conditions such as high cardiac output states, subaortic obstruction, significant aortic regurgitation, and intracardiac shunts, the proximal velocity (V1) can be significant (> 1.5 m/s), leading to an overestimation of the pressure gradient if the modified (rather than the simplified) Bernoulli equation is not applied. Finally, alterations in the blood viscosity, such as an increase in hematocrit to 60%, may lead to an underestimation of gradients, as 1/2 p may be higher from an increase in the mass density of blood. APPLICATIONS OF THE BERNOULLI EQUATION

Peak and Mean Gradients. The Bernoulli equation most commonly used to determine the peak instantaneous gradients across stenotic valves. The peak instantaneous gradient is measured with continuouswave Doppler, and most echocardiography machines can automatically calculate the peak gradient by simply positioning the cursor at the highest point of the velocity envelope (Fig. 5-19). is

10 0 AP = - (Vz2 -V12l + 2

f dvdt ds+ Rf,v) 1

FIGURE 5-18. Principles of the Bernoulli equation.

Peak Instantaneous Gradient = 4 · (V""'k )2

110 I CHAPTERS Mean pressure gradients are cal.culatcd as the average of multiple successive peak instantancom gradients measured over time dwing the particular ejection phase (see Fig. 5-19).

Intrac:ardiac PreaUK Measumnentl. Estimation of intracard.iac chambers is one of the most common forms of application of the modiflcd Bernoulli equation. This method requires the presence of a regurgitant jet or the pn:sencc of a shunt jet. The estimation

of intracatdiac pressures is perfonned in the following

steps (Fig. 5-20)2 : 1. Utilization of continuous--wave Doppler to measure the peak velocity of the jet 2. Conversion of peak velocity into a pressure gradient with the Bernoulli equation 3. Estimation of pressure in the origination chamber (Pac>

FIGURE 5-19. Measurement of peak and mean gradients. Mean pressure gradients are calculated as the average of multiple successive peak Instantaneous gradients measured over time. Receiving chambet' - Right atrium

Originating chamber - PA

Poc.f!V sys!Olrc prer.sure

PAC- RV dlaslallc pttUUre

4v2 (TR jet}+ PRc (Estimated CVP)

Poe (PA dlastollc pressure)-4v2 {PI jet)

Originating chamber - Right ventricle

Receiving chamber - fW

FIGURE S-20. Chamber pressure estimation. PA, pulmonary artery; RV; right venttide; CWD, continuous-wave Doppler; CVP, central venous pressu~ PI, pulmonary insufficiency; PAD, pulmonary artery diastolic pressure; 1R, fJicuspid regurgitation.

QUANTITATIVE ECHOCARDIOGRAPHY I 111

4. Estimation of pressure in the receiving chamber (PRc;) 5. Calculation of pressures (Fig. 5-20): a. Poe= 4v2 + PJlG b. pRC p OC - 4r

3. Left ventricular end-diastolic pressure (LVEDP} from an aortic regurgitant (AR) jet: LVED P = Diastolic Blood Pressure - 4(VEnd-DiostolicAR )

2

=

Using this methodology, numerous intraca.rdiac pressures can be measured depending on the presence or absence of regurgitation jets:

MEASUREMENT OF RESISTANCE Systemic vascular resistance (SVR) and pulmonary

vascular resistance (PVR) are typically calculated

Right Heart Pressures 1. Right ventricular systolic pressure (RVSP) using tricuspid regurgitant (TR) jet: RVSP = 4(VPokTR)2 +Right Atrial Pressure (CVP) In the absence of pulmonic stenosis or right ventricular outflow tract obstruction, RVSP is equal to pulmonary artery systolic pressure. 2. Right ventricular systolic pressure in the presence of a ventricular septal defect (VSD): RVSP =Left Ventricular Systolic Pressure -4(VPeokvso>2

3. Pulmonary artery mean pressures (PAMP) using pulmonary regurgitant (PR) jet: PAMP = 4(VPakPR)2 +Right Atrial Pressure (CVP)

4. Pulmonary artery diastolic pressures (PADP) using pulmonary regurgitant (PR) jet:

from invasive hemodynarnic measurements; however, Doppler echocardiography can provide a noninvasive assessment of vascular resistance. Units for measuring vascular resistance are dyne·s·cm - 5, pascal seconds per cubic meter (Pa·s/m3), or mm Hg/Umin, which is referred to as a Wood unit (WU). The WU value is multiplied by 8 to conven to Pa.sfm3 or by 80 to obtain the value in dyn·s·cm-5• Normal SVR values range from 10 to 14 WU, whereas a normal PVR is 1 WU. The ratio of peak mitral regurgitant vdocity to the time-vdocity integral of the LVOT flow (VMR/ TVILvPT) measured by D°l.pler echocardiography has been shown by Abbas et al to correlate positivdy with SVR measurements (WU) obtained invasively (r = 0.84, 95% er= 0.7 to 0.92). Furthermore, a calculated ratio greater than 0.27 identified patients with devated SVR (> 14 WU) with 70% sensitivity and 77% specificity, whereas a ratio less than 0.2 had a 92% sensitivity and 88% specificity to identify SVR less than 10 WU. Similarly, Doppler echocardiography has been shown to provide a clinically reliable, noninvasive method to determine PVR8:

2

PVR(WU)=~·

PADP = 4(VEnc1-0toS10nc PR ) + Right Atrial Pressure (CVP)

5. Pulmonary artery systolic pressure (PASP) in the presence of a patent ductus arteriosus (PDA): PASP = Systolic Blood Pressure - 4(VPeok PDA )2

Left Heart Pressures 1. Left atrial pressure (LAP) from a mitral regurgitant (MR) jet: LAP = Left Ventricular Systolic Pressure - 4(VPokMR)2 In the absence of aortic stenosis or left ventricular outflow tract obstruction, systolic blood pressure can be substituted for left ventricular systolic pressure. 2. Left atrial pressure in the presence of a patent foramen ovale (PFO) with a left-to-right shunt: LAP= 4(VPokPFo)2 +Right Atrial Pressure (CVP)

VTIR\'OT

10

=

where VTR peak tricuspid regurgitant velocity and VTIRVar = right ventricular outflow tract time-velocity integral. Funhermore, the ratio of V TR/ VTIRvar compared favorably to invasive PVR mea0.87 to 0.96), and a surements (r 0.93, 95% er ratio greater than 0.175 had a sensitivity of 77% and a specificity of 81 % to determine PVR greater than 2 WU.8 Scapellato et al9 have also described a method of estimating PVR using the pre-ejection period (PEP), acceleration time (AcT), and total systolic time (TT) derived from pulmonary systolic flow:

=

=

PVR = -0.156 +{1.154 · [(PEP/AcT)/TT)]} Although these methods have the advantage of being simple and easily applicable, they may not be as reliable in patients with pulmonary arterial hypenension {PAH). Haddad et al10 reponed that the ratio of systolic pulmonary anery pressure/(HR X VT~OT) correlated very well with invasive measurements of PVR indexed to

112 I CHAPTERS body surfuce area (PVRI; r = 0.86; 95% CI = 0.76 to 0.92). A cutoff value of 0.076 provided a sensitivity of 86% and specificity of 82% to determine PVRI greater than 15 WU/m2 .A cutoffvalue of0.057 increased sensitivity to 97% but decreased specificity to 65%. Similarly, Kouzu et al11 showed that the ratio of the peak tricuspid regurgitant pressure gradient over the time-velocity integral of right ventricular outflow (PGTRNTI 01') provided a reliable estimation of PVR over a wil: range of PAH values and from various causes, including intracardiac shunts. In addition, a PGTRNTIRV01' ratio greater than 7.6 was suggestive of poor prognosis fur patients with PAH without an intracardiac shunt.

Measurement of Contradility A relatively load-independent index of left ventricular systolic performance is peak dP/dt, or the maximum rate of rise of left ventricular pressure during systole. The echocardiographic method fur deriving this parameter is based on the continuous-wave Doppler recording of the mitral regurgitant spectrum, wherein the time fur velocity to rise from 1 to 3 mls is measured, and the pressure change from 1 to 3 m/s is calculated by the Bernoulli equation as 32 mm Hg 4 X {32 - 12). dP/dt is then calculated with the following equation: Left Ventricular dP/dt = 32 · 1000/dt in Milliseconds

Normal values for this parameter are 1610 ± 290mmHg/s. Right ventricular dP/dt may be calculated using the continuous-wave tricuspid regurgitant spectrum in a manner analogous to the approach used for left ventricular dP/dt. Because even hypertensive right ventricular pressures are typically lower than those of the left ventricle, the convention is to make the calculation based on the rise in velocity between 1 and 2 m/s. The pressure change from 1 to 2 m/s is calculated b:l the Bernoulli equation as 12 mm Hg 4 X (22 - 1 ). dP/dt is then calculated as: Right Ventricular dP/dt = 12 · 1000/dt in Milliseconds

A value greater than 1000 mm Hg/s is generally associated with normal right ventricular function.

CHAMBER QUANTIFICATION 12 There has been a lack of standardi7.ation of values fur cardiac chamber quantification with echocardiography, particularly TEE. Whereas normative values have been recommended for chamber quantification using transthoracic echocardiography, 12 the same is not true for TEE. 13 The same normative values are generally applied

to quantification performed by TEE; however, alterations in prdoad and afterload with institution of general anesthesia or sedation should be taken into consideration. To make reliable measurements with echocardiography, it is essential that all conditions be optimized for image acquisition, display, and archiving. The echocardiographer should make an effort to minimize translational movements of the heart, make adjustments to maximize image resolution, avoid apical foreshortening of the left ventricle, and optimize endocardial definition. Furthermore, it is important to identify systole and diastole with simultaneous display of the electrocardiogram (ECG) and to make measurements at the appropriate point in the cardiac cycle. For patients with arrhythmias, it is critical that measurements be averaged over multiple cardiac cycles.12

Cardiac Cycle End diastole is identified temporally along the ECG tracing as the onset of the QRS complex. However, end diastole can also be defined as the frame after mitral valve closure, or as the frame with the largest cardiac dimension. End systole is defined as the frame preceding mitral valve opening, or the frame with the smallest cardiac dimension. 12

Quantification of Left Ventricle (LV) A variety of echocardiographic techniques have been proposed to quantify LY dimensions and volumes (Table 5-1). Of the many potential LY measurements, septal wall thickness (SWT), inferolateral (posterior) wall thickness (PWf), and internal dimensions during systole (LVIDs) and diastole (LVIDd) are the most clinically relevant. PWT and SWf are best assessed in the transgastric mid-papillary short-axis view (Fig. 5-21) in diastole. LY diameters by TEE are ideally measured from the transgastric long-axis, transgastric two-chamber (Fig. 5-22), and transgastric shon axis mid-papillary views.13 LYID is measured at the minor axis of the LY (i.e., at the tips of the mitral valve leaflets), and the range for normal systolic and diastolic measures at this level are 32.4 ± 3.7 mm (males), 28.2 ± 3.3 mm (females) and 50.2 ± 4.1 mm (males), and 45.0 ± 3.6 mm, respectively (Table 5-2). 12 Although 2D or M-mode can be used to make these measurements, temporal resolution is better, with M-mode leading to more accurate measurements. When M-mode is applied, the distance between leading-edge echoes is measured. The current method of choice for LY volume measurement is the biplane method of disks (modified Simpson rule). It is based on modeling the left

QUANTITATIVE ECHOCAROIOGRAPHY I 113

Table 5-1. Advantages and llmltatlons of left ventricular quantification methods

.

.

~

•

·-

'1 . •

I

. ;1

Unear M-mode

20-guided Volumetric Biplane Simpson

~~

ji"r.;i°7i ·,"';'°,

- Reproduclble - High frame rates - Wealth of published data • Most representative in normally shaped ventricles - Assures orientation perpendiOJlar to ventricular long axis

- Beam orientation frequently off axis - Single dimension may not be re~tatlw In distol'ted ventricles • Lower frame rates than in M-mode - Single dimension only

- Corrects for shape distortions - Minimizes mathematlc assumptions

- Apex frequently foreshortened - Endocardlal dropout • Relies on only two planes - Few accumulated data on normal population - Based on mathematical assumptions - Few accumulated data - Lower temporal resolut!on - Image quality dependent - Less published data

Area length

- Partial correction for shape distortion

3Ddatasets

- No geometTlcal assumptfon - Unaffected by foreshortening - More accurate and reproducible compared to other imaging modalities

Mass M-modeor 20-gulded

Area length Truncated ellipsoid

oH

- Wealth ofaccumulated data

- AllOW5 for contribution of papillary muscles - More sensitive to distortions in ventTicular shape

- Inaccurate in ventricles with 1t!9ional abnormal!tles - Beam orientation (M-mode) - Small errors magnlfted • Overestimates LV mass - Insensitive to distortion in ventricular shape - Based on a number of mathematical assumptions - Minima! normal data

Data from Lang RM, Badano LP, Mor-Avl V, et at Recommendations for cardiac chamber quantification by e with the LA, the RA size should be estimated from multiple echocardiographic windows. It is also believed that RA volume may be a more accurate and reproducible estimate of size than a linear measure.

THREE-DIMENSIONAL QUANTIFICATION 30 echocardiographic data allow for reliable and precise quantification of geometric parameters in addition to the flow-dependent variables described in this chapter. Techniques previously employed to view and analyze computed tomography and magnetic resonance data are now routinely used for analyzing echocardiographic data as well. Multiplanar reconstruction (MPR) is the most common and useful tool in this context. New software permits nonorthogonal planes to be generated and adjusted, allowing customized interrogation of irregular anatomy, such as that seen in echocardiographic images (Fig. 5-25). Planes can be rotated and readjusted, enabling the operator to obtain optimal views for making linear as well as planimetric measurements. Measurements acquired in this fashion are useful in quantifying dimensions of heterogeneous structures, thereby improving the accuracy of calculations based on those dimensions.

Aortic Valve Aortic-valve area calculations based on the continuity equation assume that the LVOT is circular, that the flow is laminar, and that the ultrasound beam is in perfect alignment with the flow. In practice, the LVOT has been shown to be heterogeneous in nature, with major and minor axes. Accounting for just one of the two axes as the LVOT diameter may underestimate or overestimate aortic valve area, and in turn the severity of aortic stenosis as assessed by the echocardiographer.16 Planimetry on reformatted sections from 30 volumes offers the ability to trace the exact shape and size of the LVOT cross-section, enabling the operator to use an accurate area measurement for calculations.

Mitral Valve The mitral valve is a complex, three-dimensional structure with a hyperbolic-paraboloid shape. Its nonplanar and noncircular shape makes it an especially good candidate for 30 analysis. For example, reformatting planes through a 30 dataset helps delineate the positions of anterior, posterior, lateral, and septa! points on the annulus, aiding in accurate computation of annular diameters. Modern software also offers the opponunity to obtain other metrics of 3D geometric integrity in the form of nonplanarity angle,

annular height-commissural width ratio, tenting volume, etc. Although these metrics have yet to gain widespread adoption, their use in the clinical domain is expected to increase in the future.

REVIEW QUESTIONS Select the one best answer for each question. 1. Frequency is defined as: a. Number of wavelengths passing through acertain point b. Number of pulses passing through a certain point c. Number of positive deflections of a wave passing through a certain point d. Number of negative deflections of a wave passing through a certain point e. Number of pulses divided by the number of wavelengths 2. The units of frequency are: a. Meters/second b. Pulses/second c. Centimeters d. Seconds e. Hertz 3. Frequency determines: a. Resolution b. Brightness c. Contrast d. Compensation 4. The Doppler principle is based on the: a. Change in speed of the returning sound waves b. Change in speed of emitted sound waves c. Change in frequency of the returning sound waves d. Change in angle of the returning sound waves e. Change in resolution 5. The Doppler shift is most accurately calculated when the angle between the emitted and reflected sounds is: a. 90 degrees b. 30 degrees c. 0 degrees d. 45 degrees e. 120 degrees

6. The underestimation of Doppler shift is significantly increased when the angle of reflection increases more than: a. 15 degrees b. 30 degrees c. 10 degrees d. 20 degrees e. 25 degrees

118 I CHAPTERS 7. Misalignment of the Doppler beam with the blood flow: a. Can cause underestimation of the gradient b. Can cause overestimation of the gradient c. Does not affect the calculation of gradient d. Affects the gradient calculation, but the correction factor is built into the calculation e. Occurs only during transthoracic echocardiography 8. During continuous-wave Doppler interrogation: a. Sound waves are emitted continuously but received intermittently b. Sound waves are emitted intermittently but received continuously c. Sound waves are emitted and received continuously d. Sound waves are only emitted and not received by the transducer e. Sound waves are not emitted and only received 9. Continuous-wave Doppler: a. Is time-gated b. Measures the lowest vdocity in the pathway of the beam c. Is not affected by the angle between the emitted and reflected signals d. Can be used to avoid aliasing e. Can only be used in conjunction with color flow Doppler 10. Pulsed-wave Doppler: a. Should be used to detect high vdocities to avoid aliasing b. Utilizes the time dday to analyzc the reflected signals reaching the transducer c. Analyzes all the returning signals in the pathway of the ultrasound beam d. Is not affected by the angle between the emitted and the returning signals e. Generates "shaded" envdopes because it samples all the vdocities in its pathway 11. Pulse repetition frequency: a. Is inversely related to the depth of placement of the sample volume b. Is determined by the source (i.e., the transducer and the medium) c. Is the number of cycles per second generated by the transducer d. Is directly related to pulse repetition period e. Is exactly half of the Nyquist limit 12. High pulse repetition frequency Doppler: a. Utilizes continuous-wave Doppler to analyzc multiple high vdocities b. Is only used to analyzc tissue motion

c. Is based on analysis of successive pulsed-wave Doppler sample volumes to analyzc velocities at multiple locations in series d. Considerably increases the spatial accuracy of the pulsed-wave Doppler e. Is a combination of pulsed-wave and continuous-wave Doppler 13. Color-flow Doppler: a. Is a continuous-wave Doppler signal b. Is a combination of continuous- and pulsedwave Doppler signals c. Does not alias d. Is a pulsed-wave Doppler signal e. Leads to an increase in the pulse repetition frequency 14. Doppler tissue imaging: a. Is used to assess high-velocity and low-amplitude signals b. Can be used to grade aortic valve stenosis c. Is designed to detect low-vdocity myocardial tissue velocities d. Cannot be used to analyze diastolic function e. Is not angle dependent 15. Which one of the following is not an assumption of the continuity equation? a. Nonlaminar flow b. Constant diameter of the outflow tract c. Measurement of the Doppler velocity-time integral exactly at the measurement of the outflow tract diameter d. Parallel alignment of the Doppler beam with blood flow e. Flat profile of the blood flow 16. The greatest source of error in the continuity equation is: a. Calculation of the velocity-time integral b. Misalignment of the Doppler beam c. Measurement of the left ventricular outflow tract diameter d. High velocity of blood e. The presence of severe stenosis 17. The proximal isovelocity surface area method for the diagnosis of mitral stenosis: a. Is based on calculation of mean gradient across the mitral valve b. Is based on identification of isovelocity shells of flow acceleration on the left ventricular aspect of the mitral valve c. Is based on the continuity equation d. Requires an accurate calculation of the mitral annular diameter e. Utilizes the peak transmitral E velocity obtained by the pulsed-wave Doppler

QUANTITATIVE ECHOCARDIOGRAPHY I 119 18. Which one of the following is not a component of the Bernoulli equation? a. Proximal velocity {V1) b. Distal velocity (V2) c. Density of the liquid (p) d. Diameter of the blood vessel (D) e. Viscous resistance (R) 19. In the simplified Bernoulli equation, which of the following components of the original equation is not ignored? a. Distal velocity {V2) b. Proximal velocity (V1) c. Distance over which the pressure decreases (ds) d. Resistance (R) e. Density of blood (p) 20. Which of the following cannot be estimated with the modified Bernoulli equation? a. Peak gradient b. Peak right ventricular systolic pressure estimation even in the absence of tricuspid regurgitation c. Pulmonary artery end-diastolic pressure in the presence of pulmonary regurgitation d. Left atrial pressure in the presence of mitral regurgitation 21. Which of the following statements about identification of cardiac cycle stages by echocardiography is not correct? a. End diastole can be defined as the onset of the QRS complex on ECG. b. End diastole can be defined as the frame after mitral valve closure. c. End diastole can be defined as the frame with the largest left ventricular dimension. d. End systole can be defined as the frame with the smallest left ventricular dimension. e. End systole can be defined as the frame preceding aortic valve closure. 22. Left ventricular dimensions should be measured at: a. Left ventricular major axis at the base of the papillary muscles b. Left ventricular minor axis at the tips of mitral

leaflets c. Base of the left ventricle at the level of the mitral annulus d. In the deep transgastric window at 110 degrees e. Mid-esophageal position at 0 degrees 23. M-mode: a. Cannot be used for chamber quantification b. Can only be used to assess wall thickness c. Measures slightly higher left ventricular dimensions as compared to two-dimensional echo for the same left ventricle

d. Can only be used to calculate left atrial diameter e. Can only be used to measure end-diastolic diameter of left ventricle 24. Left ventricular diameters are best measured: a. At right angles to the axis of the ultrasound beam b. At 0 degrees (parallel) to the long axis of the left ventricle c. At 45 degrees to the long axis of the left ventricle d. At 120 degrees to the long axis of the left ventricle e. At the minor axis of the left ventricle, regardless of the rotation 25. The normal right ventricle has: a. More volume than the left ventricle b. Less volume than the left ventricle c. The same volume as the left ventricle d. A volume that changes with every beat due to excessive compliance e. A fixed volume despite changes in preload and afterload 26. The recommended view for right ventricular chamber quantification by transesophageal echocardiography is: a. Mid-esophageal four-chamber view b. Mid-esophageal long-axis view c. Deep transgastric view at 120 degrees d. Mid-esophageal short-axis view of the right ventricular inflow and outflow at 50 degrees e. Transgastric view at 90 degrees 27. The recommended view for measurement of the right ventricular outflow tract is the: a. Mid-esophageal right ventricular inflow-outflow view between SO and 60 degrees b. Mid-esophageal four-chamber view c. Mid-esophageal long-axis view at 120 degrees d. Transgastric view at 120 degrees 28. Speed of propagation of ultrasound waves: a. Is not determined by the tissue in which it travels b. Can be changed on the ultrasound system c. Is a multiple of frequency (Hz) and amplitude d. Does not change with changing frequency for a specific medium e. Is 1540 m/s in lung tissue 29. Duty factor of an ultrasound system is: a. The percentage of time the system is emitting the pulse b. Measured as cycles/second c. Determined by the source of the sound wave and the medium d. Fixed and cannot be changed e. Directly related to the amplitude of the wave

120 I CHAPTER 5 30. Which of the following is not a component of the Doppler equation? a. Transmitted frequency b. Change in frequency c. Cosine theta d. Speed of sound e. Frame rate 31. The phenomena of the returning frequency being higher than the transmitted frequency is called: a. Phase shift b. Positive Doppler shift c. Negative Doppler shift d. Fourier transformation e. Wave analysis 32. Range ambiguity can be defined as: a. Inability to utilize the focus control b. Poor two-dimensional image leading to inaccurate measurements c. Inability of the pulsed-wave Doppler to measure high intracardiac velocities d. Inability of the continuous-wave Doppler to locate the site of the high velocity e. Aliasing observed during Doppler tissue imaging 33. During pulsed-wave Doppler interrogation, the depth of the "sample volume": a. Is automatically calculated by the ultrasound system

b. Is fixed and cannot be changed c. Can be changed by the sonographer d. Keeps changing automatically with the increase/ decrease in velocity e. In irrelevant, because all the velocities in the Doppler path are measured 34. During pulsed-wave Doppler echocardiography, the size of the "sample volume": a. Is fixed and cannot change b. Can be changed by the operator c. Is determined by the speed of the blood d. Is determined by the frequency change 35. The Nyquist limit is: a. One-half of the pulse repetition frequency b. Twice the pulse repetition frequency c. Equal to the pulse repetition frequency d. One-fourth of the pulse repetition frequency e. Four times as much as the pulse repetition frequency 36. A low-frequency transducer will enable the transducer to record: a. Higher velocities at a given depth without aliasing b. Lower velocities at any given depth without aliasing c. The same velocities without aliasing

d. Lower velocities with aliasing e. Higher velocities at greater depths 37. Aliasing during color flow Doppler examination: a. Occurs at a higher velocity than during pulsedwave Doppler examination of the same flow b. Occurs at a lower velocity than during pulsedwave Doppler examination of the same flow c. Occurs at the same velocity as during pulsedwave Doppler examination of the same flow d. Does not occur because it is based on continuous-wave Doppler e. Is only determined by the depth of the color flow Doppler interrogation 38. Error may be introduced when using the pulmonary valve for cardiac output calculation with continuity equation because: a. It has a dynamic diameter during the cardiac cycle b. The flow is nonlaminar c. There is a low velocity of ejection d. There is always regurgitation e. There is always poor alignment of the Doppler beam 39. Regurgitant volume through the mitral valve can be calculated by: a. Comparing the stroke volume at the aortic and mitral valves b. Comparing the stroke volume at the mitral and tricuspid valves c. Comparing the stroke volume at the aortic and tricuspid valves d. Comparing the stroke volume at the aortic and pulmonary valves 40. Calculation of left ventricular {LV) mass is performed by: a. Subtraction of the LY volume enclosed in the endocardium from the LY volume enclosed in the epicardium b. Measuring the LY mass from images obtained from the CT scan c. Assuming the LY to be of a perfect circle d. Transthoracic echo only e. Cardiac magnetic resonance imaging only 41. Indexing of normal left ventricular (LV) dimensions to body surface area leads to: a. Overestimation of LY diameters in females b. Underestimation of LY hypertrophy in obese individuals c. Underestimation of LY hypertrophy in normalsized individuals d. Overestimation of LY diameters in obese individuals e. Underestimation of LY hypertrophy in females

QUANTITATIVE ECHOCARDIOGRAPHY I 121 42. The right ventricle: a. Can be comprehensively visualized in the midesophageal windows b. Wall thickness should be measured in the deep transgastric position c. Diameter should be measured in the midesophageal long-axis view at 135 degrees d. Is crescentic in shape e. Is more noncompliant than the left ventricle 43. Left atrial size should be measured at: a. End diastole when it achieves its greatest dimension b. End systole when it achieves its greatest dimension c. Mid-diastole when all its walls can be visualized d. Mid-systole when it achieves its greatest dimension e. Early systole when it achieves its smallest dimension 44. Left atrial dimensions: a. Are of not much clinical significance b. Are useful only for planning mitral valve surgery c. Are useful to quantify and follow the response to therapy in diastolic dysfunction d. Cannot be accurately calculated with transthoracic echocardiography e. Can be reliably performed with transesophageal echo 45. M-mode echocardiography: a. Has a better temporal resolution due to a higher frame rate b. Has a better spatial resolution due to a higher frame rate c. Is used to visualize slow-moving intracardiac structures due to a lower frame rate d. Cannot be used in conjunction with color flow Doppler e. Is ideal to measure higher gradients due to a high frame rate

d. Cannot be performed e. Requires only the calculation of left ventricular internal diameter during systole 48. A patient is found to have a peak velocity of 6.3 m/s on continuous-wave Doppler interrogation of the aortic valve in the deep transgastric window. Based on the Bernoulli equation, the peak gradient across the aortic valve is: a. lOOmmHg b. 120mmHg c. 164.5 mm Hg d. 158.8 mm Hg e. 132.9 mm Hg 49. The peak gradient across the aortic valve is found to be 39.6 mm Hg. Based on the Bernoulli equation, the corresponding peak velocity across the valve would be: a. 4 m/s b. 3.15 m/s c. 2 m/s d. 5.15 m/s e. 1.5 m/s For questions 50-53: A 60-year-old female suffers a cardiac arrest during a total hip replacement. An emergent TEE is performed and the following TEE data are obtained: Pulmonary artery diameter = 2.5 cm Pulmonary artery velocity-time integral = 11 cm LVOT diameter = 2.0 cm LVOT peak velocity = 1 m/s Aortic valve peak velocity= 4.5 m/s Tricuspid regurgitant jet peak velocity = 4 m/s Heart rate = 100 beats/min CVP = 15mmHg Systemic blood pressure = 90/40 mm Hg

46. Which of the following methods of calculating left ventricular volume is not recommended: a. Area-length method b. Biplane disk summation c. Teichholz d. Three-dimensional volumetric

50. Based on these data, the stroke volume of the patient is: a. 25.5 mL b. 35.8 mL c. 60.4 mL d. 53.9 ml e. 58.2 ml

47. Left ventricular mass calculation with TEE: a. Does not show any correlation with LV mass measured with TIE b. Generali/ measures more LV mass, greater than 6 gm/m as measured with TIE c. General?' measures less LV mass, less than 6 gm/m as measured with TIE

51. Based on these data, the cardiac output of the patient is: a. 2.5 Umin b. 3.8 Umin c. 5.4 Umin d. 6.5 Umin e. 4.5 Umin

122 I CHAPTER 5 52. Based on these data, the aortic valve area by continuity equation is: a. 1.5 cm2 b. 1.1 cm2 c. 0.9 cm2 d. 0.69 cm2 e. 0.81 cm2 53. The estimated peak right ventricular systolic pressure in this patient would be: a. 35 mm Hg b. 66.4mmHg c. 57 mm Hg d. 79mmHg e. 45.9mmHg For questions 54-57: During a routine intraoperative TEE examination, the following data are obtained: LVOT peak velocity = 0.5 m/s LVOTVfI = 12 cm LVOT diameter = 2.15 cm Heart rate= 64 beats/min Aortic valve peak velocity= 4.4 m/s Aortic valve Vfl = 22 cm 54. The peak gradient across the aortic valve would be: a. 44mmHg b. 33mmHg c. 77 mmHg d. 85mmHg e. 66mmHg 55. The stroke volume in this patient would be: a. 23.5 mL b. 22.3 mL c. 43.5 mL d. 37.8 mL e. 51.9 mL 56. The cardiac output in this patient would be: a. 3.5 L/min b. 2.8Umin c. 4.2 Umin d. 5.1 Umin e. 1.9 Umin 57. The aortic valve area in this patient is: a. 2.0 cm2 b. 1.1 cm2 c. 1.0 cm2 d. 0.7 cm2 e. 0.9 cm2 For questions 58-59: During an intraoperative TEE examination for mitral regurgitation {MR), a proximal flow convergence is noted at a Nyquist limit of 50 cm/s,

with a proximal isovelocity surface area (PISA) radius of 1.0 cm and a peak MR jet velocity of 5 mls. The patient's blood pressure was 110/60 mm Hg. 58. Based on the PISA equation, the effective regurgitant orifice area (EROA) in this patient is: a. 0.62 cm2 b. 0.71 cm2 c. 0.55 cm2 d. 0.43 cm2 e. 0.21 cm2 59. Calculate this patient's LAP. a. 5mmHg b. BmmHg c. lOmmHg d. 14mm Hg e. 19mm Hg For questions 60-64: A 48-year-old male is undergoing coronary artery bypass graft surgery. During the intraoperative TEE examination, it is noticed that he has moderate left ventricular dilatation, with at least 2+ mitral regurgitation. The following data are obtained: LVOT diameter = 2.5 cm LVOT VfI = 15 cm Mitral annulus diameter= 3.7 cm Mitral annulus VTI = 12 cm PISA radius = 0.7 cm PISA aliasing vdocity = 45 emfs Peak mitral regurgitation jet vdocity = 445 cm/s Mitra! regurgitation Vfl = 180 cm 60. The stroke volume through the LVOT in this patient would be: a. 73.6 cm3 b. 82 cm3 c. 55 cm3 d. 45 cm3 e. 66 cm3 61. The stroke volume through the mitral valve would be: a. 100 cm3 b. 118 cm3 c. 147 cm3 d. 129 cm3 e. 133 cm3 62. Regurgitant volume in this patient would be: a. 66.8 cm3 b. 55.4 cm3 c. 44.9 cm3 d. 76.8 cm3 e. 59.3 cm3

QUANTITATIVE ECHOCARDIOGRAPHY I 123

63. The regurgitant fraction in this patient would be: a. 55.3% b. 66.8% c. 42.9% d. 55.2 % e. 33.9% 64. Based on the PISA equation, the mitral regurgitant orifice area is: a. 0.51 cm2 b. 0.31 cm2 c. 0.39 cm2 d. 0.48 cm2 e. 0.42 cm2 65. The maximum vdocity through a persistent patent ductus arteriosus is 4 m/s and the blood pressure is 90/60 mm Hg. The pulmonary artery systolic pressure is: a. 4mmHg b. 26mmHg c. 74mmHg d. 90 mmHg e. 116mm Hg For questions 66-68: During the intraoperative TEE examination of a 58-year-old male undergoing coronary artery bypass graft surgery, it is noticed that he has tricuspid and aonic regurgitation. His blood pressure is 110/60 and his CVP is 10 mm Hg. Continuous-wave Doppler examination of the pulmonic and aortic valves revealed the following profile: Peak pulmonary regurgitant velocity = 1.69 m/s End-diastolic pulmonary regurgitant velocity = 1.43 m/s End-diastolic aortic regurgitant vdocity = 2.2 m/s 66. Calculate the pulmonary artery mean pressure. a. 12.2 mm Hg b. 14.8 mmHg c. 16.3mmHg d. 18.1 mmHg e. 21.4 mm Hg 67. Calculate the pulmonary artery diastolic pressure. a. 12.2mmHg b. 14.8 mmHg c. 16.3 mmHg d. 18.2mmHg e. 21.4 mm Hg 68. Calculate the left ventricular end-diastolic pressure. a. 18.2mmHg b. 24.8 mmHg c. 40.6mmHg d. 46.1 mm Hg e. 50.4 mm Hg

69. The continuous-wave spectral Doppler interrogation of an MR jet showed a 42-ms period between 1 m/s and 3 m/s of the MR velocity. The LV dP/dt is: a. 402 mm Hg/s b. 505 mm Hg/s c. 761 mm Hg/s d. 978 mm Hg/s e. 1006 mm Hg/s

REFERENCES 1. Weyman AE. Primcpln anti Prama of Echocartliography. 2nd ed. Philaddphia, PA: LWW; 1994. 2. Anderson B. Echocartliography: The Normal &izminlllWn and Echocartliographic MtllSUrtments. Hoboken, NJ: John Wiley & Sons; 2007. 3. Alam M, Warddl J, AnderMon E, et al. Characccristics of mittal and tricuspid annular velocities determined by pulsed wave Doppler riMue imaging in healthy subjects. J Am Soc Echocartliogr. 1999;12:61S-628. 4. Nishimura RA, Miller FA Jr, Callahan MJ, et al. Doppler cchocardiography: theory, instrumentation, technique, and application. Mayo C/jn Proc. 1985;60:321-343. 5. Quinones MA, Orto CM, Stoddard M, et al. Recommendations for quantification of Doppler echocardiography: a report &om the Doppler Quantification Task Force of the Nomenclature and Standards Committee of the American Society of Echocardiography. JASE. 2002; 15: 167-184.

6. Miyatak.c K. Yamagishi M, Tanaka N, et al. New method fur evaluating left ventricular wall motion by color-codcd tissue Doppler imaging: in vitro and in vivo studies.] Am CoU CllTriioL 1995;25:717-724. 7. Abbas AE, Fortuin FD, Patd B, er al. Noninvasive measurement of systemic vascular resistance using Doppler echocardiography. ]ASE. 2004;17:834--838. 8. Abbas AE, Fortuin FD, Schiller NB, et al. A simple method fur noninvasive estimation of pulmonary vascular resistance.] Am Coll Cardiol 2003;41:1021-1027. 9. Scapcllato F, Temporelli PL, Eleuteri E, et al. Accurate noninvasivc estimation of pulmonary vascular resistance by Doppler echocardiography in patients with chronic failure heart fulure. ] Am Coll CardioL 2001;37:1813--1819. 10. Haddad F, Zamanian R, Bcraud AS, et al. A novel non-invasive method of estimating pulmonary vascular resistance in patients with pulmonary arterial hypertension. ] Am Soc Echocardiogr. 2009;22:523--529. 11. Kouzu H, Nakatani S, Kyorani S, et al. Noninvasive estimation of pulmonary vascular resistance by Doppler echocardiography in patients with pulmonary arterial hypertension. Am ] Cardiol 2009;103:872-876. 12. Lang RM, Badano LP, Mor-Avi V, et al. Recommendations for cardiac chamber quantification by echocardiography in adulu: an update &om the American Society ofEchocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocartliogr. 2015;28:1-39, e14. 13. Hahn RT, Abraham T, Adams MS, et al. Guidelines fur pcrfurming a comprehensive transesophagcal cchocardiographic

124 I CHAPTER 5 examination: recommendations from the American Society of Echocardiography and the Society of Cardiovascular Aneschesiologists. JAm Soc &hocardiogr. 2013;26:921-964. 14. Haddad F, Couture P, Tousignant C, et al. The right ve.ntticle in cardiac surgery, a pcrioperativc perspective: II. Pathophysiology, clinical importance, and management. Anesth Analg. 2009;108:422-433.

15. Haddad F, Couture P, Tousignant C, et al. The right ventricle in cardiac surgery, a perioperativc perspective: I. Anatomy, physiology, and assessment. Antsth Ana{{. 2009; 108:407--421. 16. Jainandunsing JS, Mahmood F, Matya! R. et al. Impact of three-dimensional cchocardiogtaphy on classification of the severity of aortic stenosis. Ann ThoTllc Surg. 2013;96: 1343-1348.

Anatomical Variants and Ultrasound Artifacts Katherine Grichnik, Wendy L. Pabich, and Atif Y. Raja

Anatomical variants are those variations in normal anatomy that could be misinterpreted as pathological conditions. Many anatomical variants occur as remnants of embryological development and fetaI circulation, commonly visualized in the atria. Anatomical variants can be differentiated from artifacts (or errors in interpretation) as they persist despite sonographic changes in transducer frequency, gain, compression, or depth; and are seen in multiple image planes. Ultrasound artifacts usually occur due to a violation of the assumptions inherent to all ultrasound systems. Fundamentally, ultrasound imaging assumes that sound travels in a straight line, travels directly back from a reflector, and travels at exactly 1540 m/s through soft tissue. Additionally, it is assumed that the ultrasound beam is very thin, reflections are entirely from structures within the main axis of the beam, and the intensity of reflections is related only to the tissue characteristics of the reflector. 1 Artifacts can be distinguished from anatomical variants as they tend to cross known anatomical planes and boundaries and usually disappear with alternative imaging planes or sensitivity changes such as changes to the Doppler baseline or the pulse repetition frequency. Thus it is vital to be knowledgeable about the common anatomical variations and ultrasound imaging artifacts to ensure accurate echocardiographic interpretation and to avoid unnecessary interventions.2

THE EMBRYOLOGY OF ANATOMICAL VARIANTS 3 In the fourth week of gestation, the atria and the sinus venosus evolve and merge with the embryological heart. Initially, the sinus venosus receives venous blood from left and right sinus horns (Fig. 6-lA and B).Soon thereafter, the veins to the left sinus horn are obliterated and the remnants become the coronary sinus. The right sinus horn enlarges to create the smooth-walled part of the right atrium (RA), which displaces the trabeculated tissue of the primitive RA into the periphery and into the right atrial appendage (RAA), resulting in the prominent pectinate muscles

that are characteristic of the atrial appendages. Right and left venous valves mark the junction of the original right sinus horn and the primitive RA. The left venous valve disappears as it fuses with the developing atrial septum. The right venous valve of the right sinus venosus horn develops inferiorly into (1) the valve of the inferior vena cava (IVC), or the eustachian valve, which directs fetal blood flow from the NC across the foramen ovale; and (2) the valve to the coronary sinus, or the thebesian valve (Fig. 6-2). Superiorly, the convergence of the smooth and trabeculated tissue of the RA results in the crista terminalis. Concurrently, the atrial septum forms with migration of the septum primum toward the endocardial cushion. The septum secundum forms through invagination of the atrial walls and migrates to cover the fenestrations formed in the septum primum. Eventually septum primum and septum secundum fuse, leaving the foramen ovale as the only residual interatrial communication. Incomplete coverage of the septum primum fenestrations leads to the formation of a secundum atrial septal defect (ASD). Persistent separation of the septum primum and septum secundum without atrial septal tissue deficiency results in patent foramen ovale.4 Congenital abnormalities of the interatrial septum will be further discussed in Chapter 19. In the left atrium (LA), the smooth tissue of the pulmonary veins is incorporated into the wall of the left atrium and similarly displaces the primitive atrial trabeculated tissue almost entirely into the left atrial appendage (LAA). The ridge of tissue at the junction of the left superior pulmonary vein and the trabeculated left atrial appendage is called the ligament of Marshall or, more colloquially, the coumadin ridge {because this structure was initially misinterpreted as a thrombus requiring anticoagulation). Another variant occurs during the formation of the coronary sinus. Normally, the distal end of the left common cardinal vein degenerates, and the proximal portion connects via the left brachiocephalic vein to the right brachiocephalic vein, forming the superior vena cava (SVC). The left posterior cardinal vein also degenerates, and the remnants of the left sinus horn, receiving venous

126 I CHAPTER 6 Bulbuscordls

A

Left sinus horn

Right sinus hom

B

Right sinus horn

FIGURE '-t. (A) Right and left sinus venosus horns as they join the developing heart.:. (B) The remnant of the left sinus venosus horn becomes the coronary sinus, which Joins the right sinus venosus horn on the posterior aspect of thedeveloplng heart:.

Septum secundum

SeptUm prfmum

valve of coronary sinus or

thebeslan valve

FIGURE '-2. Anatomy of the right atrium demonstrating the crlsta termlnalls, atrial septum, and the eustachlan and thebeslan valves.

ANATOMICAL VARIANTS ANO ULTRASOUND ARTIFACTS I 127 drainage from the heart, become the coronary sinus. Failure of the left posterior cardinal vein to resorb .results in a persistent left superior vena cava. (PI.SVC) that drains into and dilates the coronary sinus (see Chapter 19).

ANATOMICAL VARIANTS BY LOCATION The anatomical variants are best clas&i6ed by primary location, although some variant structures may be present in more than one cardiac chamber (Table 6-1).

crcsccnt.-sbapcd tissue at the posterior aspect of the IVC. It can be found in multiple views, including tbe ME bicaval view and right ventricular (RV) inflow-oudlow views (Fig. 6-4). It may even appear to extend from the IVC to the border of the fossa ovalis and thus appear to bisect the right atrium. However, in distinction to triatriatum dexter, the eusw::hian valve is distinguished by a lack of flow distwbancc on color flow Doppler examination.6 Although tbe eustacbian valve is of no physiological consequence, it may be confused with an intracardiac thrombus, cause turbulent atrial blood flow, complicate IVC cannulation, or serve as a site for endocarditis or thrombus formation.7

Right Atrium CRJml TERMINALIS

The crista terminalis is a vertical ridge ofsmooth myocardiwu located at the jWlction of the SVC and the RA. forming a sttuctw:e that appears to protrude longitudinally into the RA. This structure is often visualized in the midesophageal (ME) bicaval view and should not be misinterpreted as thrombus or tumor (Fig. 6-3). Of note, the crista tcrminalis is thought to be a location where atrial uchydysrhytbmias originate due to the high density of adrenergic nerve 6bcrs, and thus may be a site for ablation therapy. 5 EUSTACHIAN VALVE

The Eustachian globally valve is an embryological remnant that usually regresses in adulthood, but can be seen in about 25% of individuals as a prominent

FIGURE 6-3. The Crista termtnalls Is shown at the arrow.

Table6-1. Anatomical location of common variants

Crista tenninalis Eustachian valve Thebeslan valve Chlari network Right atrial appendage Persistent fossa ovalis lnteratrial septum aneurysm Upomatous lnteratrial septum Trabeculatlons and pectlnate muscles Coronary sinus: dilated and persistent left SVC Right atrial appendage Central lines Padng and AICD wires

Coumadin ridge Trabeculatlons and pecUnate muscles Left atrial appendage Transverse sinus

Moderator band Pulmonary artery catheters Pacing and AICD wires

Trabeculations False tendons and LV bands Calc!fled chordae tendlneae Lambl's exaescence

128 I CHAPTER 6

FIGURE 6-5. The thebeslan valve (arrow) Is shown at the mouth of the coronary sinus. FIGURE 6-4. The eustachian valve is shown at the

arrow. A pulmonary artery catheter Is also seen Inferior to the eustachlan valve as a round structure In the right atrtum creating an acoustic shadow.

THEIESIAN V Al.YE

Called the "gatekeeper of the coronary sinus,"8 the Thebesian valve is a structure that can be seen as a thin piece of tissue guarding the entrance to the coronary sinw. PrC$Cnt in up to 80% of individuals, it can be visualized in the ME fuuHlwnber view with the probe slightly advanced. or in the ME modified bicaval view inferior to the left atrium in the atrioventticular groove (Fig. 6-5). Although it i& morphologically varied., thebesian valves are clas&ified according to their shape as semilunar, fi:nesttated, biconcave, or bandlike, according to their composition as membranous, fibromuscular, fibrous, or mwcular and the atcnt to which the valve covers the coronary sinus ostium. The valve serves to prevent retrograde flow into the coronary sinus during atrial contraction and is inconsequential wtless it inhibits ca.nnulation of the coronary sinus for a retrograde cardi.oplegia catheter or biventrkular pacing wire placement, as some variants can occlude more than 50% of the coronary sinus ostium.8 CHIARI NnwORK

The Chiari network is a remnant of sinus venoausderivcd structures that is seen a& a thin, fcncstrated, mobile, membranous structure within the RA. It is most highly associated with the rvc opening; however, the primary site of origin can vary to include the RA wall, intcratrial septum, or the coronary sinus.9 It should be distinguished &om thrombus or vegetation as it can be seen moving in the RA in multiple

FIGURE 6-6. The Chlarl network Is shown at the

arrow. imaging views (Fig. 6-6). The structure can be further delineated with the use of 30 imaging and may appear u a "spider web moving in the wind." It has little clinical significance except that it may cause of entrapment of right-heart cathetera and can complicate atrial septa! device occluder placement. It has also been associated with a patent furamen ovale, interatrial septa! aneurysm, and paradoxical ernbolization.6 CoRONARY SINUS (CS) AND PERSISIENT LEFT SUPERIOR VEJIA CAVA (PLSVC)

The roronary sinus courses in the atrioventricular groove superior to the mitral valve annulw10 and i& normally less than 1 cm wide and approxim.atdy 3 cm long. Echocardiographically, it can be visualized in (1) the ME four- 1.1 cm). The PI.SVC can be seen between the left upper pulmonary vein and the left atrial appendage (LAA) at the ME level (Fig. 6~10A). Injection of agitated saline into a left upper extremity vein results in. opacification of the coronary sinus from the PLSVC flow (see Fig. 6-lOB), confirming the diagnosis. PATENT foRAMEN 0vAl.E

The normal foramen ovate is an embryological remnant, which appears as a thin slice of tissue bound by thicker ridges of tissue. Up to 30% of the population may have a probe patent furamen ovale (PFO), but it may be greater than 50% in patients yotmger than 55 years of age who have had a stroke as a consequence

130 I CHAPTER 6

A

FIGURE 6- 7J. Adrawing ofa persistentforamen ovale.

B

FIGURE,_ 7O. (Al The persistent left superior vena cava Is seen as an echolucency {o"ow) above the left atrial appendage (LAA) In lieu of the tissue ridge representing the coumadtn ridge {ligament of Marshall). (B) Agitated saline bubbles (a"ow) are seen entering via the coronary sinus Into the right atrium and right ventricle after injection into a left arm vein.

of righMo-lcft intracardiac shunting (Fig. 6-11) .14 Transesophagcal cc:hocardio~phy (fEE) evaluation of the fora.men ovafel5,l should include 2D/3D assessment for intcratrial movement and color flow Doppler assessment, optimized for measwement of lower-velocity flow. Injection of agitated saline ("bu~ ble study") along with a Va.lsalva maneuver is used to provoke right-to-left shunting. After a Valsalva mancuver produces a decrease in RA volume, agitated saline is injc,tcd and the Valsalva released (when the microbubbles arc Arst seen to enter the RA) in order to transiently increase RA pressure over LA pressure. Admixture of agitated saline with small quantities of blood has been reported to improve the acoustic signal of the m.icrobubbles. The bubble study is positive if bubbles appear in the left atriwn within three to six cardiac cycles {Fig. 6-12).4

FIGURE 6-72. Positive bubble study in a patient with a patent foramen ovale (PFO). The arrow points to the PFO through which bubbles (left ofarrow) have entered the left atrium {LA). RA, right atrium.

ATRIAL SEPl'AL ANEURYSM

An atrial septa! aneurysm is characterized by an undulating atrial septwn that moves between atria during the cardiac cycle {Fig. 6-13).17 It has been defined as being more than 1.5 cm in size and/or enending into either atrium by 1.5 cm or more (Fig. 6-14), but variable grading systems c::rist, largely based on the extent of excursion into the left and ~t atrium (see Appendix F).Atrial septa! aneurysms have been asso-ciatcd with PFO and Cbiari network and may pre-dispose to thrombus formation, resulting in potential paradoxical embolism and stto~. 17 Percutaneously

ANATOMICAL VARIANTS ANO ULTRASOUND ARTIFACTS I 131

FIGURE 6-13. An lnteratrlal septal aneurysm Is demonstrated at the arrow. LA, left atrium; RA, right atrium.

FIGURE 6-'15. Llpomatous hypertrophy of the lnteratrial septum. The thin flap of the fossa ovalis is seen in between the hypertrophied sections of the atrial septum.

FIGURE 6- 14. The Image demonstrates the use of M-mode to measure the exairsion ofan interatrial septal aneurysm.

FIGURE 6-'16. Pectlnate muscles are demonstrated In the periphery of the right atrium as small, round echo densities-like •pearls on a string;"

inserted closure devices fur PFOs m.al be efficaciow in patients with paradoxical emboli.1 An atrial se~ t21 aneurysm may also impede efforts of wire passage into the superior vena cava in preparation for femoral venous cannulation.

is estimated to be between 1% and 8%. It usually occurs in older, obese people, and there may be a higher incidence in women.

LIPOMA'IOUS HYPERTROPHY OF THE ATRIAL SEPTUM

TRABECULA110NS AND PECFINA'IE MusaES

The interatrial septum may be markedly thickened, mimicking an infilttative or pathological proce&s. However, this benign finding can be seen to involve primarily the superior and inferior portions of the interattial septum, sparing the fossa ovalis, and thus leading to the "dumbbell-like" (Fig. 6--15) appearance. The ec:hogcnic: fut may also involve the right atrial wall, a Snding that is associated with coronary artery disease. L9 The prevalence of lipomatous hypenrophy

Muscle bands can exist on all endocardial surfu.ces of the heart, known ech.oc:ardiographically as ttabeculations. In the right and left atria these muscle bands are known as pectinate muscles, whicb cowse across the anterior endocardial surfu.ces, including both appendages. Pcc.tinate muscles are more prominent in the RA than in the LA (Fig. 6--16) and more apparent in the LAA than the RAA. Prominent pcc:tinate muscles can be distinguished from a mass or thrombus by their

132 I CHAPTER6

FIGURE 6- 17. Ligament of Marshall is shown at the arrow. It may look like a Q-tfp and separates the left upper pulmonary vein and the left atria I appendage. uniform texture and density, as well as movement that is in synchrony with cardiac tissue. In distinction, thrombus is often asynchronous with cardiac motion and is auociated with arrhythmias such as atrial fibrillation or low-flow states due to obstructive valvular disorders, such as mitral stenosis. Of note, trabeculations can be particularly prominent in the RV. and RV hypenrophy can ac:c:cntuatc these trabcculations making measurements of RV wall thickness difficult.

FIGURE f-'18. Three-dlmenslonal Image of the Ilg~ ment of Marshall (arrow). LAA, left atrial appendage; LUPV, left upper pulmonary vein.

RIGHT ATRIAL APPENDAGE (RAA)

The RAA is most commonly seen in an ME bicaval view where the crista terminalis sepatates the SVC and RAA.. Occasionally, the prominent trabcculations or pectin.ate muscles can also be seen. The RAA can also appear as an echo-free space anterior to the ascending aorta and near the right ventricular oudlow tract in the ME aortic valve long--axis view. The RAA should not be forgotten as a site for thrombus formation during conditions such as atrial fibrillation. Although the risk of systemic emboli is low from the RAA, it is theoretically possible with a patent foramen ovale (PFO). An. abnormally large RAA may also trap devices (such

as a PA catheter) during their placement.

Left Atrium LIGAMENT OF MARsHAU.

The atrial tis.sue between the left upper pulmonary vein (LUPV) and the LAA is known as the ligament of Marshall (LOM). LOM is the embryological vestige of the left common cardinal vein. It has many appearances, including that resembling a "Q-tip" (Fig$. 6-17 and 6-18) and has historically been misinterpreted as a thrombus, leading to its common m7crcnce as the "Warfarin" or "couma.din" ridge. The LOM contains

FIGURE f-'19. Anormal left atrial appendage Is shown. LAA, left atrial appendage.

muscle bundles (Marshall bundles), bas been identified as a source for paroxysmal atrial fibrillation, and is an important landmaik to the elec:trophysiologist.20 LEFT AlRIAL APPENDAGE (LAA)

The LAA is best seen in an ME two-chamber view where it is separated from tbe left superior pulm~ nary vein by tbe ligament of Marshall. (Fig$. 6-18 and 6-19). It can be heavily trabeculated with pectin.ate muscles and is associated with thrombus formation

during low-flow states. Pectinatc muscles arc distinguished from thrombus by similar density and tex:turc to other LAA tissue, as well as their synchronous movements with sunounding cardiac tissue. Due to

ANATOMICAL VARIANTS ANO ULTRASOUND ARTIFACTS I 133

A

B

FIGURE 6-20. {A) Thrombus (I.AA) seen in a biplane image of the left atrial appendage. (B} Pulsed Doppler flow in the left atria! appendage from a patient with atrial flbrlllatlon demonstrating flow greater than 40 cm/s.

the posterior location of the LAA. TEE is superior uansthoracic echocardiography (TTE) for examination of the LAA to identify thrombus as a potential source for cardiac embolism in patients with a history of transient iS-24). lAMBL'S ExCRESCENCES/PAPILLARY FIBROELASTOMAS Lam.bi's excrescences (a type of papillary fibroelas-

toma) an: flliform .structures arising from valvular leaflets, wually the aortic valve (AV), and may be known

ANATOMICAL VARIANTS AND ULTRASOUND ARTIFACTS I I lS

FIGURE 6-25. Ulmbl's excrescence Is shown at the arrow.

as "valvular strands." Some haVl: opined that they are simply accllula.r strands covered by cndothd!um aris-ing from the line of closure of the valvc26 (Fig. 6-25). Lambl's cxc:resc:enccs arc controversial, as they have been associated with, but not proven to ea.we, sttokc. The decision tD Clcise these when noted as an incidental finding ii wriable and largely dictated by a h.i&tory of cmbolic cvcnts.27 Further, distinguishing Lambl's acrescences from other papillary fibroelastomas, thrombi, vegetations, and other cardiac neoplasms can be challenging. Viewed with two-dimensional echocardiography, papillary fibrodastomas arc less likely to be Slamcnrous and more Iikdr to have mul· tiple fronds when compared to Lambls cx.cn:sccnces. However, thtte.dimensional cchocardiography bas been advocated to appropriately assess, diati.nguisb, and diagnose a Lambl's cxcresccnce.28 NODULE OF ARANTIUS

At. the center of the free edge of most aortic valve cusps is a small fibrous nodule known as the nodule of Arantiw. It occws at the coaptation point of the three aortic cusps and is thought to arise from the wear and tear of valvular opening and dosing.23.29 The nodule can become calcified and appear as a mass on the aortic valve lcafiets, or it can hypertrophy and contribute to aortic regurgitation.

Extracardiac Spaces PERICARDIAL EFFUSION

The normal pericardial sac is not usually well visualized with TEE, as it contains only 15 to 30 mL of pcricardial fluid. However, echocardiography is used to diagnose and/or evaluate the trca~ent for larger effusions that $Cparatc the myocardium from the

FIGURE 6-2&. A pericardia! effusion Is demonstrated atthe arrow.

pericardium, creating a.n echo-free space that is eas· ily visualized (Fig. 6-26). The clinical signifka~ce of an effiaion depend. upon the degree of ventncular and atrial compression and the ra.te of fluid a.cx:umulation, and can be identified by signs such as di~ stollc right ventricular collapse (sec Chapter 20). 0 30 echocaaliography may hdp determine the presence of scptations within the pcricard.ial space that can make thcra.peudc fluid drainage more challeng· ing. Further, the pericardium may be calcified,. futy, or thickened in a vuicty of dise:uc •ta.tea, w1tb or without concurrent effiaion, and potentially l'C$Ult in restrictive or constrictive pericarditis. Increasing use of portable echoca.rdiograpby has been adV?cated to diagnose pericardia! effusion in non-operating room settings such as the intensive care unit and the emergency room.31 •32 TRANSVERSE AND 0.LIQUE SINUSES

The visceral pericardium covers the heart and part of the great VCSM:ls, and at the reflections can cn:ate echolu.cent spaces that can be misintetprct:cd as abnormal. The tranaverae sinus is a reflection of pericardium between the posterior wall of the ascending aorta, the anterior left atrium, and the posterior pulmonary artery (Fig. 6-27). The oblique sinus is. a more infe. rior pericardial .rdl.ection located p~en~rly between the entries of the four pulmonary vcms mto the left atrium (Fig. 6-28). It is not well visualized with TEE, but may be seen on 1TE posterior tD the left a~ium in the parastemal long-axis view. At. these rdlcctions, pericardia.I fluid or fat may accumulate or _be mwn~­ prcted as ab&ccss ca:rity, cyst or even contain a hemagioma.6.33 Pericardia.I sinuses should not have any blood flow within them as demonstrated by a lack of color flow Doppler signal.

136 I CHAPTER 6

FIGURE 6-27. The transverse sinus Is shown at the arrow. It ls a perlcardlal reflection noted between the left atrium, the pulmonary artery, and the aorta. PLEURAL EFFUSION

Pleural effUsions can easily be identified by TEE, with left pleural effusions seen lateral and posterior, near the descending thoracic aorta (Fig. 6-29A) and right plewal effu&ions seen latetaJ. and superior to the liver (Fig. 6-29B). TEE has been shown to be accurate in the identification and quantification of pleural fluid in the cardiac surgical f aticnt, as well as in patients with chronic effUsions.3 Transverse perialrdill sinus WPV RLPY

LLPV

FIGURE '-28. Adrawing of the oblique pericardia! sinus, located posterior to the left atrium (LA), between the entries of the four pulmonary veins Into the LA. SVC, superior vena cava; IVc, Inferior vena cava; WPV, left upper pulmonary vein; LU'V, left lower pulmonary vein; RUPV, right upper pulmonary vein; RLPV, right lower pulmonary vein.

ULTRASOUND ARTIFACTS An artifu:t is a sttuc:ture in an ultrasound image without a corresponding anatomical tissue structure. Artif.tcu primarily occur due to the physia of ultrasound, but also result &om operator fault or equipment failurc.3S Ultra.sound machines assume that sound travels in a straight line and that echo images are only &om objccu within the main beam, that objects reflect sound once, that the distance of the reflector from the tr.wducer is related to the time necessary for the sound to ttavd to the object and back. and that the speed of sound is constant in tissue. Artifacts can be broadly categorized as (1) missing structures, (2) degraded images, (3) faJsdy perceived objects, and (4) misregistcred locations.1

Missing Strudures Missing structures are related to the resolution of the ultrasound beam or to shadowing fi:om a structure

ANATOMICAL VARIANTS ANO ULTRASOUND ARTIFACTS I 137

A

Focalzone+.

---

FIGURE 6-30. The ability to resolve two objects that

are close together is optimal at the focal zone of the ultrasound beam, as illustTated. B

FIGURE f-21. (A) Aleft pleural effusion adjacent to

the descending thoracic aorta (AO) Is seen at the arrow. (B) Right pleural effusion.

that reflects ultrasound so strongly that distal tures are not imaged or are "shadowed."

strw::~

RESOLU110N

The ability of uluasound to differentiate two separate structures in s~ace that are closely approximated is called resolution (Fig. 6-30). In general there arc three types of resolution: lateral, longitudinal/axial, and elevational. Lateral resolution allows one to dis-tinguish objects in a horizontal plane to the axis of the ultrasound beam and is determined by the beam width of the ulttasound probe. With latetal resolution artifact, two sttuctw:es that are closer together than the width of the ultrasound beam will appear as a single merged structure. Thus, a small reflector such as an air bubble may also be displayed as a wide line rather than a round point. Lateral resolution is best at the fuc:al point, where the beam is the nar~ rowcst. Longitudinal or axial resolution allows one to

distinguish objects in a longitudinal plane along the axis of the ulttasound beam and is related to spatial pulse length. Thus, transducer frequency, bandwidth, and pulse duration all play a role. A longitudinal resolution artifu:t occurs when one reflection is created from two structures that are closer than one-half the spatial pulse length. Higher frequency, wider bandwidth, and shorter pulse duration imaging have better axial resolution. Elevational resolution refers to the abiUty to distinguish between two objects that lie vertical to the axis of the ultrasound beam and is related to the beam height and thickness. Thus, elcvationa1 resolution is also best at the fucal point where the beam is the narrowest. Acousnc SHADOWING The high-density materials in prosthetic valves. patches, and im,Plants, as well as heavily calcified structures, have high acoustic impedance, which can prevent an ultrasound beam from transmitting through the medium. This causes an ccholuccnt "shadow" beyond the dense object (Fig. 6-31). Luge shadows can be problematic, as they can ob.ttruct the ewluation of important cardiac structures (Fig. 6-32).36

I l8 I CHAPTER 6

FIGURE 6-33. Acoustic shadows appear away from

the prosthetic valve in the deep transgastric fivechamber and transgastric long-axis views, allowing valve assessmenL FIGURE 6-31. The Image demonstrates two acoustic shadows from a blleaflet prosthetic valve (In the closed position in this image).

of interest and the second strong reflector several times. Strong rdlectors include calcified structures, metallic objects, catheters, and air/fluid interfuces. The successive rdlections retumin_g to the transducer result in repeated, equally spaced image& extending from the object, away from the transducer, and can cross anatomical boundaries. Less commonly, reverberations can occur when a strong ultrasound signal returns to the transducer from a single reflector and

is reflected back to the tissues. Once again, rq>cated

FIGURE 6-32. An illustration of how acoustic shadowing impairs prosthetic valvular assessment in the midesophageal four-chamber and midesophageal aortic valve long-axis views.

and alternative views may be required. For example, a prosthetic valve in the aortic position ia best evaluated in the transgastric long-axis or deep transgastric 5-chamber view so that acoustic shado"i!:fsfrom the proathesi& does not obscure perivalvular or other valve dysfunction (Fig. 6-33). An eqe Jhai.lbw is a special type of shadowing that results ttom the refraction and divergence of sound along the edge of a curved structure.

Degraded Images REV'ERBERATIONS

Reverberations typically occur when the primary ultrasound wave encounters a sccon~ strong reflect.or before returning to the transduccr.3 While the transducer is receiving the primary echo, the remaining ultrasound \W.VC can travel between the primary object

images of the structure appear on the screen, but this time at distances that are multiples of the actual object's distance from the transducer (Fig. 6-34.A and B}. Reverberations are commonly seen in the descending thoracic aorta. One can determine that reverberation has occurred by aamining the image for displacement parallel to aortic walls (in distinction to the free movement of a flap, for aample}, blood Row superimposed on the artifu:t during color flow Doppler imaging, and similar blood velocities on both sides of the image.37 Closely spaced reverberations

that form a single line deep to the echo-dense object are called "1met tail or ring down artifact (Fig. 6·34C).

Acoumc NOISE/NEAR-FIELD CWTTER Structures too close to the transducer can be obscured by high-amplitude oscillations of its piezoelectric de· ments in a phased array system. This is often observed in the LA and the descending aorta when imaging with a TEE probe, and can be improved by adjust-

ing the gain settings. It is very noticeable with epiaortic and epicardial scanning, and can be minimized by physically separating the transducer from the tissue of interest with fluid or gel ENHANCEMENT

Enhancement can be viewed as the oppo.sitc of acoustic shadowing and occurs when the ultrasound beam

ANATOMICAL VARIANTS AND ULTRASOUND ARTIFACTS I I 39

B

c

:::--

c

:::--

c

>

A

c FIGURE 5-34. (A) An lllustratlon of how reverberations are fonned when the surface of the ultrasound probe Itself serves as a reflector. (8) Reverberations generated by a percutaneous left ventricular assist device cannula seen traversing the aortic valve (AV) In the mldesophageal AV long-axis view. (C) Comet-tall artlfact (a"ow) generated by

a mltral ring. has traveled through a region with abnormally low attenuation or encounters a weak reflector.1•35 The returning echo is of higher amplitude, and therefore

a deeper object appears more reflective (brighter) than it should. It is commonly seen with the anterior pericardium in a ttansgastric view. Adjusting the ultrasound tim~gain compensation can minimize enhancement.

FIGURE 5-35. An illustration of how refraction results in a misplaced ultrasound image.

Falsely Perceived Objects REFRACTION AR'nFACT

An ultrasound machine assumes that sound trav-

ds through a homogeneous media in straight lines. However, when the sound wave crosses an interface of tissues or Auid with different propagation speeds, the ultrasound beam can be rcfuttcd and change

direction. The ultrasound system also assumes that sound travds in a straight line from the transducer and will therefore place a second copy of an object seen in the path of the refracted wave, side by side with (at the same depth as) the true image of the object (Fig. 6-35).

140 I CHAPTER 6 MIRROR IMAGES

Mirror image artifu;ts are produced when an ultra· sound beam travels between two strong reflectors (such as the near and far side of the aona), result· ing in a .second copy being placed deeper to the real structure. The structure that is visualized as the mir· ror is seen on a direct line between the transducer and the artifa.ct. and the true rdlector and artifact are equal distances from the mirror. Mirror images that occur commonly in the descending aorta and in the aortic arch arc sometimes referred to as a rcver· beration, but if there is only one copy, it is more aptly described as a mirror (Figs. 6·36 and 6·37). Not only can two--dimensional ultrasound result in a mirror artifact, but color flow Doppler (such a& that placed in the aorta) can also result in a mirror image, creating a "double-barreled aorta."'S Mirror artifacts can appear in any image plane, often causing

FIGURE f.-36. Mirror image artifact of the descending aorta of both the two-dimensional image and color flow Doppler.

confusion about the identity, nature, and pathology of the mirror image.

Misregistered Loc•tions SIDE LOBES

Although the ultrasound maclllne assumes that one primary ultrasound beam is generated, in reality, the lateral edges of the ultrasound transducer can generate extraneous (side) but weaker beams of ultrasound that diverge from the direction of the main ultrasound beam. However, because the ultrasound machine assumes that there is only one beam, any rdlected signals from such enraneous, side-lobe beams are interpreted as if they resulted from the direction of the main beam. When the weaker side ultrasound beams contact very reflective suu.aures, a silk.Jobe artifact appears as a curvilinear object at a unifunn distance from the transducer due to its oacillatioM (Fig. 6·38).1 Side-lobe artif.a.cts create uncertainty when they appear as an unexe!=cted object or linear structure in a cardiac chamber' (Fig. 6·39) or when imaging fur the presence of aortic dissection.37 Unlike true di~tiow (Fig'. 6-40), side-lobe artifu:ts tend to be displaced paralld to aortic walls and have simi· lar blood flow velocities on both sides of the artifact. Imaging with multiple planes can distinguish the true reBector from the artifu:t. SPEED ERRORS A speeti mTJT artifact occurs when the sound wave travels through an object that lw a propagation speed different from that of soft tissue. If the propagation speed is slower than that in soft tissue, reflectors arc placed deeper on the itnage than they really are because sound .i& traveling slower than the ultrasound system assumes. Sim.ilarly, If the propagation speed i& faster, the reflector will be shallower. ALIASING

FIGURE 6-37. Mirror artifact of the left ventricle.

The phen~menon ~f aliasing,. which occurs with Doppler mtcrrogaoon, can mttoducc confusion regarding the direction of blood flow and can pre. vent measurement of a peak velocity. Aliasing occurs with pulsed.wave and color flow Doppler but not continuous--wave Doppler." Aliasing is produced when the Doppler frequency shift acecds one-half the pulse repetition frequency (PRF), also known as the Nyquist limit. The PRF determines the maximal Doppler shift, or maxi.mum velocity, that is reliably measured by the transducer. When the velocity of the sound wave in question is grcarer than the Ny~uist limit, the system cannot sample frequently enough to accurately detect the velocity. A. a rcault, the signal

ANATOMICAL VARIANTS AND ULTRASOUND ARTIFACTS I 141

FIGURE 6-38. An Illustration of how side lobes are formed.

FIGURE 6-40. Atrue aortic dissection in a midesophFIGURE 6-39. Aside-lobe artifact in the ascending aorta in a midesophageal aortic valve long-axis view from a calcified plaque at the slnotubular junction. Thls artlfact Is not to be confused with an aortic dissection.

is displayed as starting correctly, but once it reaches the Nyquist Um.it, it "wraps around'° the scale, appearing to come from the opposite side of the baseline (Fig. 6-41). Aliasing does not occur with continuouswave Doppler, as with this modality the sy&tem is continuously sending and receiving ultrasound; thus, it can accurately measure very high velocities. Aliasing

ageal aortic valve long-axis view. The dissection flap is seen at the arrow.

can be overcome by increasing the velocity scale to the maximum, using a lower-frequency transducer (lower Doppler shifts), sdecting a shallower depth (increased PRF), using continuou~wave Doppler, or shifting the baseline. Because color flow Doppler is a pulsed Doppler technique, it can alias as well (Fig. 6-42). When the blood flow velocity exceeds the Nyquist limit, the flow is as&igned the color on the opposite end of the color bar-giving the impression (if one was only to look at the color) that the

142 I CHAPTER6

clutter, whereas in color flow Doppler, they are known as a ghomng artifact.

blood flow bad turned around to Bow in the opposite direction (Fig. 6-43). However. this is just the color Doppl.e.r version of "wrap-around."

THREE•DIMENSIONAL ECHOCARDIOGRAPHY

GHOSTING AND CwrrER

Just as 20 cchocardiography reveals normal ana· tomical variants and is subject to the formation of artifacts, so is 30 cchocardiography. The anatomical

Movement of heart muscle or vessel walls produces very low-frequency Doppler sbifu that can some-

times be detected by ultrasound systems. In spectral Doppler. the&e low-frequency shifts are known as

FIGURE 6-43. Color flow Doppler aliases in the left ventricular outflow tract in a deep transgastric five-chamber view; the blood flow going from the left ventricle toward the aorta changes from blue to red as the velocity of flow In the outflow tract exceeds the set Nyquist llmlt.

FIGURE '-41. This Image demonstrates pulsed-wave Doppler aliasing artifact, with •wrap-around• of the Doppler slgnal.

Color·flow Doppler

Nyquist

limit

Alias .·::·m·~. ,,

,.: l I ·~ ', .· "·&·~.

~

~ .itt~~ ~.ii.

FIGURE

------·--·····-----·-------------·-········--,-42. Pulsed·wave Doppler artlfact and color flow Doppler are subject to aliasing; continuous-wave

Doppler is not subject to the same phenomenon.

ANATOMICAL VARIANTS AND ULTRASOUND ARTIFACTS I 143

Table 6-2. Three-dimensional echocardiography artifacts Type of Artifact

Acquisition

Mechanism

Image Impact

Correction

Reverberation

Any

Any

Gain

Any

Stitch

Full Volume

Reverberations impair image quality and/or may appear to lengthen the catheter Appearance of a lack of tissue posterior to strongly reflective object that may appear as a•tear• of cardiac structures Structures and orifices may appear larger or smaller than actual size Image appears fractured

None suggested

Shadow

Similar to 20, US bounces off asecond highly reflective surface within heart, such as the metal within catheters US cannot pass through a strong reflective object

Dropout

Any

Blur

Any

Railroad

Any

Bloom

Any

Changes in gain can result in asignificant variation in the size of structures Inability of sequential subvolumes to be properly aligned due to arrhythmias, breathing, probe/patient motion Weaker echoes result in poor echocardiographic signal strength with inappropriate gain settings Nonisotropic voxel assembly can lead to indistinct edges of structures Artifact of catheters with two wide Iumens with perpendicular and parallel or tangential surfaces producing strong and weak echoes The US beam can produce fringes appearing from metallic structures extending beyond the borders of the actual structure

Misdiagnosis of artifact as a real hole, communication, or perforations Structure size and width are difficult to ascertain

Rotate and angulate the volumetric dataset

None suggested

Try to obtain normal rhythm, breath hold, hold probe still Slightly overset the gain and surfaces perpendicular to ultrasound beam; monitor z-axis High suspicion

One catheter appears as two linear structures

Look for the most favorable perspective, then increase compression to merge boundaries

Metallic structures appear to have irregular, thick edges

None suggested

Abbreviation: US, Ultrasound.

Adapted with permission from Faletra FF, Ramamurthi A, Dequarti MC, et al: Artifacts in three-dimensional transesophageal echocardiography, J Am Soc Echocardiogr 2014 May;27{5):453-462.

variants are the same as seen in 20 imaging, but must be identified as such with 30 imaging. Most of the anifacts seen with 20 echocardiography are seen with 30 echocardiography, including {but not limited to) reverberation, shadow, and gain artifucts (Table 6-2).40 Two particularly rdevant artifacts in 30 imaging are stitch and dropout artifacts. A "stitch" artifuct may occur during multibeat acquisition of

a dataset due to a disturbance of cardiac rhythm, patient movement, or operator movement. In multibeat acquisition the final dataset is formed by acquiring several subvolumes which are merged ("stitched") together to create the final dataset. If any one of the subvolumes does not match the other subvolumes with respect to cardiac cycle or position, then a sharp, disjointed sliding interface occurs in the image

144 I CHAPTER 6

FIGURE d-44. A•stitch artifact• is demonstrated. This may occur with multibeat acquisition of a dataset due to a disturbance of cardiac rhythm or with patient or operator movement.

(Fig. 6-44). This 30 imaging artifact does not occur with single--beat 30 imaging because a single volume of information is being obtained without the we of subvolume linking. 40 A dropout a.rtifu:t occurs when the z..axis is not monitored properly, the gain setting is too low (no image acquired), or the gain setting is too high (leading to mulcing). Artifu:ta in 30 imaging are further detailed in Chapter 23.

Key questions to ask include the following: 1. Arc the density and texture of the structure the same u the rest of the heart? If yes, then the structure is likely to be a variant. 2. Does the structure move synchronously with the rest of the heart? If yes, then the structure is likely to be a variant. 3. Doe& the structure appear in multiple planes and views? If yes, then the structure is not likely to be an artifact. 4. Does the structure cro" anatomical boundaries? If yes, then it i& likely to be an artifact. 5. Use various views to reduce the impact of artifu:ts; fur example, use a deep transgastric view to assess prosthetic aortic valves and avoid acoustic shadow interference. 6. Secondary signs and clues can assist with the cliag· nosis. Far example, if the patient has poor left ventricular function and/or is in atrial flbrillation, then a thrombus in either atrial appendage: or the LV is likely. 7. Agitated saline injections can identify shuna and persistent left superior vena avae and can distinguish intracardiac spaces from c:x.tracardiac spaces. Contrast agents can be used to establish or exclude the presence of thrombus. 8. Be aware that 20 artifu:ts and anatomical variants may pmist in 30 ech.ocardiograpby. making accurate interpretation challenging.

ARTIFACTS OF DISPLAY

REVIEW QUESTIONS

The interpretation of a 20 or 3D image can be confused by inappropriate we of spectral gain, color flow sector si7.e, image depth, and/or changes in the color flow velocity scale or color flow gain. It is suggested that these settings arc standardized across all exams conducted within an institution to avoid interob.. server confusion and to choose baseline settings that reduce the chance of anifact.

Select the one but answer for each question.

SUMMARY Appropriat:c analysis of ultrasound images is necessary to diagnose both pathological and normal conditions, thereby fu:ilitating correct interpretations and interventions. Common variants and frequently occurring artifacts must be recognized and differentiated from the l:!J.°logical conditions with which they rnay be COD

•

1. Identify the structure:

ANATOMICAL VARIANTS AND ULTRASOUND ARTIFACTS I 145 a. Chiari network b. Eww:hian valve c. Pacing wire d. Venous cannula

4. Identify the variant or pathology:

2. Identify the art:ifact:

a. Atrial septa! defect

b. Crista tcrminalis c. Lipomatous hypertrophy of the intcratrial septum

d. Eustachian valve a. Reverberation b. Mirror image c. Side lobe

d.

Ncar~fldd

5. What ia the artifact seen?

clutter

3. Identify the structure at the arrow:

a. Cor triatriatum b. Myxoma c. Mitral annular calcification d. Lipomatous hypertrophy of the interatrial septum

a.

Ncar~fidd

clutter

b. Mirror image c. Acoustic shadow d. Reverberation

146 I CHAPTER 6 6. Identify the structure at the arrow:

a. Moderator band

b. Papillary muscle c. Left ventrjcuJar band d. Left ventrjcuJar thrombus 7. Identify the source of the Bow:

c. Left atrium to right atriwn via patent foramen

ovale d. Left atriwn to right atrium via atrial septal

defect 8. Identify the artifu:t at the arrow:

a. Side lobe a. Right atrium to left attiwn via patent foramen

b. Mim>r image

ovale b. Right atriwn to left atrium via acrjal septal defect

c. Reverberation

d. Range ambiguity

ANATOMICAL VARIANTS AND ULTRASOUND ARTIFACTS I 147

9. Identify the structure at the arrow:

a. '&ansvcrse sinus b. Oblique sinus c. Ascending pulmonary artery

d. Brachiocephalic vein 10. Identify the sttuaure at the a.now:

a. Myxoma of the atrial septwn b. Nodule of Arantius c. lntcratrial septal hypertrophy d. Superior vcna cava. thrombus

11. What does the following image illustrate?

a. Persistent left superior 'Vala cava b. Normal coronary sinus c. Denrocardia d. Persistent right superior vcna cava

12. What is the atructure at the anow?

a. Persistent left superior 'Vala cava

b. Left atrial append.age c. Transverse sinus

d. Aacend.ing pulmonary artery

148 I CHAPTER 6 13. What is the artifu:t at the arrow?

a. Side lobe

b. Aortic dissection c. Revcrbm.tion d. Comet tail

14. What is seen in the periphery of the right atrium?

a. Right atrial myxoma b. Pcctin:1ttc muscle c. Lunbl's cxcrcscence d. Nodule of Arantius

15. Identify the structure at the arrow:

a. Chiari network b. Ewtachian valve c. Pacing wire d. Venous cannula 16. What doe. the following image demonstrate?

a. Fibroelastoma

b. Lunbl's acre&eence c. Flail aortic valve d. E.ndocarditis

ANATOMICAL VARIANTS AND ULTRASOUND ARTIFACTS I 149 17. What is the structure at the mow?

a. Crista term1nalls

b. Eustachian valve c. Thebcsian valve d. Ligament of Marshall 18. The arrow demonstrates:

a. Continuo11>wave Doppler aliasing

b. Overgain of the color flow Doppler c. Baseline shift of the color flow Doppler d. Color flow Doppler aliasing

19. The structure at the arrow .ia:

a. Ebstcin anomaly

b. Eumchian valve c. Normal tricuspid valve d. Patent foramen ovale 20. Based on this image, what is the likdy ae/JitumaJ anatomical variant?

a. Atrial scptal defi:ct b. Ventricular septa! defect c. Chiari network d. Eu.ttachian valve

150 I CHAPTER 6 21. The ccholuccncy at the arrow ia:

23. The arrow dcmonmatCl:

a. Acowtlc shadowing

b. Side lobe a. Transvenc sinus

b. Oblique sinus c. Inferior vcna caw. d. Coronary sinus

c. Reverberation

d. Mirror image

24. The suucture at the arrow is:

22. Identify the structure at the arrow:

a. ~t atrial appendage thrombus

b.

Lcfi: auial appendage thrombw

c. Left atrial appendage pcctinate muscle d. Left upper pulmonary vein dot

a. Side lobe b. Papillary muscle c. Moderator band d. False tendon

ANATOMICAL VARIANTS ANO ULTRASOUND ARTIFACTS I 151 25. The arrow points to an artifa.ct called:

a. Ncar·neld clutter b. Enhancement c. Acowtic shadow

d. Side lobe

26. The structure at the arrow is:

a. Eustachian. valve

b. Miual valve c. Tricuspid valve

d. Thcbcsian valve

27. The structure at the arrow .is:

a. Rifdit ventricular cyst b. Infuior vena cava c. Aortic outflow tract d. Dilated coronary sinus

I 52 I CHAPTER 6 28. The structure at the arrow is:

a. Thrombus b. Tricuspid valve c. P~tinate muscles

30. The structure at the urow is:

d. Crista terminalis 29. The structure at the arrow is:

a. Crista terminalis

b. Ligament ofMarshall c. Interauial septwn

d. Eustachian va1ve

a. b. c. d.

Crista terminalis Eustachian valve Thrombus Puhnonary artery catheter

ANATOMICAL VARIANTS ANO ULTRASOUND ARTIFACTS I 153 31. The space at the arrow is:

33. The sinus venosus leads to the formation of. a. Eustachian valve. crista terminalU, and moderator band b. Crista tenninalis, eustacltian valve, and thebesian valve c. Eustachian valve, moderator band, and transverse sinus d. Crista tcnninalis, transverse sinus, and thebesian valve

34. The purpose of the thebesian valve is to: a. Direct superior vena cava blood Bow in utcro

b. Direct inferior vena cava blood flow in utero c. Direct blood flow into the coronary sinus d. Prevent retrograde blood flow into the coronary sinus

35. An atrial septal aneurysm is associated with: a. Tbebesian valve and patent foramen ovale

b. Chiari network and moderator band c. Chiari netWork and patent furamen ovale d. Thebesian valve and Ch.iari network a. Pericardia! dfusion

b. Right atrium c. Mirror image d. Right ventricle 32. The space at the mow is:

36. Lipomatow hypertrophy of the interatrial septum is associated with: a. Coronary artery disease b. Patent furamen owle c. Ch.iari network d. Persistent left superior vena cava 37. The transverse sinus is seen between the: a. Left atrium, left upper pulmonary vein, and aorta b. Right auium, right upper pulmonary vein, and aorta c. Left atrium, pulmonary artery, and aorta

a. b. c. d.

Right upper pulmonary vein Left upper pulmonary vein Right atrial appendage Tricuspid valve annulus

d. Right atrium, pulmonary artery. and aorta 38. The crista tcrminalis separates the: a. Superior vena caw. from the eustach.ian valve b. Superior vena caw. from the right atrial appendage c. Left atrium from the ascending pulmonary artery d. Right atrium from the transverse sinus 39. Discrimination of two objects can be improved by: a. Imaging at the fuc:a1 zone and ~ing fu:quency b. Decreasing the depth and increasing frequency c. Increasing the depth and increasing frequency d. Imaging at the fucal zone and increasing depth 40. Acoustic shadowing is caused by: a. A change in the ultrasound medium b. Dense structures wjth high acoustic impedance c. High-amplitude oscillations of pifl.odecuic crystals d. The ulttasound beam bouncing between reflective swfu:es

154 I CHAPTER 6 41. A patent forarnen ovale is best diagnosed using: a. Agitated saline injection into a peripheral left arm vein b. Agitated saline injection with a Valsalva maneuver c. Appearance of bubbles in the left atrium in six cardiac cycles d. Appearance of bubbles in the right atrium in two cardiac cycles 42. Pectinate muscles may be distinguished from thrombus by: a. Being associated with atrial fibrillation b. Being similar in density to the right atrial appendage tissue c. Undulating throughout the cardiac cycle d. Appearing in different areas in various TEE views 43. Anatomical variants associated with the conduction system of the heart include: a. Moderator band, persistent left superior vena cava, eustachian valve b. Persistent left superior vena cava, eustachian valve, ligament of Marshall c. Ligament of Marshall, left upper pulmonary vein, moderator band d. Left upper pulmonary vein, moderator band, persistent left superior vena cava 44. Nodules of Arantius are: a. Associated with ventricular dysrhythmias b. Located on the ventricular side of the mitral valve leaflet c. An important landmark for aortic dissections d. Located in the free edge of the aortic valve cusps 45. Pericardia! fat may be confused with: a. Pericardia! effusion b. Moderator band c. Left ventricular thrombus d. Atrial septa! defect 46. Side lobes occur due to: a. A change in acoustic medium and density b. Reflection from an object with high density c. Extraneous divergent beams from the transducer d. High-amplitude oscillations of piezodectric

crystals 47. Mirror images always appear: a. On a straight line with and deeper to the real structure b. On a straight line with and more shallow than the real structure c. Lateral from and deeper to the real structure d. Lateral from and more shallow than the real structure

48. The oblique sinus is seen: a. Anterior to the left atrium, right atrium, and ascending aorta b. Posterior to the left atrium between the inlet of the pulmonary veins c. Superior to the superior vena cava and crista terminalis d. Inferior to the right atrial appendage and coronary sinus 49. The coronary sinus: a. Is guarded by the eustachian valve b. Is a pericardia! reflection c. Is in the atrioventricular groove d. Is normally 2 cm wide and 3 cm long

SO. The eustachian valve: a. Directs blood flow in utero toward the foramen ovale b. Is associated with the superior vena cava c. Oscillates randomly within the right heart d. Is associated with right heart volume overload

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cardiogmphy. 2014;31(4):Ell l-El14. 8. Katti K, Patil NP. The Thebesian valve: gatekeeper to the coronary sinus. C/inAnat. 2012;25(3):379-385. 9. Moral S, Ballesteros E, Huguet M, et al. Differential diagnosis and clinical implications of remnants of the right valve of the sinus venosus.] Am Soc &hocardiogr. 2016;29(3):183-194. 10. Tops LF, Van de Veire NR, SchuijfJD, et al. Noninvasive evaluation of coronary sinus anatomy and its relation to the mitral valve annulus: implications for percutaneous rnitral annulopla.sty. CimdatiDn. 2007;115(11):1426-1432. 11. Agrifuglio M, Barili F, Kassem S, et al. Sutureless pate.h-andglue technique for the repair of coronary sinus injuries.] Thorat: CartliDvasc Surg. 2007;134(2):522-523.

ANATOMICAL VARIANTS AND ULTRASOUND ARTIFACTS I 155 12. Povoski SP, Khabiri H. Persistent left superior vena = review of the literature, clinical implications, and relevance of alterations in thoracic central venous anatomy as pertaining to the general principles of central venous access device placement and venography in cancer patients. WorldJ Surg Oneal 2011;9:173. 13. Sheikh AS, Mazhar S. Pmistent left superior vena cava with absent right superior vena = review of the literature and clinical implications. Echocttrdiogrrtphy. 2014;3 l (5) :674-679. 14. Furlan AJ, Reisman M, Massaro J, et al. Closure or medical therapy for cryptogenic stroke with patent foramen ovale. New Engl] MeJ. 2012;366(11):991-999. 15. Augoustides JG, Weiss SJ, Ochroch AE, et al. Analysis of the interattial septum by transesophagcal echocardiography in adult cardiac surgical patients: anatomical variants and correlation with patent furamen ovale. ] CanliotboTllf: Vase AMsth. 2005;19(2): 146-149. 16. Di Tullio MR. Patent foramen ovale: echocardiographic detection and clinical relevance in stroke. J Am Soe &hocardiogr. 2010;23(2):144-155; quiz 220. 17. Ren JF, Callans DJ, Marchlinski FE. Patent foramen ovale and paradoxical systemic embolism: can we determine high.risk characteristics by echocardiography? ] Am CoU CardioL 2015;65(2):221-222. I 8. Wahl A, Krumsdorf U, Meier B, et al. Transcatheter treatment of atrial septal aneurysm associated with patent foramen ovale for prevention of recurrent paradoxical embolism in high-risk patients.]Am CoU Ctmlio/. 2005;45(3):377-380. 19. Chitkara M, Godelman A. Lipomattnu Hypertrophy ofthe /nm-atrial Septum. New York: Oxford University Press; 2014. 20. Hwang C, Chen PS. Ligament of Marshall: why it is important fur atrial fibrillation ablation. Heart Rhythm. 2009;6(12 Suppl):S35-S40. 21. de Bruijn SF, Agema WR, Lammers GJ, et al. Transesophageal echocardiography is superior to transthoracic echocardiography in management of patients of any age with transient i&chemic attack or stroke. Stroke. 2006;37(10):2531-2534. 22. Ruiz-Arango A, Landolfo C. A novel approach to the diagnosis of left atrial appendage thrombus using contrast echocardiography and power Doppler imaging. Eur] &hoctm1iogr. 2008;9(2):329-333. 23. Viles-Gonzalez JF, Kar S, Douglas P, et al. The clinical impact of incomplete left atrial appendage closure with the Watchman Device in patients with atrial fibrillation: a PROTECT AF (Percutaneous Closure of the Left Atrial Appendage Versus Warfarin Therapy for Prevention of Stroke in Patienu With Atrial Fibrillation) substudy. ] Am CoU CardioL 2012;59(10):923-929. 24. Loukas M, Klaassen Z, Tubbs RS, et al. Anatomical observations of the moderator band. Clin Anat. 2010;23(4):443-450.

25. Philip S, Cherian KM, Wu MH, er al. Left ventricular f.ilse tendons: echocardiographic, morphologic, and histopathologic studies and review of the literamre. Pediatr NunaJDL 2011;52(5):279-286. 26. Auger D, Pressacco J, Marcotte F, et al. Cardiac masses: an integrative approach using echocardiography and other imaging modalities. Heart. 2011;97(13):1101-1109. 27. Jaffe W, Figueredo VM. An example ofLambl's excrescences by transesophageal echocardiogram: a commonly misinterpreted lesion. &hocardiography. 2007;24(10):1086-1089. 28. Dumaswala B, Dumaswala K, Hsiung MC, et al. Incremental value of three-dimensional transesophageal echocardiography over two-dimensional transesophagcal echocardiography in the assessment of Lambl's acrescences and nodules of Arantius on the aortic valve. Echoetmliography. 2013;30(8):967-975. 29. Ho SY. Structure and anatomy of the aortic root. Eur J &hotardiogr. 2009;10(1):i3-il0. 30. Sagrista-Sauleda J, Mcree AS, Soler-Soler J. Diagnosis and management of pericardia! effusion. World ] CardioL 2011;3(5):135--143. 31. Hoit BD. Pericardia! disease and pericardia! tamponade. Grit Cart Met/. 2007;35(8 Suppl):S355-S364. 32. Nagdev A, Stone MB. Point-of-care ultrasound evaluation of pericardia! cffus.ions: does this patient have cardiac wnponade? Rmucitation. 2011;82(6):671--073. 33. Fitzsimons B, Koch CG. Transvellie sinus hemangioma. Anntbesia anti Analgesia. 2008;106(1):63-64. 34. Howard A, Jackson A, Howard C, Spratt P. Estimating the volume of chronic pleural effusions using transesophageal echocardiography.] Ctmliothorac Vase AMsth. 2011;25(2):229-232. 35. Pamnani A, Skubas NJ. Imaging artifacts during transesophagcal echocardiography. AnestbA~. 2014;118(3):516-520. 36. Barbetseas J, Brili S, Stamatopoulos I, et al. Pitfalls leading to misdiagnosis of a normally functioning prosthetic aortic valve as stenotic. Echoeardiography. 2007;24(7):773-779. 37. Vignon P. Spencer KT, Rambaud G, et al. Differential transesophageal echocardiographic diagnosis between linear artifacts and intraluminal flap of aortic dissection or disruption. Ch~rt. 2001;119(6):1778-1790. 38. Skubas N, Brown NI, Mishra R. Diagnostic dilemma: a pacemaker lead inside the left atrium or an echocardiographic beam width artifact? AnestbA~. 2006;102(4):1043-1044. 39. Bandyk DF. Ultrasound instrumentation and physics: a review with test questions. Snn Vase Surg. 2013;26(2-3):59-66. 40. Faletra FF, Ramamurthi A, Dequarti MC, et al. Artifacts in three-dimensional transesophageal echocardiography.] Am Soc &hocttrdiogr. 20 I 4;27(5):453-462.

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Assessment of Cardiac Structure and Function

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Assessment of Left Ventricular Systolic Function Linda D. Gillam, Konstantinos P. Koulogiannis, and Leo Marcoff

The assessment of ventricular systolic performance is one of the most important roles of perioperative echocardiography. Ventricular function is a key determinant of cardiac output, and global or regional dysfunction may be present before surgery or develop de novo perioperatively. Patients with coronary disease are particularly at risk. The ability of the echocardiographer to recogniu such abnormalities is critical to optimal patient care. In most clinical settings, the assessment of ventricular systolic function is performed qualitatively and relies heavily on the scanning ability and trained interpretive eye of the echocardiographer. The ability to accurately assess global and regional ventricular systolic function is one of the most difficult transesophageal echocardiographic (TEE) skills to acquire, and there is no shortcut to supervised training and ongoing continuous quality improvement, ideally with access to an independent gold standard. 1 Paradoxically, whereas quantitative methods may require more time for image acquisition and processing, interpretation of the results of such approaches may be relatively straightforward. All the methods presented in this chapter were first described using transthoracic imaging methods and have been extrapolated to the transesophageal approach. However, it is worth noting that, in some situations, studies directly validating TEE-based applications have not been performed. Because right ventricular (RV) performance is arguably equally imponant, methods of assessing RV function are discussed in Chapter 9.

THE PHYSIOLOGY OF VENTRICULAR FILLING AND CONTRACTION: PRESSURE-VOLUME RELATIONS A basic understanding of ventricular physiology, in particular pressure-volume relations, is essential to appropriate utilization of available methods of assessing left ventricular (LV) systolic performance. The cardiac cycle includes three basic phases: ventricular contraction, relaxation, and filling. LV contraction is initiated when, as a result of rising cytosol calcium levels, the actin and myosin filaments increase

the degree to which they overlap, resulting in sarcomere shortening. As more and more cardiomyocytes are activated, the LV begins to contract and LV pressure rises. The LV pressure continues to rise until it overcomes the left atrial pressure, at which point the mitral valve closes. During isovolumic contraction, the period between rnitral closure and aortic opening, the LV pressure continues to rise. When it exceeds the aortic pressure, the aortic valve opens and blood is ejected. As ejection continues, LV pressure peaks and begins to decrease. When it decreases below the aortic pressure, the aortic valve closes and ejected blood continues to be propagated through the systemic circulation. On a cellular level, calcium is taken up by the sarcoplasmic reticulum, and the myofilaments enter a state of relaxation. Because the mitral and aortic valves are in a closed position, ventricular volume remains constant. This period is known as i.sovolumic rr:laxation. With continued relaxation, LV pressure decreases further and the mitral valve opens. LV filling occurs in response to the gradient between the left atrium and the ventricle. This first period of filling is known as the early diastolic filling period. A second, later component occurs after atrial contraction. One method of displaying the phases of the cardiac cycle is by plotting pressure versus volume, thus creating pressure-volume loops (Fig. 7-1). It might appear that indices of systolic performance should focus exclusivdy on isovolurnic contraction and ejection. However, the diastolic filling portion of the pressure-volume loops is also relevant because it addresses the concept of preload, which, as described later, is an important determinant of many of the most commonly used indices ofsystolic function. A discussion of diastolic function itself may be found in Chapter 8.

ASSESSMENT OF GLOBAL VENTRICULAR SYSTOLIC PERFORMANCE Load Dependence Overall cardiac performance is perhaps best measured by cardiac output or stroke volume (cardiac output/heart

160 I CHAPTER 7

Volume FIGURE 7-'J. Left ventricular pressure-volume loop. Pressure is plotted along the y-axis and volume along the x-axis. The four sides of the loop correspond to the following: A-isovolumic contraction, B-systolic ejection, C-isovolumic relaxation, and D-diastollc filling.

rate). These reflect not only ventricular systolic and diastolic function, but also function of the cardiac valves and pericardium. Ventricular systolic performance, in turn, is a function of intrinsic myocardial contractility and loading conditions. Thus, in dis-cussing measures of ventricular systolic function, it is important to recognize that many of these are load dependent and that only a few are pure indices of myocardial contractility. Preload is defined as the wall stress at end diastole, or the load the ventricle experiences before contraction is initiated. It is a function of venous return. Afterload is the wall stress during ventricular contraction, or the load against which the ventricle ejects. In the absence of mechanical obstruction to ventricular emptying, such as aortic stenosis, it is a function of the systolic blood pressure. An appreciation of the effect of loading conditions is particularly important in the intraoperative setting, where dynamic changes in loading typically occur. Preoperatively, preload may be reduced due to the patient's fasting status or, perhaps, from aggressive diuresis as treatment for the patient's underlying heart disease. In the noncardiac setting, an acute event associated with blood loss or fluid shifts may have led to hypovolemia. Induction of anesthesia is sometimes associated with vasodilation that may further reduce preload. In cardiac surgical patients, preload may be reduced after cardiopulmonary bypass if underlying shunts or regurgitant valve lesions have been corrected. This is compounded by the significant

vasodilation that is typical of the period immediately after cardiopulmonary bypass. Abrupt shifts in afterload can also occur in the perioperative period. Anesthetic agents may reduce afterload, and surgical correction of outflow tract obstruction, such as aortic valve replacement for aortic stenosis, may compound the effect. These changes do not invalidate the use of load-dependent indices of systolic function, but their effect must be understood if one is to use these measures appropriately. In simple terms, load dependence refers to the fact that, for the same degree of intrinsic ventricular contractility, the index of systolic function will vary with the degree to which the ventricle is filled and/ or the pressure against which it ejects. For example, in the presence of severe mitral regurgitation, a ventricle with normal contractility will have an LV ejection fraction (LVEF; a load-dependent index) that would be considered elevated in a normally loaded heart. Conversely, in the same setting, an LVEF that would be considered normal for a normally loaded heart would, in fact, indicate depressed function. Table 7-1 lists indices of ventricular systolic performance that can be derived with echocardiography.

Chamber Dimensions The normal shape of the LV is symmetric with two relatively equal short axes and with the long axis running from the base through the mitral annulus to the apex. In the long-axis views, the apex is rounded,

Table 7- 'J. Load-dependent and loadindependent indices of ventricular function Load-Dependent Indices

Cardiac output Doppler tissue imaging: peak systolic velocity Wall stress Ejection Phue Indices Fractional shortening Fractional area change Ejection fraction Velocity of circumferential fiber shortening

l.old-lndependent Indices

End-systolic elastance Preload recruitable stroke work Preload adjusted maximal power Strain rate

lsovolumetric Phase Indices

Maximum dP/dt (afterload insensitive, preload sensitive) Abbreviation: dP/dt, Rate of rise of left ventricular pressure during systole.

ASSESSMENT OF LEFT VENTRICULAR SYSTOLIC FUNCTION I 161 so the apical half of the ventricle resembles a hemiellipse. The basal half, however, is more cylindrical. Initial evaluation of global systolic performance includes measurement of the linear dimensions of the LV cavity. Chamber dilation or hypenrophy often provides the first diagnostic clues of the underlying pathophysiology. The major long-axis measurement of the ventricular dimension is made from the apical endocardium to the plane of the mitral valve by using a midesophageal four-chamber view (see Chapter 4). The minor shon axis is measured perpendicular to a point one-third of the length of the long axis, moving from the base to the apex. Short-axis dimensions are often easier to obtain accurately with TEE and involve measurement of the end-diastolic anterior-posterior or medial-lateral diameter at the midpapillary level. Although the most recent American Society of Echocardiography (ASE) Recommendations for Chamber Quantification2 acknowledge that there are challenges to obtaining TEE images that are truly equivalent to their TTE counterparts, they recommend that the same range of normal values for LV and RV dimensions and chamber volumes be used for both TEE and transthoracic echocardiogram (TTE). The normal range fur the LV end-diastolic dimension is 42.0 to 58.4 mm for men and 37.8 to 52.2 mm for women.2 Care must be taken to ensure that the papillary muscles are excluded from the line of measurement. All end-diastolic measurements should be taken from the frame before mitral valve closure or the frame in the cardiac cycle in which the ventricular dimension or volume is largest.2 LV wall thickness is best determined from a transgastric long-axis or midpapillary short-axis view using M-mode or two-dimensional (2D) imaging. Normal ranges for septa! and posterior wall thickness are 0.6 to 1.0 cm for men and 0.6 to 0.9 cm fur women. 2 Although increased wall thickness is often viewed as being synonymous with left ventricular hypertrophy, this is incorrect, as left ventricular hypertrophy refers to increased LV mass, and LV mass may increase without an increase in wall thickness. LV mass is the total weight of the myocardium and is equal to the product of the volume of the myocardium and the specific density of cardiac muscle. LV mass can be derived from the transgastric midpapillary short-axis view by using a simple geometric cube formula: LV Mass= {1.04· [(LVID + PWT + IVST) -LVID 3

3

]}

. 0.8/- 0.69 where LVID is the end-diastolic internal dimension (diameter), PWT is the inferolateral (posterior) wall thickness, IVST is the interventricular septa! thickness, 1.04 is the specific density of the myocardium, and 0.8 and 0.6 are correction factors. Calculation

of LV mass by TEE yields measures that are comparable to those obtained with TTE, with currently recommended upper normal values for body surface area-corrected mass being 43 to 95 wm2 for women and 49 to 115 m2 for men.2 Although alternative approaches for volume and mass assessment that use 2D areas rather than linear dimensions have been developed for TTE, the frequent inability of TEE to image the full length of the LV (apical foreshortening} argues that these methods may not be suitable for TEE. Three-dimensional approaches theoretically might overcome these problems; however, the current ASE Recommendations consider the normal ranges by 3D to be less robust than those for 2D, arguing against the routine use of 3D TEE for absolute volume and mass determinations.2

w

Cardiac Output Cardiac output is the product of stroke volume and heart rate. Whereas right heart catheterization using Swan-Ganz catheters is common in the perioperative period and provides the most widely used method for deriving cardiac output, the thermodilution method may be invalid in the setting of tricuspid regurgitation. Further, the devices are expensive, and placement may be risky in some patients, such as those with right-side cardiac masses. Echocardiographic methods are not used routinely for cardiac output determinations, in large part for logistic reasons. However, they are well validated and may provide an alternative or adjunct to the thermodilution approach. Echocardiographic measures of cardiac output are based on the continuity equation, which states that in the absence of valve dysfunction or shunting, blood flow is constant throughout the heart. Thus, cardiac output is equal to the forward flow across each of the cardiac valves. For a given valve, this assumption will be invalid if there is significant regurgitation or if valve flow reflects the augmented flow of a shunt lesion. Because of the circular and relatively fixed geometry of the ventricular outflow tracts and semilunar valves, and the relative ease of echocardiographic imaging of these sites, stroke volume calculations typically are derived by measuring forward flow across the LV outflow tract,3•4 aortic valve,5·6 or, less commonly, RV outflow tract.7 Although several methods have been proposed for measuring transmitral and transtricuspid flows, the complex dynamic geometry of the orifices of these valves makes them less desirable. The measurement of the stroke volume starts with the velocity time integral, the integrated area under the curve of a pulsed Doppler spectrum. This represents the length of a column of blood moving through the targeted point in the heart per beat and

162 I CHAPTER 7 has units of distance. Multiplying the vdocity time integral by the cross-sectional area of the sampling site yidds stroke volume. Cross-sectional area is calculated by using the formula for the area of a circle ('ITr2), where r is the cross-sectional diameter divided by 2. The product of stroke volume and heart rate is cardiac output. Although these methods were originally validated with transthoracic imaging, they have been successfully transposed to the transesophageal approach. The most widdy used method is shown in Fig. 7-2. The vdocity-time integral is recorded from a deep transgastric view of the LV outflow tract, and the LV outflow tract diameter is measured using a midesophageal long-axis view.3·4 Ideally; the diameter should be measured at the same location as the velocity-time integral. Measurement of the LV outflow tract diameter from a transgastric view is less de.iliable because it rdies on the lateral resolution of the image rather than on the superior axial resolution used when the measurement is taken from a midesophageal window. Once the stroke volume is calculated (cross-sectional area X velocity-time integral), multiplication by the heart rate yields cardiac output. Commercially available echocardiographic systems have software packages designed to facilitate these calculations, typically included in the more extended analysis needed for Qp/Qs shunt calculations. However, it must be understood that although shunts or valve regurgitation do not invalidate this calculation as a measure of flow at the site being interrogated, these flows may no longer reflect forward systemic cardiac output. For example, in the presence of aortic regurgitation, LV outflow tract flow will include the forward flow (cardiac output) and the regurgitant flow. Another caveat relates to the presence of valvular stenosis, where prestenotic accderated flow signals and signals at or distal to the stenosis must be avoided. A potential alternative to the Doppler imaging approach is to determine LY volumes at end systole and end diastole. The difference between the two measurements is the stroke volume (equal to LY enddiastolic volume minus LY end-systolic volume), which, when multiplied by heart rate, yidds cardiac output. Echocardiographic methods for determining LV volume are described at greater length in subsequent sections dealing with LVEF.

Ejection Phase Indices Echocardiographic images provide a series of methods for measuring the reduction in chamber dimension that occurs with systole, typically expressed as: (End-Diastolic Value) - (End-Systolic Value). OO% 1 End-Diastolic Value

These ejection phase indices of systolic function include fractional shortening, fractional area change, and ejection fraction (EF). FRACTIONAL SHORTENING AND VELOCrTY OF CIRCUMFERENTIAL FIBER SHORTENING

The simplest ejection phase index is fractional shortening, defined as: (End-Diastolic Diameter) - (End-Systolic Diameter) . OO% 1 End-Diastolic Diameter

This method dates back to the M-mode era of TIE. Although theoretically of value in the symmetrically contracting heart, its ability to provide a sense of global ventricular function is limited when there is regional dysfunction. Thus, its use is waning. For reference, the lower limit of normal when using a transthoracic approach is 25% in men and 27% in women.2 Normal values using transesophageal views were reported to be similar but were derived from a smaller series of anesthetized patients.8 A variant of fractional shortening is the velocity of circumferential fiber shortening (Vcf), defined as: Vd = Fractional Shortening · 1/Ejection Time

Ejection time can be measured on M-mode or LY outflow tract spectral Doppler. The lower limit of normal is 1.1 circumferences/second. Although it has been suggested that this is less prdoad dependent than EF, this measure is rardy used in the clinical setting and has largely been replaced by other measures of systolic function in the research setting. FRACTIONAL AREA CHANGE (AREA EJECTION FRACTION)

The tomographic slices of the LY provided by 2D echocardiography provide another easily derived ejection phase index: fractional area change or area ejection fraction. This is defmed as: (End-Diastolic Area) - (End-Systolic Area) . OO% 1 End-Diastolic Area

Originally described using transthoracic short-axis or apical views of the LV, this index can be derived with TEE by using transgastric short-axis views. Due to the apical foreshortening that is inherent in the TEE midesophageal four-chamber view, this parameter is not generally derived through this window. Although ventricular areas typically are outlined and measured by manual planimetry, systems with automatic

ASSESSMENT OF LEFT VENTRICULAR SYSTOLIC FUNCTION I 163

A

8

c

FIGURE 7-2. Schematic representation of the measurement of cardiac output based on volumetric flow across the left ventricular outflow tract. Note: This method should not be used in the setting of significant aortic valve disease. (A} Using the deep transgastric 5-chamber view, the sample volume is placed in the left ventricular (LV} outflow tract just proximal to the aortic valve. This yields the spectral tracing shown to the right. The shaded area represents the velocity-time integral (RV, right ventricle). (B} Representative transesophageal image demonstrates alignment of the image so that the line of Doppler interrogation is parallel to blood flow. (C) The diameter of the left ventricular outflow tract Is measured by using a mldesophageal long-axis view. These measurements are analogous to those used In calculating aortic valve area with the continuity equation.

164 I CHAPTER 7 boundary detection can automate the process and provide real-time displa}'li of area and calculated fractional area change. Fractional area change derived from TEE and manual planimetry has been shown to correlate with EF when using nuclear methods as a reference standard in a variety of clinical settings.9--11 Automated boundary detection approaches have been developed, although they are not universally available without resorting to oflline assessment with vendorneutral imaging software that would be impractical for intraoperative clinical use. 12 Acceptable interobserver and intraobserver variabilities also have been demonstrated, 12 although Bailey and associates, in a study of pediatric patients with congenital heart disease, suggested an error of approximately 10% under optimal conditions. 13 In symmetrically contracting ventricles, values have been shown to be similar at multiple shortaxis levels (60 ± 6%, mean ± standard deviation). 14 It must be emphasized that although such approaches may be valid in patients with symmetric ventricular contraction, they have limited value in patients with regional wall motion abnormalities. Further, the presence of an excellent correlation between fractional area change and LVEF does not mean that the two values are identical. Thus, although it may be conceded that determinations of fractional area change are the most widely used means of quantitating ventricular function with TEE, the reader is encouraged to use the terms fractional area change or area ejection fraction rather than simply ejection fraction when referring to these calculations. The term ejection fraction should be reserved for calculations based on ventricular volumes {see later). A normal fractional area change is at least 36%. There has been a single report that correcting fractional area change for afterload (FAC afterload corrected (FACac) = FAC x log ([MAP - RAP]/CI) x 100%) provides a relatively load-independent index of contractilicy, l5 but additional confirmatory reports are necessary before recommending its routine use.

in the hands of an operator with good scanning and interpretive skills. Note is made, however, of an increasing trend to quantitative approaches facilitated, in part, by improvements in overall image quality, increased access to 30 methods, emphasis on the importance of using contrast agents when images are suboptimal, and an increasing number of clinical scenarios in which precise LVEF quantitation is essential (e.g., candidates for defibrillators or cardiac resynchronization therapy).

Quantitative Approaches Quantitative approaches mandate excellent images with good endocardial definition and no apex-base foreshortening. Although the former is rarely a problem with TEE, the latter is common. Apex-base displays are typically optimized by using a midesophageal window with the transducer held in a retroflexed position, but it may be impossible to obtain an image that is not foreshortened. This may account, in part, for the fact that TEE-derived volumes generally: underestimate those derived with other approaches, l6 although a close correlation between TEE and TIE measurements of LY volumes and ejection fraction has been reported.17 In using the midesophageal window, it may be necessary to move the imaging focus toward the apex and/or reduce the transducer frequency in order to optimally define the apical endocardium. Although this section will focus on 20 approaches, it is followed by an overview of newer three-dimensional (30) approaches.

(2D) The Simpson rule method (biplane method of disks) is currently the recommended 20 method to assess LVEF by the ASE recommendations for chamber quantiflcation.2 It is based on modeling the LY as a series of stacked cylindrical disks capped by an elliptical disk apex. The volume for each cylindrical disk is quantified by using the equation: MODIFIED SIMPSON RULE METHOD

VOLUME MEASUREMENT AND EJECTION FRACTION

The universal language for assessing LY systolic performance is left ventricular ejection fraction (LVEF). Indeed, LVEF is measured routinely in invasive angiographic studies and with noninvasive echocardiographic, nuclear cardiologic, computed tomographic, and magnetic resonance methods. Although there are several quantitative echocardiographic approaches for calculating LVEF, a semiquantitative visual assessment is still widely applied in clinical transthoracic and transesophageal echocardiographic studies. This requires a trained eye. Although less desirable for research applications, this approach may be adequate in the clinical setting

V

= (7r · D,f 2 ·

0/2:) H

where D 1 and DJ. are orthogonal diameters of the cylinder, ani:l His the height of the cylinder. The elliptical disk calculation uses a different equation:

where A is the area of the ellipsoid segment, h is the height of the ellipsoid segment, and a and b are radii of the total ellipsoid. The disks are summed for systole and diastole to yield diastolic and systolic volumes. The difference in

ASSESSMENT OF LEFT VENTRICULAR SYSTOLIC FUNCTION I 165

volumes is then divided by the end-diastolic volwne to cakulatc ejeetion fraction: Ejection Fraction = {End-Diastolic Volume)-(End-SystolicVolume). 10096 End-Dlastollc Volume

Fortunatdy, the operator can rdy on ulttasoW\d system software to make these calculations; otherwise, these calculations would be a laborious process (Fig. 7-3). These methods have been validated in vivo using TEE, IO.l6 and the major advantage of this approach is that it makes no assumptions concerning LV geometry. For individuals more than 20 years of age, EF in the range of 53% to 73% should be considered normal.2 AREA•LENGTH MElMOD (20)

There arc several cchocardiographic methods for cilculating LV volume based on modeling the LV as one

or more geometric figures. 18 One of the m.o&t common, the area-length method, models the LV as a cylinder hemiellipsoid. It is traditionally obtained on transthoracic images from the apical four-chamber and parastemal shorHxis (papillary muscle) views. With TEE, a midesophagcal four.chamber view is used to determine the major axis length, and the area is planimetered by using a short-axis view at the level of the mitral valve. Volume= (5· Area· Length)/6

The azea-length method has been validated extensively with the transthoracic approach and, to a lesser degree, TEE.10.16 A similar approach, the diameter-length method, models the LV as a pTtJlate ellipsoid: Volume= (11"· 01· 02 Length)/6

FIGURE 7-3. Illustration of the ultrasound calculatlon of ejectton fraction using the Simpson method of disks. The method of disks rs applied In the mldesophageal two-chamber view at end dtastole and end systole {panels A and B) and In the mldesophageal four-chamber view at end diastole and end systole (panels C and D), with a resultant ejection fraction of 60.2%

166 I CHAPTER 7 where Dl and lYl arc orthogonal abort--axii diameters.16 In both approaches, it is important to avoid oblique short-axis images.

is rnc:asurcd, and dP/dt is calculated. with the following equation:

QuANllTAllVE DETERMINATION OF EJECTION FRACTION

Normal values for this parameter are at least 1200 mm Hg/s.20 This calculation, which is automated in the analysis padmgs of many commercial ultrasound sys-~ is easy to perform but requires the prcscncc of wclldc6ncd rnitral n:gurgitant spectra. Although rdativcly aftu1.oad independent, d.P/dt is p.reload dependent.

Ea.eh of the previously cited methods for deriving ventricular volume can be extrapolated to yield quantitative assessments ofEF. The equation is as follows: LVEF (LY End-Diastolic volume}- (LY End-Systolic Volume) . t001l6 LV End-Diastolic Volume

LY EF of Jes,, than 52% fur men and Jes.. than 51% fur women arc suggestive of abnormal LY systolic function.2

lsovolumetric Indices (dP/dt) A more load-independent index of LY systolic performance is peak clP/dt, or the trwdJnwn rate of rise of LY pressure during systole. The echocaniiographic method fur deriving this parameter is baaed on the continuous-wave Doppler recording of the mittal regurgitant spectrum. This method ia illustrated in Fig. 7-4. As originally reported by Chen and colleagues,19 the time fur vdocity to rise from 1 to 3 m/s

dP/dt = 32· 1000/dt

W•ll Stress The common measures of LY systolic function dis-

cussed earlier do not differentiate between abnor-

malities of contra.ctility and alterations in afterload or preload. LY wall stres&, defined as the load opposing ejection, is therefore sometimes wed to describe systolic function. Wall stress is dependent on cavity dimensions, wall thickness, and pressure, and can be described as meridional (longitudinal), circumferential, or radial. Meridional stress is calculated from an cnd-syst:alic rnidpapillary short-axis view as: C1,.

= 1.33·

PCA/ A,)· 103 dyne/cm2

where P represents LY peak pressure, A, is LY cavity area, and Al" represents LY myocardial area (area of

the muscle m the short-axis view). Normal values for meridional stress are 86 ± 16 X 103 dync/cm2• Circurnfcrcntlal stress is calculated from a midcsophagcal fuur-dwnbcr view as: (f

_

c

[

(133PJAJ

I

- [-volume loops under variable

ASSESSMENT OF LEFTVENTRICULAR SYSTOLIC FUNCTION I 167

Slope = End-systolic elastance

Volume

FIGURE 1-5. calculation oftime-varying elastance based on variably loaded pressure-volume loops. A family of loops is created by abruptly changing preload, typically with inferiorvena caval occlusion. End-systolic elastance is the slope ofthe line connecting the endsystolic points of each loop and is a load-independent index of contractility.

loading conditions. In the invasive or intraoperative setting, such families of curves typically are created by abruptly reducing preload through caval occlusion. A similar but less dramatic decrease in preload can be achieved with the intravenous administration of nitroglycerin. End-systolic elastance is defined by the slope of the line joining the end-systolic points. An extension of this approach is the determination of preload-recruitable stroke work. Stroke work is the integrated area within a pressure-volume loop. It is possible to calculate stroke work for the variably loaded loops and to plot this as a function of enddiastolic volume. The slope of this linear relation is preload-recruitable stroke work, another relatively load-independent index of contractility. Values for end-systolic elastance and preload-recruitable work can be approximated with echocardiographic short-axis images and automatic boundary-tracking algorithms.23, 24 In these approaches, area becomes a surrogate for volume. Pressure must be recorded invasively, typically by transmitral placement of a high-fidelity catheter. Specialized computer analysis capabilities are needed to plot the pressure-area loops and calculate elastance or preload-recruitable work. Values for endsystolic elastance and preload-recruitable stroke work are dependent on the size of the left ventricle, so it is impossible to precisely define a normal range. To study the effect of volatile anesthetic agents on myocardial contractility, Declerck and coworke!s23 evaluated 23 patients undergoing bypass surgery with TEE by using several indices of cardiac performance derived

by automatic boundary-tracking technology. These included fractional area change, velocity of circumfi:rential shonening, end-systolic elastance, and preloadrecruitable stroke work. They reported that fractional area change and velocity of circumferential fiber shortening had poor sensitivity in detecting changes in contractility when compared with end-systolic dastance and prdoad-recruitable stroke work. Similar observations were made by Gorcsan and associates.25 Another variant of these methods is the measurement of preload-adjusted maximal power (stroke work/ end-diastolic volume2) validated by Mandarino and colleagues.26 Stroke work is the area within the pressure-volume loop. When echocardiographically derived pressure-area loops are substituted, the formula becomes: Preload-Adjusted Maximal Power Index Integrated Area within Pressure-Area Loop (End-Diastolic Area)112

To date, none of these pressure-area approaches have been used clinically. However, they provide essential research tools in studies of dynamically changing contractility. This is particularly true in settings where changing loading conditions invalidate load-dependent indices, as is typically the case perioperatively.

ASSESSMENT OF REGIONAL LV FUNCTION Because coronary revascularization is one of the primary indications for cardiac surgery and coronary disease is frequently present in patients undergoing noncardiac procedures, an understanding of the coronary vascular bed and the recognition of regional wall motion abnormalities is an important element of perioperative echocardiography. Regional dysfunction may he present preoperativdy, develop de novo during surge~ or resolve intraoperatively after revascularization. 2 ,28 Worsening wall motion after coronary artery bypass graft (CABG) surgery should be considered a prognostic indicator of adverse cardiovascular outcome. Swaminathan and colleagues29 demonstrated in 1412 CABG surgery patients that subjects with worse regional wall motion immediately after surgical coronary revascularization had a two-fold increased risk of death, myocardial infarction, or need for additional revascularization within the subsequent two years after surgery. The echocardiographic manifestation of myocardial ischemia is impaired regional contraction, typically measured in terms of reduced wall thickening and/or abnormal endocardial excursion. The latter typically is assessed visually and described in

168 I CHAPTER 7 .semiquantitative terms: hypokinesit (mild, moderate, or severe), akinc&.i&, or dyskinesis. Hypokinesis is defined as reduced endocardia.l c:itCUnion, akinesis as the absence of endocardia.1 excunion. and dyskincsis as outward systolic cndocardial motion. The term 11neurysm is used to describe segments in which there i.s diastolic deformity and dyskincsis, a frequent a.uociarion. Normally, the myocardium thickens by at least 30% [(cnd-syatolic thickness - cnd-dWtolic thickncss)/(end-diastolic thickness) X 100). Thickening of 10% to 30% is considered mildly redua:d, and less than 10% thickening is considered severely impaired. Recognition of regional dysfunction i.s fu:ilitated by the presence of at least one normally contracting and thickening segment, which serves as a reference; however, because diffuse coronary disease may create the situation in which there l& regionally variable dygfunction with no truly normal segment (i.e., all segments are abnormal but to different degree&), identification of abnormal contraction patterns based solely on a comparison to adjacent ventricular segments can be misleading. A complete assessment of LV regional performance requires multiple vicm that incorporate midcsopbageal and transgastric viCW5 (sec Chapter 4). A complete ech.ocardiographic evaluation of regional function is intrinsically redundant in the &C114e that each 1egment and each vascular bed are seen in more than one view. The apparent presence of a wall motion abnormality in a single view should prompt a careful rcevaluation of the iIDa.gel to ensure that there hu not been an interpretive error due to translation of the heart or suboptimal views (off~ or apically fore&hortened). Measurementa of S)'1tolic wall thickening may be useful supplements to the visual assessment of endocardia.l excursion. With TEE, the most difficult area to image is the LV apa. This is best seen with midesophageal views, typically with the probe in a retroflexed position and focus moved to the fu field. Transgasoic shon· and long-axis views aL.o may be used, with an emphasis on avoiding oblique imaging planes and ensuring that the imaging pla.nea reach the apex rather than simply the base of the papillary muscles. Al•essmcnt of the seprum and inferior wall may be difficult when the septal contour is distorted by primarily right-sided disease. Septa! flattening that occurs aclwivcly in diastole occurs with RV volume overload, whereas systolic scptal flarn:ning is a manifi:statlon of RV pressure overload. RV hypertension is generally aswciatcd with tticuspid regurgitation and RV dilation, ao pure RV prcasure overlod l& uncommon in the adult heart; a pattern of &eptal flattening

Baul

Mid

Apfcal

•

1nfenor Inf'eroseptal Anteroseptal lnf'erolatenl • Anterolateral • Anterior SepQI L.ite~I

Apex

FIGURE 1-6. The 17-segment model of the left ventrlde showing the basal, mid, and aplcal segments.

throughout the cardiac cycle is more common. This may falsely create the appearance of septa! and adjacent inferior wall hypokinesis. Another scrondary abnormality of the septum is the dyssynchrony that occurs in the setting of left bundle branch block, whether intrinsic or secondary to RV pacing. This create& a contraction pattern in which the septum appears to writhe, thus making it difficult to determine whether its excursion is normal. In these settings, the assessment of wall thickening may provide a better method of cx:cluding an abnor· mality of regional contraction. Seventeen-Segment Model

To •tandardiz.e the nomenclatwe for LV segmentation acrou imaging modalities, the ASE, with other subspccialty imaging societies, hu adapted a 17-segment model.'° This rcpla.ccs the 16-segment model previously used by cchocardiograpbers, the differences being the addition of an apical cap as the 17th aegmcnt and renaming the posterior, lateral, and septal segments. This scheme ls provided for reference in Fig. 7-6, while Fig. 7-7 provides a schematic assignment of each segment to a coronary vascular bed. A scmiquantitativc approach to segmental function is the wall motion score in which each scg· mcnt is as.signed a score of I to 4 (1 = normal, 2 = hypokinetic, 3 = a.kinetic, 4 = clyskinetic). These may be averaged to give a wall motion score ind.a. .Accounting for the severity of hypok:inc&.i& tramforms this scoring system to 1 = normal, 2 = mildly hypokinetic, 3 = severely hypokinetic, 4 = akinetic, and 5 = dyskinetic.

ASSESSMENT OF LEFT VENTRICULAR SYSTOLIC FUNCTION I 169

•

RCA

.

LAD LCX

FIGURE7-7. Typlcal perfusion bedsoftheeplcardlal coronary arteries. Note: There may be overtap between the beds of the left circumflex and right coronary artertes. RCA, rtght coronary artery; LAD, left anterior descending artery; LOsprcad incorporation into transcsophageal studies (sec Chapter 24 and 25).

Doppler Tissue Imaging Doppler tissue imaging (011) is a form of pulsed Doppler that focuses on the low·frequcncy, high-ampli· tude signals that return from tissue. Because the temporal raolution of on is better than that of standard 20 echocardiography, DTI has been reported to be better able to identify subtle diifuences in regional wall motion than 2D cchocanliography alone.' 1 DTI information may be displayed by coloM:oding the Doppler information and superimposing it over an M-mode or 20 image or as a vdocity·vers!JS'"time spectral display of information originating from a specific sample volume within the heart. These display options are analogous to those for pulsed Doppler data originating from

red blood cells. The major limitation of these methods is that they arc influenced by translation of the heart. Thus DTI is unable to distinguish active motion of the heart based on myocardial contraction from pwivc motion due to trnnslation. A second limitation derives from the angle dependence of tissue Doppler. Thus, as for blood cell-derived Doppler data, tissue velocities are underestimated when the direction of motion is not patallel m the line of intcttogation. When the annulus rather than any particular myocardial segment is sampled in a four-chamber view, tbe technique provides india:s of global LV performance with systolic S' and diastolic E' (early) and A' {late) waves reflecting systolic and diastolic movement toward the apex or away from the apex, respectively. Royse et al validated TEE OTI peak systolic myocardial velocity using the basal lateral wall against invasively derived preload-tt:eruitable stroke work in the operative scttinf'.'2 and Skarvan and colleagues have also suggcstcd3 that the technique may be useful in tracking systolic function in this setting. However, overlap between values for normal and abnormal segmcnu makes it impossible fur DTI S' wave to be used as the only method of assessing ventricular systolic function. Importantly, however, OTI also provides one approach to more sophisticated analyses of systolic function with strain. and strain rate determinations (see section below and Fig. 7-8).

Speckle Tracking Imaging The behavior of ultra50und in myacardium (scattering, reflection, and interference) results in 20 imagea where the myocardium is characterized by spccldcs. These speckles can be tracltcd from frame to frame throughout the cardiac cycle, and analysis of their motion can provide an angle-- and ttanslationindcpcndent tool fur measuring strain and strain rate (Fig. 7·9), as wdl as measures of ventricular twist/ torsion (see Chapter 23 and 24).

Strain end Strain Rate Imaging Strain is a dimeruionles.s quantity defined as the fractional change in length produced by the application of stress: Strain=

Length - 1 - - " ' ""''"''" • Length0

where lcn~ is the initial length. StralnRate = Strain

nme

FIGURE 7-8. Color Doppler tissue imaging of the septal wall demonstrating measurement of mean (lime green color) and color-coded segmental strain.

FIGURE 7-9. Speckle tracking imaging demonstrating measurement of longitudinal strain in a midesophageal two-chamber view.

ASSESSMENT OF LEFTVENTRICULAR SYSTOLIC FUNCTION I 171 The capability of deriving strain and strain rate echocardiographically from DTI is available in most ultrasound systems (see Fig. 7-8).34 OTI-derived strain rate is approximated by the ratio of the difference in velocities recorded at two targets over the distance between the two targets: .

~ Velocity• - Velocity &

Stram Rate =

D' 1stance

Because strain and strain rate assess the re/,ative length and motion of adjacent targets within the heart, they theoretically should be exempt from the influence of translation. Strain rate has been reponed to provide a load-independent assessment of myocardial contractility that correlates well with end-systolic elastance,35 and peak systolic strain may provide an index of regional LY function.3 6 However, when derived from OTI, the measurements are angle dependent, as demonstrated by Urheim and colleagues.34 For this reason methods based on speckle tracking have gained popularity and have become the preferred approach to strain assessment with transthoracic echo. Regardless of the approach (OTI or speckle tracking), strain rate determinations are limited by noise.37 Nonetheless, strain and strain rate imaging are valuable tools in the assessment of ventricular function, both preoperatively and perioperatively. With TIE, longitudinal strain is most widely used, hut the TEE transgastric view provides an approach for measuring radial strain and strain rate (see Fig. 7-9).3S,39 Although no normal values for strain have been established for TEE, normal values for global longitudinal strain by TIE are between -16% and -19 % with there being some vendor variability. Torsion/Twist Recently there has been renewed interest in the apexto-base rotational (twisting/untwisting) characteristics of LY contraction and relaxation. These become particularly important in understanding the response to isolated abnormalities of afterload and preload as occur with valve disease, as well as more common ischemic heart disease. 40 It is notable that the capability exists for performing these analyses with TEE using speckle tracking (see Chapter 24) or more cumbersome OTl-based approaches. Contrast Echocardiography Echocardiographic contrast agents capable of left heart opacification after an intravenous injection are valuable tools in TTE because of their ability to

improve endocardial definition. In general, the transesophageal approach provides excellent images that render contrast enhancement unnecessary. However, in patients in whom TEE images are suboptimal, particularly those who are obese or in whom there is interference by subdiaphragmatic air, contrast may facilitate endocardial border delineation. In addition, contrast may help delineate masses, enhance Doppler spectra, and define myocardial perfusion. It has been shown that contrast administration has no effect on intraoperative hemodynamics.41 If contrast is used, it is important that machine settings optimized for contrast be employed. These include harmonic imaging and low mechanical index (power). Presets for contrast imaging can be created to streamline this process.

THREE-DIMENSIONAL APPROACHES The introduction of 3D echocardiography in clinical practice has revolutionized the TEE assessment of mitral pathology and has become increasingly important in providing guidance for interventional cardiology procedures such as transcatheter valve procedures. These techniques may also be used to assist in the qualitative and quantitative assessment of ventricular systolic function, because multiple 20 images can be derived by postacquisition cropping and rotation of 30 datasets, and 3D volumes of the ventricle can be obtained using conventional 20 windows (Fig. 7-10). Single-beat acquisitions large enough to capture the LY will typically have low frame rates, but multibeat acquisition methods that create a wide-angle dataset by electronically "stitching" together partial volumes are useful, particularly in the setting of sinus rhythm. The intraoperative environment has the advantage of the possibility of briefly suspending ventilation to eliminate misalignment (stitch) artifacts that occur with spontaneous respiration. Many analyses can be quickly performed using software on the imaging system or in an offiine review station. However, as with 2D approaches, there is the caveat that it may be difficult to image the LY apex with TEE, thus limiting the accuracy of volume and LVEF determinations. That said, as with TIE, 30 TEE may help optimize derived 20 imaging of the LY through the ability to derive 2D images from the 30 volume sets that optimize the display of the true rather than a foreshortened apex. There is a theoretic advantage to 30 methods in the setting of regional LY dysfunction when it comes to volume and LVEF determinations. In a comparison of 3D to several 2D methods for assessing LYEF, the single-plane 20 Simeon approach correlated best with the 3D approach. 2 In the intraoperative study of Cowie et al, 3D assessment

172 I CHAPTER 7

FIGURE 7-70. Three-dlmenslonal Image of the left ventricle demonstrating volumetric assessment using multlplanar reconstruction and segmentation for assessment of wall motion.

of LV volume and EF was feasible in approximately 95% of patients, although it provided no clear advantage over the Simpson biplane 20 approach.43

REVIEW QUESTIONS Select the une bert answer for each item. 1. Which. of the following describes the diastolic filling phase of the LY pressure-volume loop? a. Volume rcmains constant, pressure f.ills. b. Volume remains constant. pressure .rises. c. Volume and pressure remain constant. d. Volume r.ises, pressure falls. c. Volume and pressure rise. 2. Which of the following describes the isovolumic contraction phase of the LV preS&ure-volwne loop? a. Volume remains constant, pressure falls. b. Volume remains constant, pressure r.iscs.

c. Volume and premue remain constant. d. Volume rises, pressure fulls. c. Volume and pressure rise. 3. Which of the following is the most load-independent index of ventricular contracti.lity? a. Fractional area change b. Ejection fraction c. Peak dP/dt d. End-systolic elastance e. Fractional shortening 4. For each of the following conditions, indicate whether LV prdoad is: A. Increased B. Decreased C. Unchanged a. Mitra! regurgitation b. Ventricular septa! defect c. Aortic regurgitation

ASSESSMENT OF LEFT VENTRICULAR SYSTOLIC FUNCTION I 173 d. Aortic stenosis e. Acute blood loss 5. For each of the following conditions, indicate whether LY afterload is: A. Increased B. Decreased C. Unchanged a. Mitral regurgitation b. Peri-infarction ventricular septal defect c. Aortic stenosis d. Systemic hypertension 6. Relative to the preinduction resting state, which of the following best describes the typical change in LY loading conditions after the induction of general anesthesia before cardiac surgery? a. Afterload increased, preload increased b. Afterload increased, preload decreased c. Afterload decreased, preload increased d. Afterload decreased, preload decreased 7. A 26-year-old patient with critical aortic stenosis undergoes successful aortic valve replacement. Preoperative LVEF is 45%. Immediate postoperative LVEF is 65%. What is the most likely explanation for the improvement in LVEF? a. Intrinsic myocardial contractility has acutely improved. b. Intrinsic myocardial contractility has acutely worsened. c. Afterload has acutely decreased. d. Afterload has acutely increased. e. Preload has acutely increased. B. Which of the following is not required to calculate cardiac output when using the continuity equation as applied to LV outflow? a. LV outflow tract velocity-time integral b. Heart rate c. Diameter of the LV outflow tract d. Nyquist limit (aliasing velocity) of the LY outflow tract pulsed Doppler spectrum

9. A patient with severe aortic regurgitation undergoes measurement of volumetric flow per minute across the LY outflow tract by using continuity-based methods. This will provide a measure that is: a. Identical to true forward output b. An overestimation of true forward output c. An underestimation of true forward output 10. Which of the following is the most appropriate method for determining the ejection fraction of a left ventricle with a large apical aneurysm? a. Area-length (prolate ellipsoid) b. Area-length (cylinder-hemiellipsoid)

c. Summation of disks (Simpson rule) d. Fractional area change 11. Automated boundary tracking facilitates measurement of all of the following except: a. Fractional shortening b. LVEF c. Fractional area change d. Strain rate

12. A family of pressure-volume loops is created during transient inferior vena caval occlusion. What is the slope of the line connecting the end-systolic points? a. Elastance b. Preload-recruitable stroke work c. dP/dt d. Prdoad-adjusted maximal power 13. The measurement of peak LV dP/dt requires which of the following Doppler spectra? a. Continuous wave, LY outflow b. Pulsed wave, LY outflow c. Continuous wave, descending thoracic aorta d. Pulsed wave, mitral inflow e. Continuous wave, mitral regurgitant jet 14. Doppler tissue imaging is used to record signals from the LY myocardium. These are typically: a. High velocity, high amplitude b. High velocity, low amplitude c. Low velocity, high amplitude d. Low velocity, low amplitude 15. Strain and strain rate measurements are derived from: a. Pulsed Doppler measurements ofLV outflow b. Continuous-wave Doppler measurements of LV outflow c. Automatic boundary detection: short-axis view d. Myocardial Doppler tissue imaging 16. Regional wall motion abnormalities are the hallmark ofLV dysfunction due to: a. Hypertensive heart disease b. Dilated cardiomyopathy c. Chronic severe mitral regurgitation d. Coronary artery disease 17. Using the 17-segment model of the left ventricle, akinesis of the inferoseptal segments is most likely to correspond to occlusion in which of the following coronary arteries? a. Right b. Left anterior descending c. Left circumflex 1B. Using the 17-segment model of the left ventricle, akinesis of the lateral wall segments is most likely to

174 I CHAPTER 7 correspond to occlusion in which of the following coronary arteries? a. Right b. Left anterior descending c. Left circumflex 19. Using the 17-segment modd of the left ventricle, akinesis of the apical cap is most likdy to correspond to occlusion in which of the following coronary arteries? a. Right b. Left anterior descending c. Left circumflex 20. Difficulty in imaging the left ventricle from the midesophageal views is reflected most commonly in: a. Oblique short-axis views b. Foreshortening of the apex c. Endocardial dropout of the base 21. Which of the following does not typically alter motion of the interventricular septum? a. Left bundle branch block b. Right ventricular pacing c. Right bundle branch block d. Right ventricular hypertension 22. Echocardiographic contrast agents may be used to optimize delineation of a. Left ventricular endocardium b. Left ventricular apical thrombus c. Continuous-wave Doppler spectral recording in the setting of aortic stenosis d. All of the above e. None of the above 23. Stunned myocardium is defined as: a. Myocardium after cardioversion for atrial fibrillation b. Myocardium that is hibernating c. Reperfused viable myocardium that is not functioning d. Myocardium that is functional at rest but not with exercise 24. Scarred myocardium after chronic myocardial infarction is characterized by all of the following except: a. Thinning of the wall b. More echogenic than the surrounding healthy myocardium c. Akinesis d. Speckled appearance 25. Assessment ofLV strain can be performed using: a. M-mode echocardiography b. Continuous-wave Doppler c. Contrast echocardiography d. Speckle tracking echocardiography

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30. Cerqueira MD, Weissman NJ, Dilsizian V, et al. Standardized myocardial segmentttion and nomenclature for tomographic imaging of the heart. A statement for healthcare professionals from the Cardiac Imaging Committee of the Council on Clinical Cardiology of the American Heare Association. Circulation. 2002;105(4):539-542. 31. Bolognesi R, Tsialtas D, Bacilli AL, et al. Detection of early abnormalities of left ventricular function by hemodynamic, echo-tissue Doppler imaging, and mitral Doppler ftow techniques in patients with coronary artery disease and normal ejection fraction.] Am Soc EchocllrriWgr. 2001;14(8):764--772. 32. Royse CF, Conndly KA, Maclaren G, et al. Evaluation of echocardiography indices of systolic function: a comparative study using pressure-volume loops in patients undergoing coronary artery bypass surgery. Anusthesill. 2007;62(2): I 09-116. 33. Skarvan K, Filipovic M, Wang J, et al. Use of myocardial tissue Doppler imaging fur intraoperative monitoring ofleft ventricular function. B]A. 2003;91(4):473-480. 34. Urheim S, Edvardscn T, Torp H, et al. Myocardial strain by Doppler cchocardiography. Validation of a new method to quantify regional myocardial function. Ci~n. 2000;102(10): 1158--1164. 35. Greenberg NL, Fimenberg MS, Castro PL, et al. Dopplerderived myocardial systolic strain rate is a strong index of left ventricular contraccility. Circulation. 2002; 105(1):99-105. 36. Armstrong G, Pasquet A, Fukamachi K, et al. Use of peak systolic strain as an index of regional left ventricular function: comparison with tissue Doppler velocity during dobutamine stress and myocardial ischemia. J Am Soc EchoCIZTdiogr. 2000;13(8):731-737. 37. D'Hooge J, Heimdal A, Jamal F, et al. Rq;ional strain and strain rate measurements by cardiac ultrasound: principles, implementation and limitations. Bur] Echoctmliogr. 2000; l (3): 154--170. 38. Kukucka M, Nasseri B, Tseherkaschin A. et al. The feasibility of speckle tracking fur intraopcrative assessment of regional myocardial function by cransesophageal echocardiography. ] CarriWthrm« Vmc Anesth. 2009;23(4):462-467. 39. Maclaren G, Kluger R, Connelly KA, et al. Comparative feasibility of myocardial velocity and strain measurements using 2 different methods with tran.sesophageal echocardiography during cardiac i;urgery.J CarrJWthorac V11.1cAno!Sth. 2011;25(2):216-220. 40. Scngupt1 PP, Tajik AJ, Chandrasckaran K, et al. Twist mechanics of the left ventricle: principles and application. ] Am Coll Canliol. 2008; 1(3) :366-376. 41. Erb JM, Shanewise JS. lncraoperative contrast cchocardiography with intravenous optison does not cause hemodynamic changes during cardiac surgery. ] Am Soc EchoCIZTdiov. 2001;14(6):595-600. 42. Grossgastciget M, Hien MD, Graser B, et al. Assessment ofleft ventricular size and function during cardiac surgery. An incraoperative evaluation of six two-dimensional echocardiographic methods with real time three-dimensional eehocardiography as a reference. EchoCIZTdiogmph. 2013;30(6):672-681. 43. Cowie B, Klugec R, Kalpokas M. Left ventricular volume and ejection fraction assessment with cransoesophageal echocardiography: 2D vs 3D imaging. B]A. 2013;110(2):201-206.

Left Ventricular Diastolic Function Alina Nicoara and Wanda M. Popescu

INTRODUCTION In recent years, diastolic function has received greater recognition for its impact on overall cardiac performance. Diastole is no longer regarded as a passive phase of the cardiac cycle, but rather as a complex sequence of interrelated events, which are dependent on loading conditions, heart rate, and contractility, and ultimately influence the systolic function of the left ventricle (LV). Studies have suggested that patients with diastolic dysfunction presenting for cardiac surgery are prone to hemodynamic instability and potentially worse outcomes1 and that patients with diastolic heart failure are at increased risk for decompensation in the perioperative period.2 Therefore, the perioperative echocardiographer should be familiar with the pathophysiology of diastolic heart failure and understand how to monitor and optimize diastolic function. Although advances in ultrasound technology have rendered Doppler echocardiography the clinician's "Rosetta Stone" for diastolic function evaluation, this chapter will familiariu: readers with all the echocardiographic techniques routinely employed to assess LV diastolic function, as well as more modem and sophisticated methods of diastolic function assessment, explain the significance of these diastolic indices, and provide a diagnostic algorithm to evaluate perioperative diastolic function.

CLINICAL IMPORTANCE OF DIASTOLIC DYSFUNCTION Diastolic dysfunction is defined as the inability to fill the LV to an adequate end-diastolic volume at a normal left atrial (LA) pressure. It represents a mechanical dysfunction of the LV, characterized by either impaired relaxation only or impaired relaxation and decreased compliance. Diastolic dysfunction may be absent at rest and may be unmasked by exercise, stress, or various perioperative events (tachycardia, pneumoperitoneum, positive pressure ventilation).3 Additionally, diastolic dysfunction may be present despite the absence of clinical signs and symptoms of heart failure. When these symptoms occur, the diagnosis of diastolic heart failure (or heart failure with preserved ejection fraction [EF]) is made. Therefore, whereas diastolic dysfunction

describes a cardiac mechanical abnormality, diastolic heart failure represents a clinical syndrome. Heart failure has an increasing prevalence in the United States.4 If current trends continue, 8.5 million Americans will suffer heart failure in 2030.5 Presently, heart failure is the most common cause of hospital admission in patients over 65 years of age, accounting for approximately 1 million admissions annually in the United States at a cost exceeding $15 billion.6 Nearly half of these patients, however, have a preserved EE7 The prevalence of diastolic heart failure is age dependent, increasing from less than 15% in patients younger than 45 years of age to 35% in those between the ages of 50 and 70 years, and more than 70% in patients older than 70 years.8 The increased prevalence of diastolic dysfunction in the elderly appears to be related to the coexistence of diseases associated with aging such as hypertension, coronary artery disease, aortic stenosis, and cardiomyopathies that alter the normal LV structure and lead to deterioration of the LV diastolic properties. However, the etiology of heart failure with preserved EF is multifactorial. It involves a complex interaction between impairments in left and right ventricular diastolic and systolic properties, a decrease in cardiovascular reserve, atrial dysfunction, stiffening of the arterial circulation with impaired vasodilation, and endothelial dysfunction.9 The annual mortality rate for patients with diastolic heart failure (5% to 8%) is lower than that for those with systolic heart failure, except in patients 70 years or older, where the mortality rates are similar.8 The presence of either diastolic dysfunction or heart failure with preserved EF is a predictor of morbidity and mortality, both in the general population and in the perioperative period. Therefore, the perioperative physician should assess the diastolic function as part of a risk stratification strategy.

Diastolic Dysfundion and Outcome In a recent meta-analysis using individual patient data, patients with heart failure with preserved EF had an overall lower mortality rate as compared to those with decreased EF. Nevertheless, the patients

LEFTVENTRICULAR DIASTOLIC FUNCTION I 177 with preserved EF had a higher mortality rate as compared with patients without any heart fuilure. 10 Grade III diastolic dysfunction has been associated with decreased survival in various patient po~ulations, such as after acute myocardial infarction, 1 h~ertensive patients, 12 chronic kidney disease patients, 3 and in patients with decreased EF. 14 More recent data suggest that even moderate forms of disease may affect survival. In a retrospective study including 36,261 patients, it was identified that the presence of moderate and severe diastolic dysfunction was an independent predictor for mortality, whereas mild diastolic dysfunctions did not affect survival rates. 15 Similarly, in the perioperative period, diastolic dysfunction has been associated with an increased risk of major adverse cardiac events and prolonged hospital stay. Flu et al have identified that the presence of preoperative asymptomatic ventricular dysfunction (systolic or diastolic) in patients undergoing vascular surgery is associated with increased short- and long-term morbidity and mortality. 16 Matyal et al have identified in patients undergoing vascular surgery a significant association specifically between the presence of perioperative diastolic dysfunction and postoperative heart failure, as well as an increased length of stay. 17 Swaminathan et al found that in patients undergoing coronary artery bypass surgery, the presence of worsening grades of diastolic function was associated with worse outcome (i.e., major adverse cardiac events). 18 Ferreira et al also showed that women undergoing coronary artery bypass surgery are at higher risk of diastolic dysfunction compared to men, with a significant age-gender interaction suggesting a possible age-related differential effect on diastolic dysfunction between the genders. 19 In a retrospective chart review, patients with diastolic heart failure had higher readmission rates and prolonged hospital stays as compared to matched controls.20 Additionally, in patients with severe sepsis or septic shock, the presence of diastolic dysfunction is a major predictor of mortality.21

Diastolic Dysfunction and Atrial Fibrillation Atrial fibrillation shares multiple common risk factors with diastolic dysfunction, such as age, hypertension, obesity, and diabetes. Several studies have demonstrated that diastolic impairment is associated with an increased risk for atrial fibrillation. The impact of diastolic dysfunction on the LA is three-fold: increases atrial afterload, increases atrial stretch, and increases atrial wall stress due to dilation.22 In a community-based cohort study of elderly individuals, the presence of echocardiographic indices of

diastolic dysfunction was strongly associated with an increased risk of atrial fibrillation. 23 The highest risk of developing atrial fibrillation is seen in patients with diastolic dysfunction and an indexed left atrial volume greater than 27 mUm2•24 Moreover, in patients with nonvalvular atrial fibrillation, an increase in E/e' and a decrease of e' velocity is independently associated with the development of a left atrial appendage thrombus.25 In the perioperative setting, new-onset atrial fibrillation occurs in a large patient population after cardiac surgery. It is associated with an increased risk of cerebrovascular events or even death. 26 Postoperative atrial fibrillation prolongs hospitalization and has a significant impact on the utilization of health care resources. In a prospective observational study of patients undergoing cardiac surgery, preoperative diastolic dysfunction was found to be a powerful independent predictor of postoperative atrial fibrillation. More importantly, this association increased exponentially with increasing severity of diastolic dysfunction. 27 Additionally, patients with new-onset or worsened diastolic dysfunction after cardiopulmonary bypass had an increased incidence of atrial fibrillation after coronary artery bypass surgery.28 These fu.cts have a significant clinical implication, as prophylaxis for postoperative atrial fibrillation is usually empiric. Therefore, preoperative and intraoperative assessment of diastolic function identifies high-risk patients and may allow a more selective approach to prophylactic antiarrhythmic therapy. Furthermore, preoperative decrease in LY filling pressures in patients with grade II or higher diastolic dysfunction may represent a possible strategy to decrease the incidence of postoperative atrial flbrillation.27

Diastolic Dysfunction and Hemodynamic Instability As illustrated by the previous text, the preoperative presence of diastolic dysfunction, especially advanced forms of the disease, should alert the perioperative cli~ nician that the patient may be at high risk for adverse outcomes and may be difficult to manage intraoperatively.29 Various perioperative events such as pain, hypovolemia, anemia, positive pressure ventilation, pneumoperitoneum, rate, and rhythm abnormalities directly affect the loading properties of the LY. This may result in either new-onset or worsening diastolic dysfunction with potential hemodynamic impairment. In a bariatric patient population undergoing laparoscopic gastric bypass, institution of pneumoperitoneum resulted in a decreased cardiac performance, as manifested by a significant drop in cardiac

178 I CHAPTER 8 output, and worsening of diastolic dysfunction. 3 In the cardiac surgical population, presence of moderate and severe diastolic dysfunction is associated with difficult separation from cardiopulmonary bypass30 and a more frequent use of inotropic therapy in the postoperative period. 1 Patients with diastolic dysfunction require a perioperative management strategy individualiud to their state of disease. Patients with mild forms of disease, manifested as impaired relaxation, may benefit from therapeutic strategies that decrease the heart rate, maintain sinus rhythm, and allow appropriate filling of the LY. In addition, an adequate preload is an essential factor for optimizing the cardiac performance. In contrast, patients with advanced diastolic dysfunction, manifested as decreased left ventricular compliance and increased left atrial pressures, require a strict fluid regimen, potentially guided by intraoperative transesophageal echocardiography or other noninvasive hemodynamic monitors.31 In this patient population, judicious administration of diuretic therapy may have a beneficial effect by decreasing intravascular volume and placing the patient in a more favorable position on the left ventricular pressurevolume loop.32 If vasopressor therapy is required, it is probable that the use of phenylephrine and norepinephrine will have the least impact on the diastolic properties of the heart, while vasopressin has been shown to decrease the diastolic time constant of relaxation and reduce the apical untwisting rate. 33

PHYSIOLOGY OF DIASTOLE From a clinical standpoint, the cardiac cycle has been divided into systole and diastole. Systole starts with closure of the atrioventricular valves and encompasses isovolumic contraction and ejection, finishing with the closure of the semilunar valves. At this point, diastole ensues, which comprises four phases: isovolurnic relaxation, early filling, diastasis, and atrial contraction (Fig. 8-1).

1. lsovolumic n:laxation begins with aortic valve (AV) closure and ends with mitral valve (MV) opening. During this interval, relaxation of cardiac muscle and a closed MV cause a decline in pressure. Because of the lack of blood flow and the absence of interaction with other parameters of ventricular compliance, physiologic assessment of relaxation is best achieved during this isovolumic phase and extrapolated to the other phases of diastole. Under normal conditions, the duration of this phase varies from 90 to 120 ms. Relaxation is influenced by the rate of inactivation of contractile proteins as a

result of an active, energy-dependent reentry of Ca2+ into the sarcoplasmic reticulum. In normal hearts, left ventricular relaxation occurs by "elastic recoil" using energy stored during systolic compression. A delay in the deactivation of the contraction proteins impairs the process of relaxation. 34 In addition, factors that affect intracellular Ca2+ removal may cause a Ca2 + release-reuptake mismatch, and hence lead to impaired relaxation. The preceding systolic load and its nonuniform distribution on the ventricular walls also affect ventricular relaxation. 2. The rapid filling phase starts with MV opening and extends to the equalization of pressure between the LV and LA. Under normal conditions, this phase accounts for approximately 80% of the ventricular filling and lasts from 180 to 200 ms. The persistence of myocardial relaxation and the elastic recoil of the myocardium during this phase create a drop in ventricular pressure, despite the initial increase in ventricular volume.35 Filling of the ventricle is thus thought to be the result of a "suction" mechanism rather than of a passive flow of blood into the ventricle. Equalization of atrial and ventricular pressures occurs at mid-diastole, when the rate of filling drops, representing the end of the rapid filling phase and the beginning of diastasis. The rapid filling phase coincides with and is dependent upon the continuous rdaxation of the myocardium. 3. Diastasis contributes less than 5% of the diastolic filling of the ventricle. Because myocardial relaxation has ended, filling becomes dependent mainly on the passive compliance of the myocardium, and any further increase in ventricular volume will lead to an increase in ventricular pressure. Because of its small contribution to ventricular filling, pathological changes affecting diastasis have little or no effect on overall filling. 4. Atrial, contracti.on occurs at the end of diastole; the increased LA pressure surpasses the LV pressure and generates additional forward flow from the LA to the LV. Atrial systole contributes, under normal conditions, to approximately 20% to 25% of total ventricular filling. During this phase, any additional increase in ventricular volume is coupled with an increase in ventricular pressure. The increase in atrial pressure also leads to a retrograde flow toward the pulmonary veins. Therefore, the contribution of this phase to total cardiac output depends on ventricular compliance, intrinsic atrial contractility, and ventricular pressure at the onset of atrial contraction. Diastole ends when the pressure in the LV exceeds the LA pressure, leading to MV closure.

LEFTVENTRICULAR DIASTOLIC FUNCTION I 179 Peak ejection

p

Clinical 1 IVC: I I I I

Ejection Suction

RELAXATION

CONTRACTION

I Diastasis I 1 I Passive filling I Atrial kick : FILLING

Physiological

Active relaxation

Visco-elasticity

Recoil

Compliance

i

I I

FIGURE 8-1. The first part of the graph depicts the time course of left ventricular pressure (LVP) and volume (LW) and left atrial pressure {LAP) during the cardiac cycle. According to the clinical definitions, the cardiac cycle is divided into the systolic and diastolic phases with their subdivisions: isovolumic contraction (IVC), ejection, isovolumic relaxation (IVR), rapid filling (RF). diastasis, and atrial contraction {LF). According to the physiological definitions, the cardiac cycle is divided into contraction, active relaxation, and filling phases. Note that the rapid filling phase is present in both the active relaxation and filling phases. See text for further explanations. The second part of the graph depicts the schematic representation of the determinants of intrinsic left ventricular diastolic function with respect to time. Note that active relaxation starts after peak ejection, in the second half of systole, and that the viscoelastic properties contribute to recoil during early diastole and to ventricular compliance during late diastole. (Reproduced with permission from Claessens TE, De Sutter J, Vanhercke D, et al: New echocardiographic applications for assessing global left ventricular diastolic function, Ultrasound Med Biol 2007Jun;33(6):823-841 .)

180 I CHAPTER 8 Nishimura and colleagues have proposed a physiological division of the cardiac cycle based on the loadbearing characteristics of the myocardium. From this point of view, the cardiac cycle is divided into three phases-systolic contraction, relaxation, and diastolic filling. 36 The contraction phase consists of isovolumic contraction and the first half of ejection and is characterized by a pressure increase in the LV followed by myocardial flber shortening that ultimately results in ejection of the blood into the ascending aorta. After the initial ejection, the myocardial flber will respond differently to a changing load, signaling the transition from the contraction phase to the relaxation phase. 37 The relaxation phase consists of the second half of ejection, the isovolumic relaxation period, and most of the rapid filling phase. In a normal heart, active relaxation is thought to finish at the end of rapid filling. The diastolic filling phase then includes a small portion of the rapid filling phase, diastasis, and atrial contraction. The critical insight from Nishimura et al's proposal is that myocardial relaxation begins during the second pan of ejection and continues during the isovolumic relaxation and rapid filling phase, illustrating the interdependency of systole and diastole (see Fig. 8-1). Similar to the LV, the LA cycles through passive phases, during rapid filling and diastasis, and an active phase, during atrial contraction. After MV opening, the LA pressure gradually decreases as a result of LV relaxation. During this phase, the blood flows passively from the pulmonary veins into the LA and is further suctioned into the LV. The LA functions at this time as an open conduit between the pulmonary veins and the LV. As the LY fills, the pressure gradient between the LA and LV decreases. Therefore, filling slows down and the LA reaches its end-diastolic volume. Subsequently, the LA contracts, ejecting blood into the LV. At the end of atrial systole, the LV pressure is higher than the LA pressure, and consequently, the MV closes. At this point, the LA is at its lowest volume. Following atrial contraction, the LA relaxes and is passively pulled down toward the apex of the heart by the contracting LV. Therefore, blood is suctioned from the pulmonary veins into the LA, resulting in LA filling. The LA volume just before the opening of the MY is considered the maximal atrial volume. Following MV opening, a new cycle commences. The LA functions as a barrier between the pulmonary veins and the LV. It protects the pulmonary vasculature from the wide pressure swings of the LV while at the same time it creates a passive conduit allowing LV filling from the pulmonary veins. However, the left atrial and ventricular diastolic processes are directly interrelated. Structural

and functional changes in the left atrium affect the structure and function of the LY and vice versa. The importance of the LA-LY diastolic function interplay is underscored by the fact that patients with diastolic dysfunction tolerate atrial fibrillation episodes very poorly.9

PATHOPHYSIOLOGY OF DIASTOLIC DYSFUNCTION The hallmark of diastolic dysfunction is the increased resistance to ventricular filling that produces an upward shift of the pressure-volume curve and accounts for a disproportionate increase in pressure relative to the increase in volume (Fig. 8-2).38 This ultimately leads to signs and symptoms of congestion and, in severe cases, to a decrease in ventricular filling and stroke volume. Diastolic dysfunction can be caused by intrinsic myocardial factors (e.g., alterations in calcium homeostasis, cytoskeleton, and extracellular matrix) or nonmyocardial extrinsic factors (e.g., afterload, pericardia! effusion or restriction, and right ventricular [RV] dilation).

Intrinsic Myocardial Factors Impaired calcium homeostasis is the main mechanism of impaired relaxation. Relaxation is an energy-dependent process that requires active removal of Ca2+ from the troponin C binding sites and from the cytoplasm by the sarcoplasmic reticulum.35 Removal of intracellular Ca2 + also occurs by extrusion and exchange with extracellular Na+ through the sarcolemma, and ultimately results in dissociation of actin-myosin crossbridges while consuming adenosine triphosphate. Factors that affect intracellular Ca2 + removal may cause a Ca2+ rdease-reuptake mismatch, leading not only to impaired relaxation but also to increased passive stiffness. Alterations in the extracellular matrix also affect diastolic function. Among the fibrillar proteins, proteoglycans, and basement membrane proteins that make up the extracellular matrix, fibrillar collagen is thought to contribute to the development of diastolic dysfunction by altering ventricular distensibility and increasing the resistance to filling. Alterations of collagen metabolism and fibrillar physical properties are determined by chronic changes in ventricular load, growth factors, and neurohormonal modulation, including the sympathetic nervous system and the renin-angiotensin system.8 Acute and chronic neurohumoral activation and/ or inhibition have variable effects on diastolic function. In contrast to the acute stimulation of the reninangiotensin-aldosterone system, in which arise in cardiac filling pressure is noted possibly by direct action on the

LEFTVENTRICULAR DIASTOLIC FUNCTION I 181 cardiomyocyte, chronic renin-angiotensin-aldosterone activation induces an increase in extracellular flbrillar collagen with increased passive stiffness. The effect of angiotensin on diastolic cardiac perfurmance may be related to changes in the mobilization and reuptake of cytosolic calcium.39

Nonmyocardial Extrinsic Fadors Extrinsic compression from lung or mediastinal masses and pericardia! diseases, such as effusion or constriction, result in direct compression of the ventricles, thus restricting ventricular filling. 8 Moreover, RV enlargement shifts the interventricular septum to the left, leading to an increase in LV pressure and alteration of ventricular fllling.40 Engorgement of coronary veins secondary to elevated right atrial (RA) pressure also increases myocardial blood volume and reduces the capacity of the ventricle to distend during diastole. Acute pressure or volume overload is another extrinsic cause of diastolic dysfunction. The increase in load tends to prolong ventricular contraction and to delay and shorten relaxation,41 an effect that can be reproduced by catecholamines, angiotensin, and vasopressin. Acute hypertension is a primary cause of decompensation of preexisting diastolic failure. Chronic overload as a consequence of chronic elevation of pressure (hypertension, aortic valve stenosis, or congenital disease) or chronic volume overload (valve incompetence or cardiomyopathy) produces myocardial cell hypertrophy as a compensatory mechanism.42 Hypertrophy in turn increases the likelihood of

diastolic dysfunction by impairing myocardial relaxation or by causing myocardial ischemia. Tachycardia also may produce diastolic dysfunction by increasing oxygen demand and by decreasing coronary perfusion and LV filling time, but it most often is an aggravating factor. Incomplete relaxation is a physiological response to prolonged systolic contraction (delayed systole) and leads to increased dependence on the atrial contribution to ventricular filling in late diastole. The loss of atrial contraction is often a precipitating factor in diastolic heart failure in patients with relaxation abnormalities.

INVASIVE MEASURES OF DIASTOLIC FUNCTION A physiological description of diastolic function is classically based on the analysis of ventricular volume and pressure changes over the period of a cardiac cycle. The cycle typically begins at end diastole, corresponding to the right lower corner of the pressurevolume loop (see Fig. 8-2). Measurable parameters used to describe and study diastolic function include relaxation and compliance. The effect of relaxation predominates during the first phase of diastole, whereas compliance affects mainly late diastole. In pathological situations, both parameters may interact, leading to diastolic dysfunction. 1. Relaxation can be assessed by the peak -dP/dt,

the duration of the isovolumic relaxation period (IVRT), and the time constant of relaxation (T).43 Peak-dP/dt (mm Hg/s) is the maximum

Dlastollc dysfunction

Systollc-cllutollc dysfunction - - - Normal

- - - - Normal

Dlastollc ,,, dysfunction

,,..,,,""'"

A

FIGURE B-2.

Volume

Normal

Normal

B

Volume

(A) Pressure volume relation in patients with isolated diastolic dysfunction characterized by a left and upward shift of the end-diastolic pressure-volume relation reflecting elevated filling pressures. (8) Pressure volume relation in patients with combined systolic-diastolic dysfunction characterized by a left and upward shift of the end-diastolic pressure-volume relation and also by a decline in the slope of the end-systolic pressure-volume relation reflecting decreased inotropy. CHF, congestive heart failure.

182 I CHAPTER 8 rate of LY pressure decline and is usually the lowest value of the first derivative of this pressure. The peak -dP/dt occurs at or around the time of aortic valve closure and appears to depend on aortic and LY pressures. Accurate calculation of -dP/dt necessitates invasive measurement of left intraventricular pressure. Like peak -dP/dt, IVRT is an index of pressure decline and can be assessed by Doppler echocardiography. IVRT is dependent on the timing of aortic valve closure and mitral valve opening. The time constant of relaxation (T) is mathematically derived from peak -dP/dt and measures the decay in ventricular pressure during relaxation. In humans, the T constant is equal to 30 to 40 ms, with lower values representing faster relaxation. Relaxation is considered complete after three to four time constants (120 to 150 ms). This time corresponds to the point at which peak early diastolic filling has occurred. 34 The T constant is relatively independent of preload but is affected by afterload. Impaired relaxation leads to a reduction in peak -dP/dt and prolongation ofIVRT and T. 2. Compliance is the ratio of change in volume to unit change in pressure (dY/dP) and depends on the intrinsic properties of the myocardium (myocardial compliance) and the geometric characteristics of the ventricular chamber (chamber compliance).8 Stiffness is the opposite of compliance and reflects the ratio of change in pressure to a unit change in volume (dP/dV). Chamber stiffness is not constant but increases throughout ventricular filling. Thus dY/dP and dP/dY are global indices and cannot be used to compare different ventricles.44 The relation between dP/dY and ventricular pressure, however, is linear, with a slope (K) called the modulus of chamber stiffness that is proportional to ventricular chamber stiffness. The slope becomes steeper with increases in ventricular chamber stiffness, a relation that is independent of ventricular geometry and therefore can be used to compare different patients. Examining the relation between stress (o") and strain (e:) during diastole assesses the intrinsic myocardial stiffness. Stress expresses the resisting force of the myocardium to increases in length, and strain is defined as the percentage change in muscle length during the application of a force (pressure change). The relation between do'/de: and stress is also linear, and the slope of this relation (K,,,) is the modulus of myocardial stiffness. The slope is steeper (Km increases) when myocardial stiffness increases.

ECHCARDIOGRAPHIC ASSESSMENT OF DIASTOLIC FUNCTION Although invasive microcatheter micrometry provides the most accurate measurement of diastolic function, direct measurement of these indices in the operating room is impractical. Therefore, intraoperative echocardiography, through the combination of various techniques such as two-dimensional (2D), Doppler, color M-mode, and tissue Doppler offers an attractive, efficient, versatile, and reproducible way of evaluating diastolic function and noninvasively estimating LY filling pressures. Most measured Doppler paruneters are dependent on load or heart rate and may be difficult to interpret individually; thus, evaluating one parameter would be insufficient to evaluate and understand all aspects of diastolic function. The analysis of any given parameter should always be coupled with all other parameters measured simultaneously. Also, algorithms for diastolic function evaluation are based mostly on studies conducted using transthoracic echocardiography (TIE) in patients breathing spontaneously, thus making it hazardous to extrapolate the application of such algorithms to intensive care or operative patients in whom load-dependent parameters can be altered by mechanical ventilation and/or general anesthesia.

TRANSMITRAL INFLOW The transmitral velocity profile detected by pulsedwave Doppler echocardiography directly reflects directly changes in LY filling and provides the initial basic information on LY filling dynamics and diastolic properties.45 Because the pressure gradients across the MY determine the volume and velocity of transmittal flow, transmitral Doppler flow pattern depends on LA and LY pressure. LA pressure in turn is determined by LA compliance and function, and LY pressure is determined by both LY relaxation and LY compliance.

Normal Patterns and Basic Variables Analogous to the different phases of diastole previously described, transmitral flow can be divided into four periods (Fig. 8-3). Measured parameters from the transmitral velocity profile include: 1. Iscwolwnic .reluation time (IVRI) represents the time needed for the LY myocardium to relax and for the LY intracavitary pressure to decrease below the LA pressure. IVRT is determined primarily by the timing of MY opening, which is influenced by the rate of LY relaxation and left atrial pressure.

LEFTVENTRICULAR DIASTOLIC FUNCTION I 183

- ----IVRT

___ [_____

OT

Diastasis A-dur

--r-------~--------:-------

-------------

Ar.

A

A

E

B

c

FIGURE B-3. (A) Schematic representation of the transmttral flow during dlastole. The parameters that characterize transmltral flow are IVRT, lsovolumrc relaxation time; E. peak velocity of early d!astollc fllllng; DT, deceleration time; A, peak velocity of atrial contraction; and A-dur, duration of A wave. (B) Transmltral flow recorded with pulsed-wave Doppler from a mldesophageal four-chamber by tTansesophageal echocardlography. (C) Transmittal flow showing an L·wave during diastasis. Ac, aortic valve closure.

2. E- wave is a downward deflecting wave generated by transmitral flow during early filling. Peak E velocity depends on the LA pressure at MV opening, the relative driving force between the LA and LY, minimal LV diastolic pressure, rompliance of the LA, and the rate of ventricular .relantion.-46 3. The deceleration time (DT) of the E velocity is the interval from peak E to the point of intersection of the deceleration of .flow with the baseline. DT correlates with time of pressure equalization between the LA and LV and is a measure of LV compliance.47 4. During diastasis very little flow occurs between the LA and the LV. On OCA::aSion a separate waveform, the L waft (see Fig. 8-3C), may be seen in

patients with very low heart rates due to continued blood flow from the pulmonary veins into the LA and the LV: 5. The A wine is ge.aerated by transmittal. flow dw:ing atrial contraction. Peak A vdocity is in£lue.nced by auial contractility, residual atrial pressure, and LV compliance. 6. The duration of atrial systole (A·'Wa"ft duration) is imponant in assessing LV filling pressure and is measured as the interval from the beginning to the end of the A wave. Mitra! velocity profiles change with age despite the absence of detectable cardiac diseases. This is due to agc-rdatcd alteration in theJhysiological properties of myocardial fibcrs. Norm values with regard to

184 I CHAPTER 8 age are summarized in Table 8-1. 48 In young subjects, the rate of rdaxation is vigorous, and LV filling occurs primarily during early diastole (80%). Therefore, mittal Doppler flow shows a high E vdocity, high E/A ratio, and short DT. However, with aging, there is a gradual decrease in the rate of myocardial rdaxation, as wdl as in dastic recoil. Thus, LV filling becomes slower, resulting in a prolonged IVRT and DT and a progressive decline in the E vdocity. Because early LV filling is reduced, the contribution of atrial contraction to LV filling becomes more imponant. In most individuals, the peak E- and A-wave velocities become approximately equal during the seventh decade of life, with atrial filling contributing up to 35% to 40% of LV end-diastolic volume (see Fig. 8-4).2 ,49,50

Technical Recommendations IVRT is best acquired from a deep transgastric longaxis view with a continuous-wave (CW) Doppler recording both aortic and mitral flows (Fig. 8-5). IVRT can be measured from the end of systolic ejection to the beginning of the E wave on the transmittal flow. Common pitfalls include mistaking wall motion anifacts for aortic valve closure clicks and angulating the beam too far toward the LV outflow tract, resulting in a delay in the recorded onset of mitral flow. The measurement of the other parameters of transmittal flow is performed using pulsed-wave (PW) Doppler in the midesophageal four-chamber (ME 4-ch) view. Proper alignment of the ultrasound beam,

Table B-1. Normal transthoracic echocardiographyvalues for Doppler-derived diastolic measurements in different age groups .

Age Group (y)

.

.

Measurement

16-20

21-40

41-60

>60

IVRT(ms) E/A ratio DT(ms) A duration (ms) PVS/Dratio PVAR(cm/s) PV AR duration (ms) Septal E'(cm/s) Septal E'/A' ratio Lateral E'(cm/s) Lateral E'/A' ratio

so ± 9 (32-68)

67 ± 8 (51-83) 1.53 ± 0.40 (0.73-233) 166 ± 14 (138-194) 127 ± 13 (101-153) 0.98 ± 032 (0.34-1.62) 21 ±8(5-37) 96 ± 33 (30--162) 15.5 ± 2.7 (10. 1-20.9) 1.6 ± 0.5 (0.6-2.6) 19.8 ± 2.9 (14.0--25.6) 1.9 ± 0.6 (0.7-3.1)

74 ± 7 (60--88) 1.28 ± 0.25 (0.78-1.78) 181 ± 19 (143-219) 133 ± 13 (107-159) 1.21 ± 0.2 (0.81-0.61) 23 ± 3 (17-29) 112±15 (82-142) 12.2 ± 2.3 (7.6-16.8) 1.1 ± 0.3 (O.S-1.7) 16.1 ± 2.3 (11.5-20.7) 1.5 ± 0.5 (0.5-2.5)

87 ± 7 (73-101) 0.96 ± 0.18 (0.6-1.32) 200 ± 29 (142-258) 138 ± 19 (100--176) 1.39 ± 0.47 (0.45-2.33) 25 ± 9 (11-39) 113 ± 30 (53-173) 10.4 ± 2.1 (6.2-14.6) 0.85 ± 0.2 (0.45-1 .25) 12.9 ± 3.5 (5.9--19.9) 0.9 ± 0.4 (0.1-1.7)

1.88 ± 0.45 (0.98-2.78) 142±19 (104-180) 113 ± 17 (79-147) 0.82 ± 0.18 (0.46--1.18) 16 ± 10 (1-36) 66 ± 39 (1-144) 14.9 ± 2.4 (10.1-19.7) 2,41 20.6 ± 3.8 (13.0--28.2) 3.1 1

Data are expressed as mean ± SO (95% confidence interval). Note that for E' velocity in subjects aged 16 to 20 years, values overlap with those for subjects aged 21 to 40 years. This is because E' increases progressively with age in children and adolescents. Therefore, the E' velocity is higher in a normal 20-year-old than in a normal 16-year-old, which results in a somewhat lower average E' value when subjects aged 16 to 20 years are considered. •standard deviations are not included because these data were computed, not directly provided in the original articles from which they were derived. Abbreviations: IVRT, isovolumic relaxation time; E, early diastolic peak velocity; A, late diastolic peak velocity; E/A, ratio of early to late velocities; DT, deceleration time of early diastolic wave; PV SID, ratio of systolic to diastolic peak pulmonary vein velocities; PVAR, peak velocity of pulmonary vein reverse atrial flow; E', early diastolic peak velocity by tissue Doppler imaging; A', late diastolic peak velocity by tissue Doppler Imaging. Reproduced with permission from Nagueh SF, Appleton CP. Gillebert TC, et al: Recommendations for the evaluation of left ventricular diastolic function by echocardiography,J Am Soc Echocardiogr 2009 Feb;22(2):107-133.

FIGURE 8--4. Schematic representation ofthe mitral velocity profile at different ages in a population with no

cardiac disease.

- - ~~-v---- - ----~v---- - -vv-- - - v v--

LEFTVENTRICULAR DIASTOLIC FUNCTION I 185 with a near-zero angle of incidence to the auioventricular inflow, minimizes errors in peak vd.ocity (6% error at 20 degrees), bdps place the sample volwue in an aiea of laminar Bow, and reduces the spectral broadening. which makes measurements of flow duration and dccdcracion time difficult. Typically. there is an angle of 20 degrees between mitral inffow (normally directed toward the lateral wall) and the LV longitudinal axis. Cardiac chamber remodeling, as in patients with dilated card.iomyopathy, can increase this angle to 40 degrees; in cases ofasymmetric bypertrophic cardiomyopatby, the direction of ftow can be even more difficult to delineate {Fig. 8-6).S1 In such A

FIGURE •-s. (A) Deep transgastrlc long-axis vtew with the dotted llne Indicating a conttnuouswave (CW) Doppler beam Intercepting the aortic valve flow and the transmltral valve flow. (Asc Ao, ascending aorta; AoV, aortic valve; MV, mitral valve.) (8) The velocity pattern obtained by applying CW Doppler as shown in panel (A). The isovolumic relaxation time (IVRT) Is measured from the aortic valve closure to the beginning of the transmltral dlastollc flow.

B

.

30"

'• •• \

FIGURE B-f. Alteration of mltral Inflow with progressive cardiac dllatton. Flow normally Is directed approximately 20 degree laterally toward the apex. With severe left ventricular dilation, optimal beam alignment may be as much as 40 degrees or more laterally from the apex.

186 I CHAPTER 8

A

B

instances, color Doppler imaging should be used to visualize the direction of the inflow in ea.eh patient and to obtain the best alignment with that flow. le is also important to reoognize that vdocicy profiles change with the Doppler sample position within the mitral inflow tract. For accurate evaluation of diastolic function, the PW Doppler sample volume typically is placed at the mitral leaflet tips. Moving from the mitral annulus to the tip of the leaflets produces an increue in E velocity and a decreue in DT (Fig. 8-7). However, the duration of the mitt.al A wave may be best acquired by moving che sampling gate into che annular plane of the mitral w.lve. Sample volume also should be reduced (1.5 to 2.0 mm) to obtain 1barper limit& of the spectral cnw-lopc and the most accurate DT. Further, the aliasing li.tn.it should be maintained between 0.7 and 1 m/s, the velocity Alter should be reduced (between 200 and 600 Hz) to improve visualization of low flows, a sweep speed of 50 to 100 mm/s should be implemented, and an average of three beats should be recorded..S1 The use of low·velocity filters is of par· ticular importance for the measurement of time inter· vals, which can be masked by the numerous anifu:ts seen at u:ro ba.scline. Normal w.lues fur the trarumi~ tra1 flow parameters are provided in Table 8~ I . Abnormal Pattarns

In diastolic dysfunction, three abnormal transmittal filling patterns have been described: impaired relaxation, pscudonormal, and restrictive filling. IMPAIRED REUXA110N PATTERN

c FIGURE B-7. Doppler envelope at different levels of the atrioventricular valve apparatus: the annulus, midportion of the leaflets, and tips af leaflets. Moving from t he mitral annulus to the tip of the leaflets

produces an Increase In peak velocity and a decrease of deceleration time. (A) Annulus. (BJ Mid portion of tile

The initial manife5tation of diastolic dysfunction is abnormal relaxation and i.s often seen in pacienu with hypertension and coronary artery disease, and in the elderly. Abnormal relaxation is ch.aractcri7.cd by a I.ow.:r rate of LY p~urc decay during isovolumic relaxation causing a delay in MV opening, which translates into a prolonged IVRT. Abnoimal LY relaxation al.so results in a lower pressure itraf{ient between IA and LY during early Alling. which leads to a compromised. early Alling and a slow equalization of pres.sures between LA and LV. This compromised early filling is compensated for by a forceful atrial contraction. Hence, che impalled. relaxation pattern ii charaacrizcd by a dccrea5C in peak E wave, an increase in peak A wave, an E/A ratio less than 1, and a prolonged OT (Fig. 8-8).

leaflets. (C) Tips of leaflets. PsEUDONORMAL PATTERN

As diastoUc dysfunction progresses, an alteration in LY compliance cruues and ahift& the filllng of the LY on che steeper portion of the pressure-volume relation. In this situation an increase in LY volume will

LEFTVENTRICULAR DIASTOLIC FUNCTION I 187

lead to a disproportionate increase ofLV pres.sure, and ultimatdy to a compe.naatory incrca&e of LA preS&ure. The inaeasc of LA pressure reestablishes the normal LA-LV pressure gradient. and therefore improves LV filling during the rapid filling phase. However, the "normalization" of diastolic filling is obtained at the cost of increased LA pressure, which is associated with a host of detrimental effects (LA enlargement, possible atrial arrhythmias, and ultimately heart failure). The normalized pressure gradient between LA and LV is ttanslated on the mitral inflow vdocity profile into a normal E/A ratio, normal DT, and normal IVRT. The pseudonormal pattern represents a transition period between isolated relaxation abnormality and disease progression toward dcc:rcascd compliance.49,50 Because the pattern "normalizes" due to an increase in preload, prefoad reduction using a Valsalva maneuver, reverse Trendclenburg position, or nittoglycerin administration will unmask. diastolic: dysfunction by changing the pseudonormal pattern to an impaired rdaxation pattern. In contrast, when diastolic function is normal,

A

the decrease in preload will result in a dcc:rcase in both peak. E and A velocities with an Wtc:hangcd ElA ratio.so Methods used to distinguish. a normal from a pseudonormal pattern are sununarized in Table 8-2. RESTRICTIVE P~ERN

In late stages of diastolic dysfunction, the LV compliance decreases drastically and leads tD severely increased inttacavitaty diastolic pre&aure and LA pressure. Patients with this type of abnormality have either isolated severe diastolic dysfunction (restrictive caidiomyopathy) or concomitant significant systolic dysfunction (dilated cardiomyopathy). The increased LA pressure results in an earlier MV opening and higher initial transmittal pressure gradient, producing a fast acceleration of blood flow into the LV during the rapid filling phase. Because the ventricle is very stiff. the LV pressure will rue rapidly to equaliu with LA pressure. Atrial contraction at the end of diastole will oontribute very little to the filling of the noncompliant LV, as increased LV pressure will terminate

B

FIGURE 8-8. Examples of mitral inflow reoorded with pulsed-wave Doppler. (A) Impaired relaxation. (8) Restrictive pattern. (E, early filling peak velocity; A, late filling peak velocity.) Table 8-2. Various methods to differentiate the pseudonormal from normal mltral flow pattern8 Cl!nlcal elements 20 echocardiography evidence of LV remodeling 20 echocardiography evidence of LA pressure elevation Preload reduction through dynamic maneuvers Doppler evidence ofelevated fllllng pressure byPVF

Age >70 years; hypertrophlc or ischemlc cardlomyopathy Hypertrophy, dilation, scars of myoosrdial infarction LA enlargement with h~tory ofatrial fibrillation or mitral valve disease Unmasked mttral Inflow pattem of Impaired relaxatton Systolic fraction 1). The systolic 6lling fraction is the ratio of systolic time-velocity integral (TVI) to the sum of the systolic and diastolic TVIs, with normal values being greater than or equal to 55%.

Technical Recommendations The PVF velocity profile is obtained by PW Doppler interrogation of the flow in the left or right upper pulmonary veins. Both upper pulmonary veins enter the attiwu in an anterior-to-posterior direction and are thus suitable for Doppler interrogation, whereas the lower pulmonary veins typically course in a lateral·t~ medial direction, entering the atrium almost perpendicular to the Doppler beam, making them less than optimal for routine assessment of PV ffow. The left

52

A

8

FIGURE 8-9. (A) Schematic representation of a normal pulmonary venous flow pattern. (8) Pulmonary venous flow recorded with pulsed-wave Doppler in 1he left upper pulmonary vein. There is an antegrade systolic flow with a biphasic pattern (S1 and S2), an antegrade diastolic flow {0), and a retrograde diastolic flow {AR). AR-dur, duration of the retrograde flow in late diastole.

190 I CHAPTER 8 upper pulmonary vein can be visualized lateral to the left atrial appendage by withdrawing the probe slightly from the ME 4-ch view and then turning to the left. Depending on the orientation of the heart within the mcdiastinum, advancement of the multiplane angle between 30 and 60 degrees may be necessary in order to align the Doppler beam parallel with the PV flow (Fig. 8-10). The right upper pulmonary vein can be visllalizcd in a modified bicaval view by withdrawing the ttansesophageal ecbocardiogram (TEE) probe and advancing the multiplane angle to 110 to 130 degrees until the .right upper pulmonary vein is seen lateral to the superior vena cava (see Fig. 8-10). Color flow Doppler with low-velocity settings is also useful in locating the pulmonary veins and assists in aligning

the Doppler beam with the laminar blood Bow. The PW Doppler sample ia positioned 1 to 2 cm into the PV. beyond its insertion into the left atrium. As with mitral inflow recordings, the velocity filter should be reduced in order to improve visualization of low Bows, a ~ecp speed of 50 to 100 mmls should be implemented, and an average of three beats should be recorded. To minimize the impact of changes in intra.thoracic pressures on PV flows, all measurements must be made at end expiration or during apnea. A small sample volume (1 to 2 mm) can produce a weak specttal signal containing excessive wall motion arti&as; therefore, increasing the sample volume from 2 mm to 3 to 5 mm may improve an inadequate signal. However, a large sample volume (>5 mm) as well as a Doppler g:Un set too high could result in a dense Doppler signal with spectral broadening. Wall motion arti&as are common in PV recordings and often mask the AR wave. Although these artifacts are difficult to eliminate completely, a slight angulation of the ttansducer beam or placing a larger sample volume (4 nun) further into the PV may improve the flow velocity signal.51 As the sample volume is moved into the pulmonary vein, the PVF profile is influenced more by pulmonary arterial pressure.71 Although the PVF profile is a more sensitive index of LA pressure when the sampling volume is placed at the atriovenous junction, in orde.r to obtain a clear Doppler signal, the sample volume has to be located 1 to 2 cm into the pv:s1

A

As stated earlier, because the LA functions as a passive conduit for flow during diastolic early filling. the PVF 0-wave vdocity correlates well with the mitral. ~wave velocity. In an isolated relaxation abnormality, the PVF D-wave, following the pattern of the transmittal Bow E wave, is diminished, resulting in an increase in the pulmonary venous systolic fractlon (S> > 0) and an increased S/D ratio (Fig. 8-11). In these patients, PVF AR-dur duration greater than transmitral mitral inflow A-dur may indicate an earlie.r stage of reduced LV compliance, as well as inaeased LV end-diastolic pressure)2 As diastolic dysfunction progresses to the pseudonormal pattern, the abnormally elevated LA pressure is associated with a decrease in forward systolic flow ("blunted" systolic pattern) and a more prominent diastolic velocity, resulting in a decreased systolic fraction (S30 ms) (see Table 8-3). In patients with fT'll,ie III diastolic dysfunction (restrictive filling), LV filling is determined by the very high LA pressure and the poor compliance of the LV. The elevated LA pressure results in an earlier opening of the mitral valve, accelerated early filling with very fast equalization of pressures between LA and LY, and very small contribution of the atrial contraction to the filling of the noncompliant LV (E/A >2, DT < 160 ms, IVRT < 60 ms). The very high LA pressure is supported by systolic filling fraction less than 40% on the PVF and average E/E' ratio > 13 (septal E/E' > 15, lateral E/E' > 12) (see Table 8-3). Treatment with diuretics in these patients by decreasing the intravascular volume, and therefore the filling pressures, may produce changes in the mitral flow

Table 8-3. Classification of different stages of diastolic dysfunction with mitral flow, pulmonary venous flow, propagation velocity, and mitral annular velocity

TMF E/A DT(ms) IVRT(ms) PVF PV-S/PV-D PV-AR {cm/s) ARdur-Adur Vp

Nonnal

Impaired Relaxation

Pseudonormal

Restrictive Filling

1-2 150-220 60-100

200 >100

0.8-1.5 150-220 >100

;::2 1 13 and septa! E/e'> 15 are considered abnormal), LA maximum volume index >34/mUm2 , and peak tricuspid regurgitation (TR) velocity >2.8 m/s. LY diastolic dysfunction is present if more than half of the available parameters meet the cutoff values (Fig. 8-14A). The 2016 ASE update also recommends using the same variables in order to estimate LY filling pressures in patients with underlying myocardial disease with reduced or preserved LVEE When the transmitral flow pattern shows an E/A S 0.8 with a peak E velocity S50 emfs, the mean left atrial pressure (LAP) is either normal or low with a corresponding grade I diastolic dysfunction. When the transmitral flow pattern shows an E/A > 2, LA mean pressure is elevated, corresponding to grade III diastolic function. When the transmitral flow shows an E/A S 0.8 with a peak E velocity > 50 cm/s or if the E/A ratio is >0.8 but 14 2of3 or 3 of3 Negative

2-TR velocity> 2.8 rn/s 3-LA Vol. index> 34mVm2

2of3 or 3 of3 Positive

When only 2 criteria are available 2 negative

Normal LAP Grade I Diastolic Dysfunction

1 positive and 1 negative

Cannot determine LAP and Diastolic Dysfuntion Grade

2posltlve

jLAP

jLAP

Grade II Dtastollc Dysfunction

Grade Ill Dlastollc Dysfunction

B FIGURE 8-14. (A) Algorithm for diagnosis of left ventricular (LV) diastolic dysfunction (BJ Algorithm for estimation of LVfilling pressures and grading LV diastolic function in patients with depressed LV ejection fraction (EF) and patients with myocardial disease and normal LVEF. (Reproduced with permission from Nagueh SF, Smiseth OA, Appleton CP, et al: Recommendations for the Evaluation ofLeftVentricular Diastolic Function by Echocardiography: An Update from the American Society of Echocardiography and the European Association of Cardiovascular lmaging,JAm Soc Echacardiogr 2016 Apr;29(4):277-314.)

LE FT VENTRICULAR DIASTOLIC FUNCTION I 20 I E'velocity

/

E'~10cm/s

~ E'6 and diastolic predominance with prominent V- and A-wave reversals on the HVF; and (3) restrictive filling: FJA > 2.1, DT of the E wave D) are consistent with grade I diastolic function with impaired relaxation pattern. The patient has a prolonged PR interval (first-degree AV block), which leads to a fused E-A pattern on the transmitral Bow. In spite of evidence of ddayed relaxation, Yp is normal (Vp = 61 cm/s). This occurs most likdy in the setting of LY hypertrophy with a small LY cavity and normal ejection fiac:tion, one of the limitations of interpreting propagation velocity.32

Case2 A 62-year-old morbidly obese patient (BMI 48 k:glm2) with a history of hypertension presented for laparoscopic gastric bypaas. Hia most recent TTE showed a normal LY ejection :fraction and normal diastolic function with no valvular abnormalities.

After induction of general anestbcsia, inuaoperative TEE assessment of diastolic function showed normal values of the septa! and lateral E' vdocities (septa! E' = 13 emfs) as well as normal filling pressures (EIE' = 8) (Fig. 8-lSA). Following abdomen insufflation for the Iaparoscopic procedure, another assessment of diastolic function showed that the septa! E' velocity decreased significantly (E' = 5 emfs). and the E/E' was consistent with severely elevated left atrial pressures (E/E' = 20) (Fig. 8-18B). The LY ejection fraction was preserved throughout. Following desufflation, the E' vdodties and the E/E' normaliud (septa! E' = 9cm/s, E/E' = 9; Fig. 8-18C). The cardiovascular structwal changes seen in obesity arc represented by an increase in arterial and left ventricular chamber stiffness, resulting in clinical or subclinical forms of diastolic dysfunction. In this setting. the institution of pneumoperitoneum with

A

B

c

D

FIGURE B-17. {A) Transmltral flow: A, peak velocity of atrial contraction; E, peak veloclty of early fllllng. (B) Pulmonary vein flow: 0, peak velocity of the diastolic component; S, peak velocity of the systolic component (C) Tissue Doppler Imaging: E~ early diastolic veloctty of mltral annulus by tissue Doppler Imaging; A' mltral annulus velocity during atrtal contraction. (D} Propagation velocity.

204 I CHAPTER 8

A

B

,

"'

•w

.•.

lO

I

TO 8 '1

r

r.1, 1!

-

''

I

..• 11 ...9'-

,. I

""

•

·-"

I' ., ,

;\ ·~-.

I

,.

/\

'

AM ('r .1bdQn'INl dC'~u f! l,it>on

c FIGURE 8- 78. (A) Tissue Doppler Imaging of the septaI mlt.Tal annulus at baseline. (8) Tissue Doppler Imaging of the septaI mitral annulus after abdomen insufflation. (C) Tissue Doppler imaging of the septaI mitral annulus after abdomen desuffiation. E', early diastolic velocity of mit.Tal annulus.

subsequent increases in afi.crload rendered a considerable change in cardiovascular performance. This case highlights the fu.ct that various common perioperative events (i.e .. pneumoperitoneum, positive pressure ventilation) can unmask. subdinical forms of diastolic dysfunction, in particular in an "at-risk" patient population.3

CONCLUSION .Asses&ment of LV diastolic function should be an integral pan of the routine echocardiographic examination. Although frequently underestimated, diastolic dysfunction is common and can be a cause of hemodynamic instability in patients undergoing surgery or in patients in the intensive care unit. A systematic, stepwise Doppler evaluation of diastolic function complements 20 imaging and provides clinically relevant infurmation in a noninvasive and prompt fashion.

REVIEW QUESTIONS Select the one best answer for each of the following questions. 1. In patients with LV systolic dysfunction, devation of PCWP is likely to occur when E-wave OT is: a. 300 ms c. 1=65 years of age with abnormal left venuicular diastolic rdaxation. Am J QinJjoL 2003;93:54-58. Doukky R. Garcia-Sayan E, Gage H, et al. The value of dia· stolic function parameters in the prediction of left atrial appendage thrombus in patients with nonvalvular atrial fibril· lation. Clt1Jio1111Sc Uhmsormd. 2014 Feb 25;12:10. Fl-Chami MF, Kilgo P. Thourani V, et al. New-onset atrial fibrillation predicts long-term mortality after coronary artery bypass graft.] Am Coll OirJioL 2010;55:1370-1376.

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80. Castdlo R, Vaughn M, Dressler FA,

et al. Relation between pulmonary venous flow and pulmonary wedge pressure: influence of cardiac output. Am Heart]. 1995;130:127-134. 81. Klein AL, Bailey AS, Cohen GI, et al. Effects of mittal stenosis on pulmonary venous flow as measured by Doppler uansesophageal cchocardiography. Am] CawJWL l 993;72:66-72. 82. Klein AL, Stewart WJ, Bartlett J, et al. Effects of rnitral regurgitation on pulmonary venous flow and left atrial pressure: an intraoperative transesophageal cchocardiographic study. J Am

Co/J Carriiol. l 992;20: 1345-1352. 83. Marcucci C, Lauer R, Mahajan A New echocardiographic techniques for evaluating left venuicular myocardial function.

Snrsirs Carriiothorac Vase Anesth. 2008; 12:228-247. 84. Nagueh SF, Sun H, Kopden HA, et al. Hemodynamic deter-

85.

86. 87.

70. Nishimura RA. Abd MD, Hade LK. Relation of pulmonary vein to mitral flow velocities by uansesophageal Doppler echocardiography. Effect of diffctent loading conditions. CiTCUlation. 1990;81:1488-1497.

71. Appleton CP. Hemodynamic determinants of Doppler pulmonary venous Row velocity components: new insights from studies in lightly sedated normal dogs. ] Am Coll CarrJioL

1997:30:1562-1574. 72. Hoit BD, Shao Y, Gabd M, et al. Influence of loading conditions and contractile state on pulmonary venous flow. Validation of Doppler velocimctty. Cimdation. 1992;86:651-659.

73. Tabata T, Thomas JD, Klein AL. Pulmonary venous flow by doppler echocardiography: revisited 12 years later. J Am Coll CarrJioL 2003;41:1243-1250. 74. Rossvoll 0, Hatle LK. Pulmonary venous flow velocities recorded by uansthoracic Doppler ultrasound: rdation to left ventricular diastolic pressures. ] Am Coll CawJWL 1993;

21: 1687-1696. 75. Yamamuro A, Yoshida K, Hozumi T, et al. Noninvasive evaluation of pulmonary capillary wedge pressure in patients with acute myocardial infarction by decderation time of pulmonary venous flow velocity in diastole. J Am Coll CawJioL

1999;34:90-94. 76. Klein AL, Tajik AJ. Doppler assessment of pulmonary venous Row in healthy subjects and in patients with heart disease.

] Am Soc Echocawiiogr. 1991;4:379-392. 77. Garcia MJ, Thomas JD, Klein AL. New Doppler cchocardiographic applications fur the study of diastolic function. ] Am Coll Gm/io/. 1998;32:865-875.

88.

minants of the mitral annulus diastolic velocities by tissue Doppler.] Am Co/J CarJWl. 2001;37:278-285. Dumesnil JG, Paulin C, Pibarot P, et al. Mitral annulus velocities by Doppler tissue imaging: practical implications with regard to prdoad alterations, sample position, and normal values.] Am Soc EchocawiWgr. 2002;15:1226-1231. Garcia MJ, Thomas JD. Twue Doppler to assess diastolic left ventricular function. Echoctmliography. 1999;16:501-508. Sohn DW, Chai lli, Lee DJ, et al. Assessment of rnitral annulus velocity by Doppler tissue imaging in the evaluation of left ventricular diastolic function.] Am Coll CarrJioL 1997;30:474-480. Nagueh SF, Middleton KJ, Kopden HA, et al. Doppler tissue imaging: a noninvasive technique fur evaluation of left ventricular relaxation and estimation of filling pressures.] Am Coll

Carriiol. 1997;30:1527-1533. 89. Rivas-Gatz C, Manolios M, Thohan V, et al. Impact of left ventricular ejection fraction on estimation of left ventricular filling pressures using tissue Doppler and Row propagation velocity. Am] Cardiol. 2003;91:780-784.

90. Ommen SR, Nishimura RA. Appleton CP. et al. Clinical utility of Doppler echocardiography and tissue Doppler imaging in the estimation ofleft ventricular filling pressures: a comparative simultaneous Doppler-catheteri7.ation study. CiTCUlation.

2000;102:1788-1794. 91. Mankad S, Murali S, Kormos RL, et al. Evaluation of the potential role of color-coded tissue Doppler cchocardiography in the detection of allograft rejection in heart uansplant recipients. Am Hurt]. 1999;138:721-730. 92. Nagueh SF, Bachinski LL, Meyer D, et al. Tissue Doppler imaging consistently detects myocardial abnormalities in patients with hyperuophic cardiomyopathy and provides a novd means fur an early diagnosis before and independently ofhypertrophy. Cimdation. 2001;104:128-130. 93. Nagueh SF, Mikati l, Kopelen HA, et al. Doppler estimation of left ventricular filling pressure in sinus tachycardia. A new application of tissue doppler imaging. CiTCUlation.

1998;98: 1644-1650. 94. Garcia MJ, Rodrigue"L L, Ares M, et al. Differentiation of consuictive pericarditis &om restrictive cardiomyopathy: assessment

212 I CHAPTERS of left ventricular diastolic velocities in longitudinal axis by Doppler tissue imaging.]Am Coll Carrliol 1996;27:108--114. 95. Rivas-Gott C, Khoury DS, Manolios M, et al. Time interval between onset of mitral inflow and onset of early diastolic velocity by tissue Doppler: a novel index of left ventricular rclantion: experimental studies and clinical application. ] Am Coll Cardiol. 2003;42:1463--1470. 96. Gillebcrt TC, De Pauw M, l!Dlmermans F. Echo-Doppler assessment of diastole: flow, function and haemodynamics. HellTt. 2013;99:55-64. 97. Soel-5 Ventricular systolic ejection of the RV is in a peristaltic manner different from the twisting and rotational motions that predominate on the left side. Right ventricular contraction is sequential, beginning with the inlet portion contracting toward the apex and ending with the infundibulum. The ejection phase begins earlier and lasts longer, and the velocity profile is characterized by a lower and delayed peak. 6-8 Ventricular interdependence is also a feature to be remembered in assessing RV {or LV) function. It is a term used to describe the dysfunction of one ventricle secondary to a disorder of the other, through direct mechanical interactions mainly due to the

involvement of the interventricular septum and the constraint of the pericardium. Under normal conditions, the septum is concave toward the LV during the entire cycle. With RV pressure or volume overload, the interventricular septum (IVS) flattens or displaces toward the LV, impairing compliance and filling.9,lO Ventricular interdependence is not only diastolic but also systolic, mediated primarily by the intcrventricular septum. Animal studies have shown that approximately 20% to 40% of the RV systolic pressure and volume outflow of the RV results from LV contraction.9

TOMOGRAPHIC VIEWS OF THE RIGHT VENTRICLE Although the vast majority of information about the RV can be obtained from a small number of images, the chamber's complexity defies standardized description or definition. The RV is located directly behind the sternum, appearing triangular shaped when viewed in midesophageal four-chamber view and crescent shaped, when viewed in cross-section, while sharing the septal wall with the left ventricle. Likewise, although it usually appears smaller than the LY, its end-diastolic volume is actually grcater.3 As the RV cannot be completdy seen in any single image, multiple scan planes are required to adequately assess RV structure and function. The RV has approximately one-fourth the mass of the LV11- 14 and performs about one-quarter of its partner's stroke work. 6 It consists of a free wall, an inferior or diaphragmatic wall, a septal wall, and an outflow tract (RVOT) region, although there is no formal segmental scheme for classifying wall motion as exists for the LV. Despite this, a series of guidelines have been developed that attempt to establish standards for measurement of global RV size and function. Most important of these are the Recommendations for Chamber Quantification, developed jointly by the American Society of Echocardiography (ASE) and the European Association of Echocardiography. 11 •15 These standards were developed by a combination of methods, including sratistical calculation of standard deviation, expert opinion, and assessment of associated outcome. It is

RIGHTVENTRICULARFUNCTION I 215

recommended that the same values be used to assess RV si2:e fur both TEE and ttansthoracic ech.ocardiography ('ITE), even though the actual images obtained may be markedly different.13 Quantification with TEE is frequently very challenging due to the inc.reased difficulty in achieving standard image planes and views.

Midesophageal Views The mUksophageal four-chamber (ME-4ch) view is probably the most useful view fur RV assessment. To image the RV; the standard ME-4ch view is obtained and the probe is then turned slightly to the right to bring the tricuspid valve into the middle of the screen

FIGURE,_ t. Midesophageal fourchamber view, with the probe turned to the patient's right side bringing the RA and RV Into view. Note the rtght ventricular enlargement and hypertrophy In this Image. RA, rtght atrium; LA, left atrium; RV, right ventrlde; LV, left ventride.

FIGURE g-2. Midesophageal four-chamber view focused on the r1ghtventrlde with short-axis (basal and mid) and long-axis dimensions marked. Abnonnal dimensions are noted In Table~1.

(Fig. 9-1, Video 1). 1 The basilar RV fu:e wall will be to the left of the screen, and the apical portion of the free wall will be in the fur fidd or slightly to the right,

depending on the orientation of the heart. It may be useful to increase the multiplane angle to 10 to 20 degtees to optimi7.e the view of the RV cavity. A norm.al RV will be no more than two-thirds the longitudinal extent of the LV, with the LV comprising the apex of the heart. From this imaging plane, the basal, mid.cavity and longitudinal diameters of the RV may be measured and systolic motion qualitatively a.sse&&ed (Fig. 9-2). In addition. color flow Doppler (CFD) and specttal Doppler analysis of tmnstticuspid flow, a.s well as tissue Doppler enmination of the tricuspid

216 I CHAPTER 9 annulw,. may be pcrfunncd from this image to evaluate possible valvular patholagy and diastolic dysfunction. The ME-4ch view is al&O an excellent view in which to quantify the right attiwu (RA) by measuring its major and minor axes and comparing it to its

Table 9-1. Reference values for right atrium and right ventride (all measurements are in millimeters)

RA

Length Minor axis diameter

RV Basal diameter Mid-diameter

Longitudinal diameter Wall thickness

2.1

Otherd•t• EIE'> 6 D>SonHVF DT 10 cmls 20. A patient is found to have a tricuspid regurgitation jet velocity of 3.69 m/s with a measured central venous pressure of 10 mm Hg. Please estimate the patient's pulmonary artery systolic pressure? a. 55 mm Hg b. 45 mm Hg c. 65 mm Hg d. 69mmHg

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6. Farb A. Burke AP, Virmani R Anatomy and pathology of the right ventricle (including acquired tricuspid and pulmonic

valve disease). Ctlrdiol Clin. 1992;10:1-21. 7. Ho SY, Nihoyannopoulos P. Anatomy, echocardiography, and normal right ventricular dimensions. Heart. 2006;92(suppl l):i2-i13. 8. Jiang L, Wiegcrs S, Weyman AE. Right Vmh"ick. 2nd ed. Philaddphia, PA: LWW; 1994. 9. Haddad F, Hunt SA, Rosenthal DN, et al. Right ventricular function in cardiOV3&cular disease, part I: anatomy, physiology, aging, and functional assessment of the right ventricle. Cirr:tdation. 2008;117:1436-1448. 10. Vitarclll A. Terzano C. Do we have two hearts? New insigha in right ventricular function supported by myocardial imaging cchocardiography. Heart Fail &v. 2010;15:39-61. 11. Lang RM, Badano LP, Mor-Avi V. et al. Recommendations for cardiac chamber quantification by echocardiography in adula: an update from the American Society of Echocardiography and the European Association of CardiOV3&CUlar Imaging. ]ASE. 2015;28:1-39, e14. 12. Lorenz CH, Walker ES, Morgan VL, et al. Normal human right and left ventricular mass, systolic function, and gender

RIGHT VENTRICULAR FUNCTION I 235 differences by cine magnetic resonance imaging. J CanJiolJllSc

Magn &son. 1999;1:7-21. 13. Maccira AM, Prasad SK, Khan M, et al. Rdi:rcnce right ventricular systolic and diastolic function normalized to age, gender and body surface area from steady-state free precession cardiovascular magnetic resonance. Eur Heart ]. 2006;27:2879-2888. 14. Sandstede J, Lipke C, Beer M, et al. Age-- and gender-specific differences in left and right ventricular cardiac function and mass determined by cine magnetic resonance imaging. Eur RtzdioL 2000;10:438-442. I 5. Lang RM, Bierig M, Devereux RB, et al. Recommendations fur chamber quantification: a report from the American Society of Echocardiography's Guidelines and Standards Committee and the Chamber Quantification Writing Group, dcvdoped in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. JASE. 2005;18:1440-1463. 16. Lee FA. Hcmodynamics of the right ventricle in normal and disease states. CanlioJ Clin. 1992; 10:59-67. 17. Mebazaa A. Karpati P, Renaud E, et al. Acute right ventricular failure-from pathophysiology to new treatments. lntmsive Care Med. 2004;30:185-196. l 8. Bronicki RA, Baden HP. Pathophysiology of right ventricular failure in pulmonary hypertcmion. Pediatr Crit Care Mui. 20lO;11:S15-522. 19. Llndqvist P. Momer S, Karp K, et al. New aspects of septal function by using I-dimensional strain and strain rate imaging. ]ASE. 2006;19:1345-1349. 20. Redington AN, Gray HH, Hodson ME, et al. Characterisation of the normal right ventricular pn:ssure-volume relation by biplane angiography and simultaneous micromanometer pressure measurcmenrs. BH]. 1988;59:23-30. 21. Klima U, Guerrero JL, Vlahakes GJ. Contribution of the interventricular septum to maximal right ventricular function. Eur j Canliothorac Surg. 1998;14:250-255. 22. Otto C. Echocanliofl"'Phk Evalua#on ofLeft and !Ught Vmlricu-lar Systolic Function. 2nd ed. Philaddphia, PA: Saunders; 2000. 23. Cacho A, Prakash R, Sarma R, et al. Usefulness of two-dimensional echocardiography in diagnosing right ventricular hypertrophy. Chtst. l 983;84: 154-157. 24. Goldstein JA. Parhophysiology and management of right heart i&chemia.J Am Coll CanlioJ. 2002;40:841-853. 25. Louie EK, Rich S, Levitsky S, et al. Doppler echocardiographic demonstration of the differential effects of right ventricular pressure and volume overload on left ventricular geometry and filling.] Am Coll Canliol. 1992; 19:84-90. 26. Little WC, Reeves RC, Arciniegas J, et al. Mechanism of abnormal interventricular septa! motion during ddayed left ventricular activation. Cirt:11!4tion. 1982;65:1486-1491. 27. Piazza G, Goldhaber SZ. The acutdy decompensated right ventricle: pathways for diagnosis and management. Chest. 2005;128:1836-1852. 28. Shanewise JS, Cheung AT, Aronson S, et al. ASE/SCA guidelines fur performing a comprehensive intraoperative multiplane transesophageal echocardiography examination: recommendations of the American Society of Echocardiography Council fur lnuaoperative Echocardiography and the Society of Cardiovascular Anesthesiologisrs Task Force for Cenifkation in Perioperative Transesophageal Echocardiography. Anesth Ana{g-. 1999;89:870-884.

29. Kasper J, Bolliger D, Skarvan K, et al. Additional cross-sectional transesophageal echocardiography views improve perioperative right heart assessment. Anesthesiology. 2012; 1l7:726-734. 30. Wilson BC, Cohn JN. Right ventricular infarction: clinical and pathophysiologic considerations. Adv Iniern Med. 1988;33:295-309. 31. Christaki& GT, Frcmes SE, Weisd RD, et al. Right ventricular dysfunction following cold potassium cardioplegia. J Thor« CanJiOIJllSc Surg. 1985;90:243-250. 32. Winkdmann J, Aronson S, Young CJ, et al. Rctrogradedelivered cardioplegia is not distributed equally to the right ventricular free wall and septum. ] Canliothorac Vase Anesth. 1995;9:135-139. 33. Denault AY, Chaput M, Couture P, et al. Dynamic right ventricular outflow tract obstruction in cardiac surgery. ] Thorac CanliOIJllSc Surg. 2006;132:43-49. 34. Bommer W, Weinert L, Neumann A, et al. Detetmination of right atrial and right ventricular size by two-dimensional echocardiography. Cimdation. l 979;60:91-100. 35. David JS, Tousignant CP, Bowry R. Tricuspid annular velocity in patients undergoing cardiac operation using transcsophageal echocardiography. ]ASE. 2006; 19:329-334. 36. Mi&hra M, Swarninathan M, Malhotra R, et al. Evaluation of right ventricular function during CABG: transcsophageal echocardiographic asses&ment of hepatic venous flow vusus conventional right ventricular performance indices. Echocardiography. 1998;15:51-58. 37. Di Mauro M, Calafiore AM, Penco M, et al. Mitra! valve repair for dilated cardiomyopathy: predictive role of right ventricular dysfunction. Eur Heart]. 2007;28:2510-2516. 38. Samad BA, Alam M, Jensen-Urstad K. Prognostic impact of right ventricular involvement as assessed by tricuspid annular motion in patients with acute myocardial infuction. Am] CardioJ. 2002;90:778-781. 39. Lopez-Candales A, Rajagopalan N, Saxena N, et al. Right ventricular systolic function is not the sole determinant of tricuspid annular motion. AmJ Canliol. 2006;98:973-977. 40. Anavekar NS, Gerson D, Skali H, et al. Two-dimensional assessment of right ventricular function: an echocardiographicMRI correlative study. Echocanliofl"'Phy. 2007;24:452-456. 41. Maslow AD, Regan MM, Panzica P, et al. Prccard.iopulmonary bypass right ventricular function i& associated with poor outcome after coronary artery bypass grafting in patients with severe left ventricular systolic dysfunction. Anesth Analg. 2002;95:1507-1518, table of contents. 42. Anconina J, Danchin N, Sdton-Suty C, et al. Noninvasive estimation of right ventricular dP/dt in patients with tricuspid valve regurgitation. Am] Canliol. 1993;71:1495-1497. 43. Imanishi T, Nakatani S, Yamada S, et al. Validation of continuous wave Doppler-determined right ventricular peak positive and negative dP/dt: effect of right atrial pressure on measurement.] Am Coll CanlioL 1994;23:1638-1643. 44. Kass DA, Maughan WL, Guo ZM, et al. Comparative influence of load versus inotropic states on indexes of ventricular contractility: experimental and theoretical analysis based on pressurevolume relationships. Cimdanon. 1987;76:1422-1436. 45. Pavlicek M, Wahl A. Rutz T, et al. Right ventricular systolic function assessment: rank of cchocardiographic methods vs. cardiac magnetic resonance imaging. Eur J Echoamliogr. 2011;12:871-880.

236 I CHAPTER 9 46. Tei C, Ling LH, Hodge DO, et al. New inde:x of combined systolic and diaiicolic myocardial performance: a simple and reproducible measure of cardiac function-a study in normals and dilated cardiomynpachy.] CtJTdioL 1995;26:357-366. 47. Haddad F, Denault AY, Couture P. et al. Right ventricular myocardial performance index predicts perioperativc mortality or circulatory failure in high-risk valvular surgery. ]ASE. 2007;20:1065-1072. 48. Vogel M, Schmidt MR, Kristiansen SB, et al. Validation of myocardial aeceleration during isovolumic contraction as a novel noninvasivc inde:x of right ventricular contraccility: comparison with ventricular pressure-volume relations in an animal modd. Circu'4tion. 2002;105:1693-1699. 49. Kjacrgaard J. Assessment of right ventricular S)'3tolic function by tissue Doppler echocardiography. DM]. 2012;59:B4409. 50. Tcrnacle J, Berry M, Cognet T, et al. Prognostic value of right ventricular twi:H:limensional global strain in patients referred for cardiac surgery. ]ASE. 2013;26:721-726. 5 L Benchimol A, Desser KB, Hasueiter AR. Right ventricular volume in congenital heart &ease. Am] Ctmiiol. 1975;36:67-75. 52. Ferlinz J, Gorlin R, Cohn PF, et al. Right ventricular performance in patients with coronary artery disease. Circulation. 1975;52:608-615. 53. Panidis IP, Ren JF, Kotler MN, et al. Two-dimensional echocardiographic estimation of right ventricular ejection fraction in patients with coronary artery disease. ] Am Coll CtmiioL 1983;2:911-918.

54. Jainandunsing JS, Matya! R, Shahul SS, er al. 3-dimensional right ventricular volume assessment. J Cttrdiothonu: V.uc Anerth. 2013;27:367-375. 55. Cacciapuoti F. Echocardiographic evaluation of right heart function and pulmonary vascular bed. lnt] C4rtiiotNzsc lm11ging. 2009;25:689-697. 56. Karhausen J, Dudaryk R, Phillips-Bute B, et al. Three-dimensional transesophageal echocardiography for perioperativc right ventricular assessment. Ann 'ThortZC Surg. 2012;94:468-474. 57. Fusini L, Tamborini G, Gripari P, et al. Feasibility of intraopcrativc three--dimensional tran.sesophagcal echocardiography in the evaluation of right ventricular volumes and function in patients undergoing cardiac surgery. ]ASE. 2011 ;24:868-877. 58. Maslow A, Comunale ME, Haering JM, et al. Pulsed wave Doppler measurement of cardiac output from the right ventricular outflow tract. Anesth Anal.f. 1996;83:466-471. 59. Brennan JM, Blair JE, Goonewardena S, et al. Reappraisal of the use of inferior vcna cava for estimating right atrial pressure. ]ASE. 2007;20:857-861. 60. Feissel M, Michard F, Faller JP, et al. The respiratory variation in inferior vcna cava diameter as a guide to fluid therapy. lntmsive Can Mui. 2004;30:1834-1837. 61. Klein AL, Leung DY, Murray RD, et al. Effects of age and physiologic variables on right ventricular filling dynamics in normal subjects. Am] Cawiiol. I 999;84:440-448.

Mitral Valve Johannes van der Weisthuizen and Justiaan Swanevelder

The evaluation of valvular heart disease has become increasingly dependent on echocardiography. Since its introduction to the operating room, transesophageal echocardiography (TEE) has played a major role in surgical decision making and anesthetic management of patients undergoing mitral valve surgery. Mitra! valve replacement has its own implications and is not free of risk, but it has empowered surgeons to develop techniques for mitral valve repair, which are becoming more and more intricate as our understanding of valve function expands. Recent outcome literature indicates strong support for repair rdative to replacement in patients with primary (organic) mitral valve pathology1•2 and for the role of intraoperative TEE in mitral valve repair. A good knowledge of mitral valve anatomy and its assessment by TEE is therefore vital for the success of any intraoperative echocardiographer.

ANATOMY AND FUNCTION OF THE MITRAL VALVE The mitral valve is located between the left atrium and the left ventricle and allows unidirectional flow of blood toward the left ventricle, prevents backward flow of blood into the left atrium during left ventricular systole, and allows unobstructed flow of blood to the left ventricle during diastole, maintaining low left atrial pressures.3 The anterior mitral valve leaflet also forms part of the left ventricular outflow tract and allows for unimpeded left ventricular ejection during systole. The normal function of the mitral valve depends on its six components, which are collectively referred to as the mitral valve complex. This complex consists of the anterior (aortic) and posterior (mural) leaflets, together with the annulus, chordae tendineae, papillary muscles, and left ventricle. Abnormalities of any of these structures can result in valvular dysfunction and should therefore be included in the comprehensive evaluation of the mitral valve.

Mitral Valve Leaflets and Commissures Two leaflets separated by two commissural areas cover the mitral valve area during systole. The anterior or aortic leaflet is situated anteriorly and to the

right, adjacent to and in continuum with the aortic valve, and occupies approximately one-third of the annular circumference. Both the aortic valve and the anterior mitral valve leaflet contribute to the socalled fibrous skeleton of the heart, and the connection between the two is sometimes described as the aonomitral continuity. The posterior or mural leaflet occupies the remaining two-thirds of the annular circumference and is much narrower than the anterior leaflet. Although the posterior leaflet appears to have less height than the anterior leaflet, they are similar in surface area. The posterior leaflet is subdivided into three scallops by clefts. The scallop adjacent to the anterolateral commissure is named PI, with P3 situated inferomedial in close relation to the posteromedial commissure. P2 is the middle scallop in between Pl and P3. Even though the anterior leaflet is not anatomically divided into scallops, the areas opposing the posterior leaflet arc correspondingly referred to as the Al, A2, and A3 segments (Fig. 10-1).4 Closure of the valve requires apposition and coaptation of the two leaflets, and this occurs along a single semilunar coaptation line. A normal leaflet overlap (coaptation height) at end systole should be about 8 to 10 mm.5 The ends of this coaptation line, called commissures, do not extend all the way to the annulus. These commissural areas are situated anterolateral and posteromedial in relation to their respective papillary muscles.

Mitral Annulus Anatomically, the annulus is formed by lateral extensions of flbroelastic tissue originating from the left and right fibrous trigones. The amount of fibrous tissue decreases toward the posterior aspect of the annulus, making this area most susceptible to dilatation. The aortomitral fibrous continuity, another area where the annulus is not well defined, is situated between the two trigones. Left atrial implantation serves as an indicator of the mitral annulus in this region. Undulations in the mitral annulus result in a saddle shape, with the commissural areas located more toward the ventricle and the intertrigonal and posterolateral areas located more toward the left atrium. The annulus has a hyperbolic paraboloid oval shape,

238 I CHAPTER 1O

FIGURE JO- J. This fullvolume 30 dataset of the heart demonstrates the mltral valve during diastole. The anterior leaflet, scallops of the posterior leaflet {P1, P2, P3), and both anterolateral and posteromedial commissures are clearly visible. AV, aortic valve; LAA.. left atrial appendage; AMC:, anterolateral mitral commissure; PMC, posteromedial mitral commissure;AML, anterior mltral leaflet.

with the intercommissural (intertrough) distance greater than the aortic to mural (interpeak.) distance. The heart is slightly tilted in the chest. with the anterior part positioned superiorly. Recent investigations have shown that the saddle shape plays an imporwit role in the distribution of forces that act on the mitral valve. The sb:.c of the annulus and the "high points" of the aad.dle vary coruid.etably during the cardiac cycle. In normal individuals during systole, the antero~­ terior diameter shortens, the overall area of the mitral valve is reduced by 25%, and the saddle shape of the mitral annulus dccpens.5

Paplllary Muscles and Chordae Tendlneae The subvalvular apparatus is made up of two papillary mwcles supporting the mittal valve leaflets by means of multiple chordae tendineae. The anterolateral papillary muscle is attached to the anterolateral left ventricular wall and supplies chordae to the anterolateral commissure and anterior halves of both leaflets. The posteromedial papillary muscle supports the posteromcdial commissurc and posterior half of both lcallets by means of chordal attachments. The mitral valve has no di.n:ct leaflet connection to the interventticular septum, as occurs with the tricuspid valve septal leaflet. Blood supply to the posteromedial papillary

muscle is usually provided by a single coronary artery. Depending on the dominance of the circulation, it can be either a branch from the ~rior descending artery or a branch from the obtuse marginal artery. The antcrolatcral papillary muscle is found in relation to the antcrolatcral commissure and receives blood supply from both the lefi: anterior descending anery via the marginal artery and from the circumflex artery via the fust obtwe marginal artery. Dual supply makes d~on of the anterolateral papillary muscle less likely.6 Chordae stretching from the papillary muscles and attaclllng to the free edge of the lcaflcts arc called primary ch.Ordae. Primary chordae ensure that the leaflet free edges remain turned down toward the LV apex during systole. Sudden-onset severe mitral insufficiency with a flail leaflet .results from disruption of the primary chords. Secondary chords also arise from the papillary mwcles but attach to ventricular aspea:s of the leaflet bases. These chords appear to play an important role in maintaining ventticular geometry, as transection of these chords during surgery oficn results in accelerated vcntticular dilatation. Tertiary chords arise from the left ventticular free wall and also attach 1D the ventricular aspect ofthe posterior leaflet in particular. The function of the papillary mwcles and chordae is to maintain the mit.ral valve coaptation point at

nr:st

MITRAL VALVE I 239 a fured. position relative to the mittal annulus during ventricular conttaction, therefore preventing lea1let prolapse. Victor and Nayak? studied the vaiiations in the papillary muscles of the normal mitral valve in 100 cases and concluded that the mitral valve apparatus, including the papillary musc:lcs, is as unique to each individual as one's own Sngcrprints. More recently. Gunnal et al dissected 116 fumia1in-prcserved hearts of human cadavers and repotted that the number of pap-illary muscles found in the series was highly variable. In fact. the presence of two papillary mwcles in the left ventricle was found in only 3.4% of specimens.8

poor apposition. Mitra! insufficiency can now occur in spite of normal leaf1et structwe.

Left Atrium The role of the left atrium in mitral valve function is not dearly defined. However, atrial contraction results in presystolic reduction in the mittal valve Atrial dilatation and loss of sinus rhythm play a role in mitral valve dysfunction.

area.'

Left Ventricular Myocardium

TRANSESOPHAGEAL ECHOCARDIOGRAPHIC ASSESSMENT OF THE MITRAL VALVE

The left ventricular myocardium determines the position of the papillary muscles relative to the mitral coaptation point. Dilatation of the left ventricle displaces the papillary muscles away from the mitral coaptation point with resultant lea1let tethering. Coaptation now occurs more toward the left ventricle (LV) apex, and traction on the secondary chords pre· vents billowing of the leaflet bases with subsequent

Two-dimensional (20) cchocardiography requires the acquisition of multiple tomographic planes with mental reconsttuction of the three-dimensional (30) sttuctwe of the valve (Fig. 10-2). Systematic 2D :wessment of the mitral valve and rdated structures is done according to the standard views recommended in the American Society of Echocardiography (ASE)/Society of Catdiovascular Ancsthesiologists (SCA) guidelines

FIGURE 10-2. The mitral valve as seen in 20 echocardiography. (A) Midesophageal four-chamber view. (8) Midesophageal mitral commissural view. (CJ Midesophageal two-chamber view. (D) Midesophageal long-axis view.

2.CO I CHAPTER 1O fur performing a comprehensive inttaoperatlve TEE exam.10 Three-dimensional echocardiography is now readily available and allows evaluation of the whole mittal valve at onc.e, with improved accuracy in the location of pathology. Standards for 3D evaluation and image display have also been proposed reccntiy.11

Two·Dlmenslonal Views for Mltral Valve Assessment MIDESOPHAGEAL FOUR-CHAMBER VIEW (ME-4cH)

This view is achieved by gently rettofiexing the probe in the midesophageal position, directing the imaging sector toward the cardiac apex through the mitral valve. In the classical ME-4ch view, which is obtained at 10 to 20 degrees, the imaging plane transects the mitral valve in an oblique plane relative to the valve commissurcs, thus showing the A3 segment of the aortic or ante.rior leaflet to the left of the display and the Pl scallop of the posterior leaflet to the right of the display (see Figs. 10-2 and 10-3). By withdrawing or anteflexing the probe slightly, the tomographic plane will transect the valve closer to the anterolateral commissure, bringing the left ventricular outflow tract (LVOT) into view,. whereas advancing or rctroflexing the probe slightly transects the valve more mward the posteromedial commissure. When the ME-4ch imaging plane is at 0 degrees (often the fivechamber rather than fuur-chamber view), the middle

FIGURE 10-3. Three-

dimensional image of the mitral valve seen from the left atrium illustrating how the valve is transected by the midesophageal (ME) twodlmenslonal views.

part of the aortic leaflet (A2 segment) and the more anterior part of P2 are seen. Any subvalvular or LVOT pathology can be visualb:ed in this view. MIDESOPHAGEAL MrrRAL (OMMISSURAL VIEW {ME COMM)

From the ME-4ch view, the multiplane angle of the probe is electronically rotated forward to approximately 60 degrees, aligning the tomographic sector with the mittal valvar commissurcs. In this view, the P1 scallop is viewed to the right of the screen and the P3 scallop to the left of the image. In the middle, the A2 segment will be seen moving in and out of view as the valve opens and closes (see Figs. 10-2 and 10-3). P2 will be behind A2 (into the screen) but is usually not visible unless it is prolapsing. Small left and right rotations of the probe will move the scanning plane view across the mitral valve parallel to the coapta~ tion line. This view is ideal fur localizing the origin of mitral regurgitation when color Doppler is applied. MIDESOPHAGEAL Two-CHAMBER VIEW (ME-2CH)

This view is achieved by advancing the multiplane angle to 90 degrees. The imaging sector c:uts through the mitral valve at an oblique angle relative to the commissures, showing the more anterior pans of the anterior leaflet (A2, Al) tD the right of the image and the more posterior parts of the posterior leaBet (P3) to the left of the image (see Figs. 10-2 and 10-3). At.

MITRAL VALVE I 241 in the commis&ural view, small left and right rotations will move the scanning line acro.u the whole mitral valve. From this view, the left attial appendage can also be evaluated for the presence of thrombi. MIDESOPHAGEAL l.oNG-Axls VIEW (ME LAX)

With the multiplanc angle between 120 and 140

degrees, the aortic valve should appear in its long axis tngetber with the mittal valve. This imaging plane cuts through the mittal valve perpendicular to the cooptation line, and in diastole clearly demonstrates the aortomitral continuity and the unfolded length/height

of A2, ~er with P2 (see Fi~. 10..2 and 10-3). Turning the probe to the right (clockwise) will show the more posterior part of the mitral valve (A3/P3). and leftwards (counterclockwise) the more anterior parts of the mitral valve (Al/Pl). Because the mid.esopbageal long-axis view intersects the mitral valve perpendicular to the coapwion line, it is the best view to measure the intetpeak distance of the annulus (Fig. 10-4) or the diameter of a mittal regurgitant jct vcna oontrac:ta in systole (Fig. 10..5). The LVOT ia also clearly visualized to assas any subaortic valve or outflow tract pathology.

FIGURE I~. This 30 animation of the MV annulus (right) Is reconstructed from a real-ttme 30 Image of the MV (left). It demonstrates the antertor-posterlor or lnterpeak distance, which Is also measured In the 20 mtdesophageal long-axis view.

FIGURE 10-5. Midesophageal long-axis view of mitral regurgitation demonstrating where the vena contracta should be measured.

242 I CHAPTER 10

FIGURE fa-& In the transgastrlc basal short-axis view (A), the mitral valve Is seen with the anterolateral mitral commissure (AMO in the far field and to the right of the image. whereas the posteromedial mitral commissure CPMO is in the near field and to the left of the image. AML, anterior mitral leaflet; PML, posterior mitral leaflet

TRANSGASIRIC BASAL SHORT-Axis VIEW (TG BASAL SAX)

From the transganric tnidpapillary short-axis view, the probe is k.ept in the flexed position and slowly withdrawn until the mittal valve is seen in the short axis. The antcrolateral commissurc, together with Al/Pl, will be in the far field and to the right of the image. whcrcu the postcromedial commis.surc and A3/P3 arc in the near field and to the left of the image (Fig. 10-6). Although quantification of mitra.I valve pathology with color Doppler u not po.uiblc in thu view, it is helpful to identify the origin of mittal regurgitation.

CH) From the transgastric basal shon--axis view, advance the multi.plane angle to 90 degrees to devdop the two-chamber view (Fig. 10-7). Th.is view is ideal for

TRANSGASIRIC Two-CHAMBER VIEW (TG 2

ewluation of the subvalvular apparatus due ro its perpendicular orientation relative to the ultrasound beams. Small left and right rotations may be needed to see both the papillary muscles and their attached chordae. It is important to complete a 2D evaluation of the mitral valve before color Doppler is applied in order to establish mcclwtlsms of mitral valve disease as well as its hcmodynamic cons~uenccs. Chamber cnlargomcnt and indirect signs of pulmonary hypcncnsion arc indicators of severe degrees of mitral valve disease, as well u long-mnding pathology.

Doppler Assessment After a comprehensive 2D examination of the valve, color Doppler is applied to all of the midc:sophageal

FIGURE 10-7. In the transgastric two-chamber view, the subvalvular apparatus can be readily assessed. In this view, the chordae (arrows) are easlly seen, and the posteromedlal paplllary muscle Is seen In the nearfteld, whereas the anterolateral paplllary muscle Is seen In the far fleld. LA, left atrium; LV, left ventricle. views. In order to achieve good temporal resolution, it is neccs.sary to keep the 2D and color Doppler sectors as small u possible but still big enough to include the whole mitral valve area of intcrrog-ation. A frame rate of at least 15 ltamcs per second is considered adequate. With color Doppler, the presence of mitral regurgitation (in systole) or mitral stenoai& (in diastole) can be demonstrated. PW&cd-wavc and continuous~wavc Doppler should be applied across the valve to quantify the degree of mitral valve disease severity, and will be &cussed later under specific headings. THREE-DIMENSIONAL AssESSMENT OF

THE MITRAL VALVE

Considerable experience is required to mentally integrate a number of 20 view& of the mitral valve into a 3D structure and then present a clear description to the surgeon. The application of real~time 3D echocardiography to evaluate the complo: structure of the mitral valve is now well documented and adds incremental value in localizing and dcmonsttatine; mitral valve pathology d:~J. repair proced.ures.!1,!Ti Presently, commercially a: • le software allows the real-time acquisition of a 3D dataset at high spatial and temporal resolution (adequate frame rates), which can be cropped and manipulated to see the mitral valve (MV) from both the left aorta (IA) and LY sidcs5 (see Fig. 10-3 and Chapter 23). The way to acquire an acceptable 3D image of the MV u to obtain a well-ddined 0-, 60-, 90- or

MITRAL VALVE I 243 120-degree view of the full structure. The biplane mode should be used to confirm in a second view, orthogonal to the acquisition view, so that the full annulus is included and in the center of the image. The acquisition can be live (lower temporal resolution, lower lateral spatial resolution) or multibeat (better temporal and spatial resolution) (see Chapter 23). The acquired dataset can be manipulated with the AV positioned at the top of the image according to recommended practice guidelines. 10 This allows the visualization of the MY "en face" from the LA side. It can also be investigated from different angles, including from the ventricular side, where the subvalvular apparatus can be visualized. Additional valuable information can be obtained when combining color flow Doppler with 30 echocardiography. This is especially relevant for patients with mitral valve stenosis or regurgitation, where it can assist in the definition of jet origin and relationship to adjacent structures. 12 All of these developments facilitate more accurate quantification of specific parameters, such as valve area (mitral stenosis), effective regurgitant orifice area (EROA), vena contracta, annular and outflow tract geometry, and ventricular volumes. 11 Postoperatively, real-time 30 echocardiography provides excellent views of both bioprosthetic and mechanical valves, as well as annuloplasty rings or bands (see Chapter 23) . 13 Postprocedure, the location of any residual transvalvular or paraprosthesis regurgitation can easily be confirmed and its severity quantified. A combined 20 and 30 TEE examination is now the gold-standard routine for preoperative planning of mitral valve surgery, guidance during the procedure, and postoperative quality assurance of the surgical results.

MITRAL REGURGITATION Etiology Mitral regurgitation (MR) results from the incomplete closure of the mitral valve leaflets during left ventricular systole, resulting in backflow of blood into the left atrium. The amount of backflow will determine the hemodynamic consequences of the mitral regurgitation and appears to be mostly affected by the area of the regurgitant orifice. Other factors that influence the amount of regurgitation include the duration of systole and the pressure gradient between the left ventricle and atrium. Normal size and function of the left atrium, left ventricle, mitral annulus, and leaflets are required to ensure a competent mitral valve complex. Dysfunction of any of these components can result in mitral regurgitation. Mitral insufficiency can be functional (secondary) or organic (primary) in nature. 14 Secondary mitral

insufficiency results from dilatory changes in left ventricular geometry due to cardiomyopathy or ischemia with subsequent malcoaptation. The leaflets and chordae are largely normal in this case. Abnormalities in the valve leaflets, chordae tendineae, or papillary muscles result in primary mitral insufficiency. Primary MR is most likely the result of degenerative disease, such as occurs in myxomatous degeneration, fibroelastic deficiency, and connective tissue disorders such as Marfan syndrome. Other causes include mitral annular calcification, rheumatic heart disease, leaflet destruction in infective endocarditis, and papillary muscle rupture after myocardial infarction.

Mechanisms of Mitral Incompetence Successful mitral valve repair has significant benefits over mitral valve replacement and is therefore the~ ferred method to address mitral incompetence. l7 Improved understanding of mitral valve function has led to the development of more complex repair techniques since first proposed by Carpentier in the 1970s and 1980s,4•18 making more lesions amenable to repair. It is therefore imperative to understand the underlying mechanism of MR. This is also reflected in the 2010 EAE guidelines for the assessment of native valvular regurgitation 14 where the emphasis had moved from grading of MR19 to functional assessment of the valve with the aim of repair. 14 Carpentier's functional classification of MR18 to describe regurgitant lesions is still used today when planning surgical repair. In this system valvular pathology is described in terms of the opening and closing motion of the leaflet (Fig. 10-8). This allows a better understanding of the etiology and type of valvular dysfunction. Assessment of the direction and origin of the MR jet with color Doppler is often helpful when describing the underlying mechanism. Improved imaging with TEE has resulted in the following proposed extension ofCarpentier's classification (Table 10-1).20 TYPE I MITRAL REGURGITATION Type I lesions are characterized by normal leaflet motion, and mitral regurgitation is caused by annular dilatation or leaflet perforation. In case of annular dilatation, one can expect to find a central regurgitant jet (Fig. 10-9A). MR jets in clefts or leaflet perforation will not originate from the mitral coaptation line, but from the defect in the leaflets with varying jet direction. TYPE

II MITRAL REGURGITATION

Type II lesions result from increased leaflet motion producing an MR jet directed away from the pathological leaflet (Fig. 10-9B). This results from

244 I CHAPTER 10

Typel~t"

Table 10-1. Modified classification of mitral regurgitation 20 Type 1

BCleft C Annular dilatation without leaflet Type2

Typell

r Type3

Type4

Typelllb~~

r -

FIGURE 10-8. Schematic representation of the functional classification of mitral incompetence as originally proposed by Carpentier.

elongated (localized prolapse) or ruptured chordae (flail leaflet), allowing the affected leaflet to move beyond the coaptation point and level of the annulus. In case of Barlow disease, multisegment symmetrical prolapse may result in a central jet. The timing of the jet can also help in revealing the underlying mechanism. MR that worsens during the latter part of systole is typical of prolapse. TYPE Ill MITRAL REGURGITATION

Type III lesions are the result of restricted leaflet motion. This category is differentiated into type IIIA, B, and C lesions. With IIIA lesions, leaflet motion is restricted during systole and diastole and is usually the consequence of rheumatic heart disease. This type of mitral regurgitation is seldom seen in isolation, as the diastolic restriction causes varying degrees of stenosis as well. The usually eccentric mitral regurgitation jet is

Normal leaflet motion with normal subann ular coaptation A Perforation

Types

tethering Excessive leaflet motion during systole A Flail leaflet BProlapse CProlapse with flail Restricted leaflet motion A Systolic and diastolic restriction as in rheumatic mitral disease BSymmetric systolic restriction as in dilated cardiomyopathy C Asymmetric systolic restriction as in ischemic heart disease Systolic anterior motion of mitral leaflets A Hypertrophic obstructive cardiornyopathy BPost-mitral valve repair CHemodynamic induced in susceptible patients (hypovolemia, inotropes) Hybrid conditions

more likely to be in the direction of the pathological restricted leaflet (Fig. 10-9C). When both leaflets are equally involved in the disease process, the jet may be centrally directed. With type IIIB lesion, symmetric systolic restriction occurs in dilated cardiomyopathy and results in a central MR jet (Fig. 10-90). Tethering of the leaflets due to displacement of the papillary muscles results in more apical coaptation. Traction on the secondary chords prevents billowing of the leaflet bases in systole, with further reduction in coaptation length. In type me lesions, asymmetric systolic restriction results from localized ventricular pathology, usually due to ischemic changes. The result is focal tethering of a leaflet with relative prolapse (not above the annular plane) of the opposing leaflet. The jet appears in the direction of the afllicted leaflet. Types IIIB and C lesions are a ventricular problem, but the leaflets themselves are not abnormal. These lesions are usually also accompanied by a dilated annulus.

IV MITRAL REGURGITATION Systolic anterior motion (SAM) of the mitral valve results in dynamic obstruction of the LVOT and dynamic mitral regurgitation {Fig. 10-10).

TYPE

MITRAL VALVE I 245

FIGURE 10-9. (A) c.arpentier type I: This midesophageal long-axis view demonstrates a central jet offunctional MR. The MV is morphologically normal. (8) c.arpentier type II: The color Doppler study demonstrates the eccentric incompetence jet directed away from the pathological posterior leaflet (C) c.arpentier Type Illa: This patient has

rheumatic disease with reduced leaflet mobility and minimal tip motion in both systole and diastole. (D) Carpentier type lllb: This midesophageal four-chamber view demonstrates restricted MV leaflet motion as found with global ventricular dysfunction. Both leaflets are pulled out of position by the chordae and dilated ventricle, leading to

tenting and poor coaptation, with a central MR jet. Conditions that worsen SAM also worsen MR. Jets are usually directed in an inferolateral direction and are most prominent in the latter half of systole when SAM occurs. Hypcrtrophic obstructive cardiomyopathy is the main cause of SAM, but SAM can also present after mitral valve repair or even in a hypovolcmic heart overstimulated. by inotropic agents. TYPE V MITRAL REGURGITA'nON

More than one underlying mechanism may be present in MR. and fuilure to recognize all may lead to fuiled repair surgery. A systematic approach is therefore still mandated, even when the invo1Wld mechanism appears obvious.

Assessment of MR Severity Two-DIMENSIONAL IMAGING

Signi6cant MR seldom oe-

cvnLwr ·

(0.78S LVOT!.n))

Alternatively. LV stroke volume is equal to the sum of the effective forward stroke volume and the regu.r· gitant volume, and therefore to the mitral annular

stroke volume {if the aortic valve is competent). The Simpson modified biplane method of disa or 3D volwuettic assessment ofLV volumes can also be used to determine forward flow across the MY. Once the regurgitant volume has been calculated. rcgurgitant fraction can now be c:alc:ulatcd: Regurgltant fraction

=

Regurgitant volume Mltral annular stroke volume

The EROA can also be calculated once regurgitant volume is known: EROA

= f\o./M~

Thi& requires continuous-wave Doppler interrogation of the MR jet and determination of the MRvr, by tracing a spectral Doppler envdope. This metho·d is limited by the fact that different cardiac cycles are used for stroke volume c:al.culation at different sites. Variation in stroke volume occurs due to changes in cardiac cycle length, as occurs in atrial fibrillation, commonly in patients with mitral valve disease. Pmdnud Law:lodty Sum.c:e Arca. Effective n:gur~ gitant orifice area can also be determined by the flow convergence or proximal isovdocity surface area (PISA) method (Fig. 10-13). In MR. flow accelerates as it approaches the regurgitant oriflce until it reaches a maximum velocity at or just distal to the anatomical orifice. This flow convergence creates hemispheric shells of increasing velocity on the upstream side of the regu.rgitant orifice. The instantaneous flow at any

FIGURE 10-13. Flowaccel· eratlon tn the region proxlmal to a regurgltant orifice forming concentric hemispheres of increasing velocity. The radius of the hemisphere should be measured from the narrowest part of the jet to the contour where aliasing occurs.

250 I CHAPTER 1O of the&e hemispheric shells is equal to the flow at the .regwgitant orifice at the same moment. By applying the principle of the conservation of energy. the effective .regwgitant or.ifice area can be calculated using the following formula:

aliasing velocity is obtained from the color Doppler legend. Next continuous--wave Doppler is applied. to the MR jet, and the maximum MR vdocity is measured from the speetral Doppler display. The formula can now be written as:

PISA flow = regurgitant orifice flow

21tr2· V;= EROA· V.,..

or

or PISA· V,= EROA·

v_

where PISA is the proximal isovdocity surface area in cm2, Va is the aliasing velocity at the proximal isovclocity SUrface in cm/s, EROA is the effective rcgurgitant orifice area in cm 2, and Yma: (Fig. 10-14) is the maximum velocity at the regurgitant oriflce in cm/s. PISA is theoretically a hemisphere, and its surface area is calculated with the following formula: PISA=2°r2 The radius of the hemisphere is obtained from a zoomed image of the mit.ral valve with color flow Doppler applied to display the regurgitant jet. The baseline of the color Doppler legend is shifted in the direction of flow in order to induce aliasing on the ventricular side of the mit.ral valve. The distance from the 6rst aliasing to the rcgurgitant orifice is measured. This is the radius of the isovelocity hemisphen:. The

FIGURE 10-14. 'The maximal systolic velocity through the regurgitant orifice can be measured by applytng continuous-wave Doppler to the regurgltantjet Togetherwlth the area of the PISA hemisphere,. It Is used to calculate the effective regurgltant orifice area and subsequently the regurgitant volume.

EROA = (2D r2·

v....

v.>

The use of the PISA method relies on a nwnber of assumptions when EROA is calculated that may influence results:

1. The ERO is not always circular. Secondary MR due to functional disease typically bas an ovalshapcd orifice dongated. along the coaptation line, and therefore the PISA surfu:c is hemiellipsoid rather than hemispherical. This results in unden:stimation of the regurgitant orifice area by using the 20 PISA method, and a lower cutoff of EROA in patients with chronic secondary MR may denote severe MR. New automated 3D methods can be used to accurately measure the PISA and overcome this problem.28 2. Another assumption is that the biggest PISA radius occurs at the time of the h~cst pressure difference between LV and IA (when Vmax is measured during mid.systole). This is not always true when the ERO is dynamic during the cardiac

MITRAL VALVE I 251 cycle. An example is secondary MR where the PISA radius is at its biggest at the beginning and end of systole and at its lowest during peak systole when mitral valve closing forces are at their peak. In mitral valve prolapse the PISA radius is at its greatest during the latter half of systole when the regurgitant vdocity has already decreased. This also results in an underestimation of the ERO. The application of color M-mode to the PISA is often useful to indicate dynamic changes in the ERO during systole. 14 It is the recommendation of the ASE that the measurement of the PISA radius and of the MR vdocity be performed at the simultaneous moments during the regurgitant phase.21 3. In the case of very severe MR, the PISA radius may be very large and containment by the LY wall may alter the shape of the flow convergence zone. Overestimates of the PISA surface may occur with subsequent overestimation of MR severity.20

Quantifying MR Severity Integrating data from multiple parameters is required when MR severity is graded. This reduces the impact of some of the limitations of certain methods and also compensates for errors in measurements that might have been made with specific methods. The hemodynamic consequences of a similar amount of MR might also differ based on the duration over which MR had devdoped. For example, chordal rupture with sudden-onset severe MR will not allow for the development of LY and LA enlargement. The small noncomplaint atrium may result in severe pulmonary congestion where a similar degree of MR that had developed over time may leave patients relatively free of symptoms. 19 MR should be graded as mild, moderate, or severe for clinical decision making. Based on EROA and regurgitant volume, provision is made to subclassify moderate MR as mild-to-moderate or moderate-tosevere. Due to limitations in 20 echocardiography, MR severity is underestimated in secondary MR Different cutoff values are used to differentiate significant MR from nonsigniflcant MR in these settings (see Table 10-2).

MITRAL STENOSIS The normal mitral valve area is 4 to S cm2 •29 Reduction of the mitral valve area to less than 2.S cm2 requires an increase in the atrioventricular pressure gradient to maintain an adequate cardiac output and often marks the onset of symptoms during exercise.30 An increase in left atrial pressure results in atrial enlargement and eventually the onset of atrial dysrhythmias, usually

atrial fibrillation. 31 New-onset atrial fibrillation typically leads to sudden worsening of symptoms due to rapid ventricular rates and loss of the atrial contribution to left ventricular filling. Elevated left atrial pressures also result in pulmonary hypenension and eventually alterations in right ventricular function and functional tricuspid regurgitation.32 As mitral stenosis progresses further, the presence of low cardiac output and atrial fibrillation is a common cause of left atrial thrombi and embolic events. Echocardiographic evaluation of patients with mitral stenosis should therefore aim to exclude the presence of intracardiac thrombi, especially when there is a history of embolic events. 33 In rheumatic mitral stenosis, left ventricular function can be reduced secondary to scarring of the basal inferolateral wall of the ventricle and by impaired diastolic function in patients with pulmonary hypertension as a consequence of septal displacement.34 Acute attacks of rheumatic heart disease can result in a pancarditis with subsequent ventricular dysfunction.

Etiology The most common cause of mitral stenosis (MS) is rheumatic heart disease.35 Progressive inflammatory reaction in valve tissue results in thickening of the leaflet tips and fusion of anterior and posterior leaflets in the commissural areas, with subsequent reduction in valve opening. In long-standing rheumatic heart disease or after recurrent episodes, varying degrees of thickening and calcification of the leaflet bodies and bases can also occur. Chordae tendineae are typically thickened and shonened, leading to reduced movement of the mitral leaflets. Mitral regurgitation commonly occurs concomitantly with rheumatic mitral stenosis. Degenerative calcification of the mitral annulus is a rare cause of mitral stenosis and mostly occurs in the presence of other diseases that accderate calcification. These diseases include certain connective tissue diseases such as systemic lupus erythematosus; rheumatoid arthritis; and also in hyperparathyroidism, systemic carcinoid disease, amyloid deposition, mediastinal radiation therapy, systemic hypertension, and aortic stenosis. Congenital mitral stenosis presents in childhood and is rardy seen. One rare congenital anomaly responsible for mitral stenosis is a parachute mitral valve. In this condition, all the chordae originate from a single papillary muscle, and mitral stenosis is the result of impaired leaflet motion during diastole. 36 Other developmental anomalies, such as car triatria~ tum or a supravalvular membrane, can also simulate mitral stenosis even though the mitral valve apparatus is usually normal.

252 I CHAPTER 10

Table 10-2. Parameters for the determination of the severity of mitral regurgitation MR severity•

. .

Miid

.

.

Moderate

Severe

.

Strudur•I MV morphology

None or mild leaflet abnormality (e.g., mild thickening, calcifications or prolapse, mild tenting)

Moderate leaflet abnormality or moderate tenting

Severe valve lesions (primary: flail leaflet, ruptured papillary muscle, severe retraction, large perforation; secondary: severe tenting, poor leaflet coaptation) Dilated*

LVand L.Asizet

Usually normal

Normal or mild dilated

Color flow jet area§

Small, central, narrow, often brief

Variable

Flow convergencell

Not visible, transient or small Faint/partial/parabolic

Intermediate in size and duration Dense but partial or parabolic

Holosystoliddense/triangular

0.8 for biplane)'

Systolic dominance (may be blunted in LV dysfunction or AF) A-wave dominant

Normal or systolic blunting'

Minimal to no systolic flow/ systolic flow reversal

Variable

E-wave dominant (> 1.2 m/s)

EROA, 20 PISA (cm2)

1.5

1.0-1.5

10 cm 2/m o Ratio of aortic diameter to body surface area >4.25cm/m2 • Aortic diameter >4.0 cm with concomitant indication for elective AVR Reproduced with permission from Tadros TM, Klein KD, Shapira OM: Asc:ertdlng aortic dllataUon associated bicuspid aortic valve: pathophyslology, molecular biology and clinical lmpllc:atlons, Circufatlon 2009 Feb 17;119(6):880-890.

FIGURE 11-11. The aortic root and ascending aorta In patients with a bicuspid aortic valve are significantly larger than matched controls with a trtcuspld aortic valve. Notice the dllatatlon of the aortic root (sinuses) and slnotubular junction. Two-D1MEHSIONAL MEASURES

Two-dimensional imaging of a stenotic aortic valve in the ME AV SAX (Video 17) and ME AV LAX views (Video 16) will typically demonstrate lea1let resttiction, calcification, commiS&ural fusion, and failed leaflet coaptation (Video 13). The ME AV SAX view can be used for measuring the aortic valve orifice area by planimetry, which has been shown to correlate wdl with other quantitative methods,56 but is also subject to error in the presence of highly pliable or heavily calcified lea£leu?7 A aoss-section that is oblique or inferior to the leaflet tips ovcre&timate& the orifice size (Fig. 11-12). It is important, therefore, to devdop an image with the smallest orifice size to ensure that the imaging plane transects the leaflet tips. To do so, the aortic valve is first imaged in the ME AV LAX, and the smallest ormcc seen on the long axis is ccntered on the image display screen. The transducer position is then stabilized within the esophagus as the multiplane angle is rotated backward to the short-axis view. In a

true short-axis cross-section, the valve should appear rdatively citcular and all three cusps appear equal in shape. Planimetry for aortic valve area is a level 2 recommendation by expert consensus and is considered reasonable when additional information is needed in selected patients.55 The ME AV LAX view provides imaging of the left ventricular out£1.ow tract, aortic valve, and aortic root. and is useful in differentiating valvular from subvalvular and supravalvular pathology. Maximal cusp separation of less than 8 mm in a long-axis view suggests critical stenosis (Fig. 11·13). whereas greater than 12 mm separation suggests nonc:ritical discasc.58 Measurements of aortic valve separation can be made with M·mode techniques, where a characteristic "box car" pattern is seen on M·mode display when the aortic valve is open, with leaflet separation represented by the width of the boxcar. In patients with membranous subaortic stenosis, M-mode assessment may show euly systolic closure of the valve (Fig. 11·14).

PEAKJETVELOCITY AND PRESSURE GRADIENTS The primary cchocardiographic technique used to quantify the severity ofaortic stenosis is Doppler echocardiography for determination of pressure gradient

274 I CHAPTER 11

FIGURE 11-12. Consequences of the ultrasound beam Intersecting the aortic valve In two different planes. The green line rt!prt!sents the beam intersecting the tips of the aortic valve, yielding an accurate estimation of the aortic valve area by planimetry. The red line represents the beam intersecting the aortic valve in a different plane, resulting in overestimation of the aortic valve area by planimetry.

FIGURE 11-13. Systolic leaflet tip distance of less than 8 mm in a long-axis view suggests critical stenosis, whereas greater than 12 mm separation suggests mild disease or less.

AORTICVALVE I 275

FIGURE 7 7-74. M-mode of the aortic valve in a patient with membranous subaortic stenosis demonstrating early dosure (arrow) of the valve.

and aonic valve an:a..5' Calculation ofva1ve area may be supponivc but is not necessary when a high-velocity/ arad,ient ia present and the valve ia calcified and immo6ile; most patients will have a valve area S 1.0 cm2 or an indacd valve area s0.6 cm2/m2 , but some will have a larger valve area due to a large body size or coaisting aonic regurgitation (AR). 1TE with multiple transducer angles may be superior in comparison to TEE to c:valuate the hemodynamic performance of the aortic valvc. 14 TEE--dcrivcd gndicna can be determined despite this anatomical limitation. yet peak transaonic velocities may be undcttstimated with TEE when compared to ITE mcasurcmenu.14 Valvular stenosis produces flow acceleration and increase in velocity, resulting in a corresponding decrease in pressure at or immediately distal of the levd of stenosis. This pressure gradient or pressure drop across the valvular stenosis is described by the Bernoulli equation: ~p

= 4(V:- "1 + Lacal Acceleration + Viscous Losses 2 )

= Pressure gradient (mm Hg) V2 =Velocity of flow (m/s) distal to the stcnosis (aortic valve) V1 = Vdocity of flow (rnls) proximal to the stenoa.i& (LVOT) Given that local aa:deration is only significant for long tubular lesions, and viscosity losses ate only important when hcmatocrlt is extremely high, these factors can be diueguded in clinical practice. Typically, V1 or the LVITT vdocity is less than 1 m/s Where dp

and therefore can be disregarded as well. This yields the commonly applied riwplif""' Bernoulli equation: b.P=4CVl b.P = 4(VAaot1c-.>"

When V1 aceed.s1.5 m/a (e.g., LVOT flow acceleration or obstruction), the ~Bernoulli equation should be utilized: ~P = 4(V: -

v,2)

V 1 is commonly elevated in the presence of aonic regurgitation, volume overload, or other high-output states. Failure to use the modified Bernoulli equation in these conditions when LVOT velocity exceeds 1.5 m/s will overestimate the pressure gradient and the severity of aortic stcnosis. Continuow-wave Doppler (CWD) is used to measure traruvalvular blood velocity in either the TG LAX or deep TG five-chamber view. The CWD cursor .i& aligned with the narrow, turbulent. high-velocity jct and the spccttal Doppler display is activated. .Accurate alignment provides a distinctive highvelocity (>3 rn/s) spectral Doppler recording that exhibits a fine feathery appearance and a midsystolic peak (Fig. 11-15). Planimctty of the spectral cnvc-lopc yicl = 4(Aorttc

Valve Veloclty)2

Peak gradients are calculated ttom velocity information and therefore do not provide additional clinical information in comparison to peak velocity. A peak velocity greater than 4 m/s and a mean gradient greater than 40 mm Hg arc suggestive of severe aortic stenosis (Table 11-2). The 2014 .American. Heart Association/American College of Cardiology guidelines for the management of patients with valvular heart disease present a management algorithm for patients with aortic stenosis based upon

severity .relies upon maximum velocity and mean pressure gradient and no longer uses AVA as an indepen· dent criterion for severity of AS. In these guidelines, valvular AS is staged from at risk (stage A). to pro-gres.sive (stage B). to asymptomatic severe (stage C), to symptomatic (stage D). Management strategies are determined by symptoms, maximal aortic velocity, mean aortic pmswe gradient, ejection fraction, and body surface area indexed aortic valve area and stroke volume.S 4 Patients with a peak velocity across the aortic valve of greater than 4.5 m/s have higher rates of symptom development and poorer outcomes, especially as peak velocities exceed 5.0 m/s and may be considen:d fur prophylactic AVR before symptom development. 59,60 Although some management algorith.nu recommend reserving AVR for only symptomatic patients with severe AS, the current literature is suggesting there may be a role for eazlier consideration of AVR in asymptomatic patients with severe

AS.s4.60.61

Gradients derived in the operating room may be significantly different from those obtained during preoperative echocardiographic studies or in the cardiac catbete.rization laboratory. A recent retrospective study of patients Wldergoing AVR for severe AS with normal left ventricular ejection fractions demonstrated discordance between AVA 40 mm or >21 mm/m2•14 Moreover. the dimensions of the right-sided chambers can provide clues to the severity of regurgitation. In conaast to mild i:cgurgitation, chronic moderate or severe TR is usually ~oc:iated with a dilated right atrium and ventricle. This is, however, not ttue in cases ofaaitc modernn: or severe TR where the chambers do not have time to rcm.odel.

Inteiventricular septum flattening with paradoxical shift the tdt at end diastole due to right ventri.cular volume ove.doad can be seen with significant TR.

to

TRICUSPID AND PULMONICVALVES I 309

A

I

lhree-Dtmenslonal Evaluation Thrcc--dimensional (3D) studies demonstrate that the TA area in healthy subjeca without ecbocardi~ graphic evidence of TR increases from midsystole to early dia&tole, then decreases during mid-dia&tole

FIGURE 12-6. UU Mldesophageal four-chamber view with colorflow Doppler showing a trlcuspld valve with trlcuspld regurgitation and catheters traversing (oflow) the valve. (8) Three-dimensional dataset of the tricuspid valve as seen en-face from the right atrium showing vegetations (arrows) of the anterior leaflet.

before increasing again in late diastole, thus showing a biphasic pattern with two peaks in early and late diastole. 15 The geometry of the TA also appeazs to be dif&rent from the saddle-shaped mitral annulus. In healthy subjects the TA is nonplanar shaped with homogeneous contraction. In patients with functional

310 I CHAPTER 12

FIGURE tz-7. Mldesophageal four-chamber view showing prolapse of both the trlcusptd valve leaflets and the mltral valve leaflets.

Doppler Evaluation

jet area can be hdpful; an area ~ater than 10 cm2 is indicative of severe insuffic:ienq.17 Doppler parameters that indicate increased severity ofTR inc:ludc a dense, triangular, and early-peaking continuous--wave (CW) Doppler signal of the tricuspid valve. The peak velocity of the TR jet may be low as a reflection of a low gradient between the right ventricle and the right atriwu {Fig. 12-13). The proximal isovdocity surface aiea (PISA) method can be applied for more quantitative assessment (Fig. 12-12B). The TR PISA method is subj~t to several pitfalls and limitations suc:h as noncircular ori6ce of regurgitation and flattening of the PISA profile due to lower velocities of the TR jet.17 In addition, severe TR is associated with systolic: flow reversal in the hepatic veins and/or the coronary sinus, similar to what is seen in the pulmonary veins in the case of severe mitral regurgitation.

Colar flow Doppler mapping can detect and provide a degree of quantification of the severity ofTR. When applied, the multiplane angle should be changed and the probe tip manipulated in order to demonstrate the largest possible jet of regurgitation {Fig. 12-12A). Doppler principles similar to those used in the assessment of mitral regurgitation c:an be used to asscs.i tricu.spid regurgitation (Table 12-2). Measuring the vena contracta, which is the narrowest portion of the jct at the orifice of the valve, is easy to perform in the midesophageal four-chamber view; the cutoff for severe regurgitation is c:onsid.eted to be 7 mm. l6,l7 In centrally directed regurgitation, measw:ement of the

Imaging of the hepatic veins can be performed by identifying the opening of the inferior vena cava (IVC) into the right atrium at a deep ME level and following the IVC into the liver. The hepatic: veins will be seen opening into the IVC (Fig. 12-14A). A lower Nyquist limit may be needed due to the lower blood velocity in the hepatic: veins, and the pulsedwavc (PW) Doppler should be placed in the hepatic vein at about I to 2 cm from the opening into the IVC. A normal flow pattern consists of larger systolic (S wave) and smaller diastolic (D wave) forward-flow waves. In addition, two small flow-reversal waves may

TR. the annulus dilates in the septa! to lateral and posteroseptal to antcrolatcral directions, resulting in a more circular TA shape. Tbrcc--dimensional imaging allows immediate identification of the leaflets and associated pathology by examining the 1V in an en-face fashion either from the right atrium (RA) or from the RV (Fig. 12-10, Video 10). Po.ttprocessing of three-dimensional datasets also enables accurate measurements of the septal-lateral and anterior-posterior diameters of the TA (Fig. 12-11). Imaging of the 1V by 30 TEE can also be challenging because of the thin appearance of the 1V lca£lets. For example, the appearance of lca£lct perforations may be due to echo dropout and should be cottdatcd with two-dimensional (2D) 6ndings, as well as presence of blood flow by color flow Doppler.

HEPATIC VEHOUS FLOW PA'mRNS

TRICUSPID AND PULMONICVALVES I 311

A.

B

FIGURE I 2-8. Ebstan anomaly. (A) Note the lower Implantation of the septaI leaflet (arrow) In the mldesophageal four-chamber view. (B) The•sall-llke"appearance of the anterior leaflet of the trlcuspld valve (panel A). Malcoaptatlon results In stgntflcant trlcusptd regurgitation (panel B).

be noted: one in late dWtole (AR wave, which. is the .result of atrial conttaction) and another in late systole (V wave, due to an upward movement of the TA toward the right atrium at the end of systolic ejection) (Fig. l:Z..14B). A blunted or reversed systolic wave is seen in patients with severe tricuspid regurgitation (Fig. l:Z..14C). However, hepatic vein flow pattern is dependent on right atrial and right ventricular compliance, abnormal heart rhythms, and respiration and all these conditions should be accoW\ted for when inte.rpreting hepatic vein flow. 17 For example, patienu

with elevated right atrial pressures or atrial nbrillation can exhibit blunting of the systolic wave in the absence ofsignificant tticuspid regurgitation. CoRONARY SINUS FLOW PATIERNS

PW Doppler sampling of the coronary sinus flow is best performed in a modified ME bicaval view, which displays the coronary sinus in its long axis in the attioventricular groove. In normal individuals with absent or mild degrees of tticuspid .regurgitation, two negative waves are noted: a late systolic wave and a

312 I CHAPTER 12

FIGURE f 2-9. Midesophageal four-chamber view with and without color flow Doppler in a patient with cartinoid heart disease

FIGURE 12-70. Three-dime~ slonal dataset of a 11tcuspld valve as seen from the right atrium. Note the fla!I anterior leaflet (anow).

diastolic wave with higher vdocity and longer duration. When severe tricuspid regurgitation is present. reversal of the systolic wave is seen. This finding has a high sensitivity and a good spcciflcity for the deu::ction of severe tricuspid rcgurgitation. 18

EmMATION OF Svsrouc PuLMONARY ARTERY PRESSURE Using CW Doppler, measurement of the peak tricuspid regurgitation jet velocity can be performed in any of the midesopbagcal views that allows optimal alignment of the tricuspid regurgitation jet with the Doppler beam. Localization of the jet is assisted by color flow Doppler mapping, and angulation of the

probe with adjwtment of the multiplane angle should

be performed in order to identify the maximal velocity jet (Fig. 12--13). Based on the simplified Bernoulli equation, the pressure gradient between the right ventricle and atrium is given by: Pressure Gradient (mm Hg) = 4 · [Peak Regurgltant Velocity (m/s)]2

When added to an estimate of the right atrial pressure, this gradient provides an approximation of the right ventricular systolic pressure, wh.icb in the absence of right ventricular outflow obstruction is

TRICUSPID AND PULMONIC VALVES I 313

FIGURE 12-11. Multiplanar reconstruction of a tricuspid valve three-dimensional dataset allows measurements of the septal-lateral diameter (white arrow) and antero-posterlor diameter (black arrow) to be performed In the transverse plane of the tr1cuspld annulus. equivalent to the ~tolic pulmonary artery pressure. Right anial pressure is commonly assessed by exarnin· ing the respirophasic changes in the diameter of the IVC. An IVC diameter less than 2.1 cm and greater than 50% change in the diameter of the IVC with inspiration indicates a tight at.rial pressure of less than. 10 mm Hg, whereas a diameter >2.1 cm and less than 50% collapse with inspiration is associated with a pressure that is above 10 mm Hg. 19 This, however, is not n::liahle in patients on mechanical ventilation or in those who do not mount a good inspiratoty effi>rt. In these patients, right anial pressure can be assessed by aamining the PW Doppler pattern of the hepatic veins, based on the following formula20: Mean Right Atrial Pressure (mm Hg) = 21.6 - (24 · SFF) where SFF is systolic filling fraction of the hepatic venous flow, which is obtained by dividing the

hepatic vein systolic velocity-time integral (Vfl) by the sum of ~tolic and diastolic VI1s. For the purpose of simplification, peak velocities can be used in lieu of Vfls.20 This method, however, has not been validated in patients with severe ttkuspid .regurgitation; instead, the right atrial pressure can be estimated in these patients at a constant of 20 mm Hg, especially in the presence of other indicators of elevated right atrial pressure (e.g., significantly distended jugular vcins). 21 More recently, Arthur et al22 fuund that measurement of the IVC diameter by TEE can provide an estimate of the centtal venous pressure (CVP) in mechanically ventilated patients. In theit study, the IVC diameter w.as measw:ed in the bicaval view (at 110 degrees) at the level of the cavo-atrial junction and

at the end of the T wave of the dec.trocardiogram. The ventilator was turned off at the time of the measure· ment to eliminate the effect of intrathoracic pressure

changes. The linear regression-derived equation

to

314 I CHAPTER 12

A

FIGURE 72-12. (A)Trlcuspld regurgitation by colorflow Doppler in the midesophageal fourchamber view

(8) Flow acceleration and proximal isovelocity profile (arrow) seen In a patient with cardnold disease and severe trlcuspld regurgitation.

B

cakulate the CVP based on the IVC diameter [CVP = (IVC diameter - 4.004)/0.751] showed a good correlation with catheter-measured CVP. Based on their

TRICUSPID STENOSIS

findings, we propose the fullowing simplified formula fur estimating the CVP based on the IYC diameter:

Tricuspid ste.n.osis is less frequently foWld in the community given the low incidence of rhewnatic hean disease, the most common cause of this valvular lesion. In areas where rheumatic heart disease is still

O/P {mmHg)=4/3· DVC diameter (mm)-41

Common Pathophyslology

TRICUSPID AND PULMONIC VALVES I 315

Table 12-2. Grading the severity of chronic TR by echocardiography Parameters

Mild

Moderate

Severe

TV morphology

Norm•I or mildly •bnorm•l lellflets

Severe vlllve lesions (e.g., flail leaflet,

RV and RA size

Usually normal Normal 50-70 emfs. *With baseline Nyquist limit shift of 28 cm/s. §Signs are nonspeclflc and are Influenced by many other factors (RV diastolic function, atrial fibrillation, RA pressure). II There are little data to support further separation of these values. Reproduced with permission from Zoghbi WA. Adams D, Bonow RO, et al. Recommendations for Noninvasive Evaluation of Native Valvular Regurgitation: A Report from the American Society of Echocardiography Developed in Collaboration with the Society for Cardiovascular Magnetic Resonance,J Am Soc Echocardiogr 2017 Apr;30(4):303-371.

prevalent, tricuspid stenosis is usually associated with involvement of other valves, namdy the mitral valve. In addition, it is frequently coupled with tricuspid regurgitation. Rheumatic disease leads to thickening of the leaflets and commissural fusion as well as involvement of the subvalvular apparatus.23 Other causes of tricuspid stenosis include endomyocardial fibrosis and carcinoid heart disease, in which fibrous deposits on the endocardium lead to thickening of the valve and leaflets that are fw:d in a semiopen position. This is invariably associated with regurgitation. When present, the increased flow from the regurgitation will lead to higher gradients across the valve. Patients with tricuspid stenosis usually have a significantly dilated right atrium. Dilatation of the right ventricle is a function of the severity of the associated tricuspid regurgitation.

Two-Dimensional Evaluation Careful examination of the tricuspid leaflets is needed to assess for thickening and/or calcifications, and for the presence of restricted mobility with or without doming in diastole (see Fig. 12-9). Planimetry of the valvular orifice in the transgastric right ventricular basal view can be attempted, but is difficult and unlikely to yidd accurate results. Lesions (tumors, large vegetations, etc.) causing mass obstruction of the valvular inlet can be identified. Information from the assessment of the other valves and chambers can hdp in determining the underlying etiology of stenosis, such as involvement of the mitral valve in patients with rheumatic bean disease or the pulmonic valve in patients with carcinoid disease. The presence of left ventricular dysfunction and apical thrombus raises the possibility of endomyocardial fibrosis as a cause

316 I CHAPTER 12

A

A

8

8

FIGURE 12-13. (A) Continuous-wave Doppler measurement of the peak tricuspid regurgitation jet velocity from the midesophageal four-chamber view. Coler Doppler is used to guide the placement of the CW Doppler cursor (peak tricuspid regurgitation gradient 65 mm Hg, calculated right ventricular systolic pressure 71 mm Hg). (B) Spectral Doppler envelope in a patient with severe trlcuspld regurgitation. Note the low-veloctty, dense, triangular Doppler proflle.The calculated right ventrlcular systollc pressure Is 29 mm Hg as a sign of right ventricular dysfunction.

for tricuspid ste.n.osis. In gene.ral, the right attium and inferior vena cava are dilated, e&pecially in chronic and more severe case&.

Doppler Evaluation Color Doppler usually reveals evidence of turbulent, hWt-veloc:ity flow. Using PW Doppler with the sample volume placed at the tip of the leallers, the RV inflow velocities can be shown to be incrca.scd (>0.7 m/s).'M

c FIGURE 12-14. Color Doppler vtsuallzatlon ofhepatfc venous flow (A). Normal hepatic vein Doppler proflle (B} characterized by a small reversal offlow after atria! contraction {AR wave), an antegrade systollc phase during atria! filling from the superior and Inferior vena cavae (S wave), a second small flow reversal at end systole (V wave), and a second antegrade diastolic filling phase (0 wave). (C) Hepatic vein flow with systolic flow reversal.

TRICUSPID AND PULMONICVALVES I 317 gradient of more than 5 mm Hg coruidered re£1.cctive of severe stcnosis. M The pres&ure half-time (P112) method using a constant of 190 (i.e., 190/P112t) can be used to estimate the orifice area,2s but is not as well validated as for mitral stcnosis and is of limited usefulness in clinical practice. Finally, in the absence of regurgitation, dividing the stroke volume measured at either the left or right ventricular outflow tract by the tricu.spid inflow Vl1 fi:om the CW Doppler recording (continuity equation) can be used to calculate the stenotic orifice area.26 An area of 1 cm2 or less is consistent with significant tticuspid stenosis (Table 12-3).24

FIGURE 72-75. Continuous-wave Doppler measurement of the tricuspid valve diastolic gradient reveals a mean gradient of 3.7 mm Hg in this patient, consistent with moderate tricuspid stenosis.

Thia ia typically performed in the midesophageal .right ventricular inflow-outflow view where the Doppler beam can be aligned with the blood flow. Assessment of the diastolic pressure gradients using CW Doppler can be performed while increasing the sweep speed (100 mm/s) fur better accuracy of mca.surcmcnts (Fig. 12-15). Also, it is recommended to average at least five cycles to account fur respiratory variations or changing cycle length in patients with atrial fibrillation. As with the other valves, the pres&urc gradient across the tticuspid depends on both the valvular orifice area and the flow across it, which is increased in the presence of concomitant regurgitation. However, current assessment of severity of tricuspid stcnosis is mainly based on the gradient alone, with a mean

SURGICAL CONSIDERATIONS RELATED TO THE TRICUSPID VALVE Tricuspid Regurgitation: When to Repair Tricuspid valve annuloplasty is the trcamlent of choice for functional TR secondary to pulmonary hypertension from left-sided. valvular heart disease. Indications for surgical repair of the TR include right heart f.ailure and moderate to severe TR. ~cently, K:usajima et al showed that untreated 2+ TR improved temporarily after mitral valve surgery, but then progressed in the mid-to-long tcrm.27 Therefore, the current recommendation is to perform a repair based upon the degree of dilation of the tricuspid annulw, regardless of the severity of TR.28 Cunent European Society ofCardiology guidelines29 state that tticuspid annuloplasty should be considered (Class Ila) even in the presence of only mild TR. whenever the tricuspid annulus exceeds 40 mm or more than 21 mm/m2 on preoperative ec:hocardiography. A similar recommendation is provided by the 2014 American

Table J2-3. Echocardlographlc findings In trtcusptd stenosls

. . Two-dimensional findings Leaflet morphology Leaflet mobility Right-side chambers• Doppler findings

Color Doppler Inflow velocity (mls}

. . . . Stenosls SIMllfty . . .

.

. .

Miid

Mod•ate

Savant

Usually normal Normal Can be normal

Thickening Moderately restricted Diiated

Thickening +/- calclflcatlons Severely restricted; doming Slgnlflcantly dilated

0.7

Turbulent inflow >>0.7

:s;2 Mean dlastollc gradient ~5 Pressure half-time ~190ms :s;1 cm2 Area by continuity equation •Mostly the right atrium and the Inferior vena cava. Right ventricular dilatation Is present when there ls associated Insufficiency. Data from Baumgartner H, Hung J, Bermejo J, et al. Edlocardiographic assessment of valve stenosis: EAEIASE recommendations for clinical practice,J Am Soc Echocordlogr. 2009 Jan;22(1):1-23.

318 I CHAPTER 12 Heart .Association/American College of Cardiolo~ guiddincs for management of valvular heart disease. More specifically the latter guidelines state that mild or mode.rate degrees of functional TR concomitant to left~heart disease arc considered suitable for correc-tion (Class Ila, Levd of Evidence C) in the presence of signincant tricu.spid annulus dilation exceeding (40 mm diameter or 21 mm/m2), whereas the indication becomes debated (Class Ilb, Level of Evidence C) in the presence of pulmonary hypertension without muked dilatation of the annulus.

Trlcuspld Stenosls For patients with symptomatic TS or a valve area less than 1 cm2, medical therapy is indfective and t.ricwpid valve replacement is the procedwe of choice.

PULMONIC VALVE Relevant Anatomical Landmarks The three cusps of the pulmonic valve are labeled the anterior, right, and left cusps. The names of the cusps arc derived from their devdopmcntal origin from the truncu.s artcriosus.4 The plane of the opening of the pulmonic valve fu:es superiorly and to the left (sec Fig. 12-1).31 Due to its anatomical position away from the esopbagua, the pulmonic valve is frequently difficult to image by TEE.

Tomographic Views MIDESOPHAGEAL AORTIC VALVE 5HORr-AxlS VIEW

The short-axis view of the aortic valve is first obtained from the mid.esophage:al. position with the multiplane angle set between 35 and 50 degrees. Withdrawing the probe slightly along with minor rotation will bring up a long-axis view of the pulmonic valve (Fig. 12-16). In thiS view, the pulmonary valve and the proximal segment of the main pulmonary artery are located to the right of the display. The anterior pulmonary cusp is seen in the fu fidd, and the right cusp is seen in the proximity of the aortic valve.~2 MIDESOPHAGEAL RIGHT VENTRICULAR INFLOW•Oun:LDW VIEW

In this view, the pulmonic valve can be visualized along its long axis to the right of the display (see Fig. 12-3). Color-flow Doppler can be used to assess fur the presence of pulmonary insufficiency (Fig. 12-17). In some patients with heavy aortic valve calcifications or a prosthetic aortic valve, acoustic shadowing can prohibit ad.equate visualization of the pulmonic valve. In addition, the direction of the pulmonary blood flow is almost perpendicular to the Doppler beam, making assessment of velocities and gradients unreliable in this view. Simultaneous orthogonal plane imaging (enabling visuali%ation of the original

FIGURE 12-16. Midesophageal aortic valve short-axis view, with the pulmonic valve clearly seen in the right-side far field. The right (R} and anterior (A) cusps of the valve are seen in this view. RA, right atrium; AL., anterior leaflet; PL, posterior leaflet.

TRICUSPID AND PULMONIC VALVES I 319

FIGURE 72-77. Mldesophageal right ventricle Inflow-outflow view. Color flow Doppler shows the presence of mild regurgitation. RVOT, right ventricular outflow tract; PV, pulmonic valve; PA, pulmonary artery.

FIGURE 72-19. Upper esophageal aortic arch shortaxis view showing the pulmonary artery in long axis. This view is useful because it aligns the Doppler beam with the flow of blood.The arrow points to the pulmonic valve. PA, pulmonary artery.

window with the multiplane anitle at approximately 90 degrees, along with rotation the probe to the left. The pulmonic valve and pulmonary artery are seen to the left of tbe display (Fig. 12-19). Slight retroflaion of the probe and an increased imaging depth are often needed to better visualize the pulmonic valve.

or

TRANSGASTRIC RIGHT VENIRICULAR INFLOW·Oun:LOW VIEW

FIGURE f 2- f 8. Short-axis view of the pulmonic valve seen with orthogonal plane imaging. In this view, the anterior (A), left (L), and right (R) leaflets can be ldenttfled. LA, left atrium; LV, left ventrtcle; LVOT, left ventrtcular outflow tract; AV, aortic valve; AO, aorta; PV, pulmonlc valve.

image on the left side of the screen [primary plane] and the secondary image (90 degrees multiplane from tbe original] on tbe right side of the screen) with tilt (-30 to +30) on the secondary plane will generate a short-axis view of the pulmonic v.alve (Fig. 1~ 18).-~3

This view is obtained from the transgastric position at the midpapillary muscle level by tuming tbe probe to the patient's left and forward rotation of the multiplane angle to 110 to 140 degrees. The right ventricular outftow tract (RVOT) and pulmonic v.alve (PV) will appear in the mid·far field, paralld to the beam, often in optimal position for color and spectral Doppler analysis (see Chapter 4). TRANSGASTRIC RIGHT VENIRICULAR BASAL VIEW

This image can be obtained from the TG-SAX. view by turning the probe toward the patient's right and anteflaion. The uicuspid leaflets are often seen in short axis, and the RVOT may be seen in the far fidd (see Fig. 12-5).

5HORr-Axts VtEW

PULMONIC REGURGITATION Common causes

This imaging plane provides a long--axis view of the pulmonic v.alve and pulmonary artery with the ultrasound beam being almost parallel to the direction of blood flow. It is obtained from the upper esopbageal

In the adult population, pulmonary hypertension leading to pulmonary artety and annular dilatation is the mott common cause of pulmonary .regw:gitation. Connective tissue disorders, such as Marfa.n

UPPER ESOPHAGEAL AORTIC ARCH

320 I CHAPTER 12 syndrome, can also lead to dilatation and insufficiency. Carcinoid and rheumatic heart disease cause restricted leaflet mobility and malcoaptation. Additional etiologies include endocarditis, trauma, congenital malformations, and complications of surgical interventions (repair of pulmonary stenosis or tetralogy of Fallot).

the slope of the Doppler envelope can provide information about the severity of the pulmonic regurgitation, with steeper slopes being associated with significant degrees of regurgitation. 38 Recently, a pressure half-time of the pulmonary insufficiency jet of less than 100 ms was found to reliably identify patients with adult congenital heart disease who had angiographically confirmed severe regurgitation.39

Two-Dimensional Evaluation Two-dimensional echocardiography is essential in defining the anatomy of the pulmonic valve. Lesions such as annular dilatation, valve prolapse, vegetations, congenital malformations, and rheumatic involvement are frequently easily identified. Thickening and restricted mobility, malcoaptation (Fig. 12-20A), and narrowing of the annulus can be seen in patients with carcinoid heart disease. 12 The presence of right ventricular dilatation in the absence of other etiologies is usually indicative of severe chronic pulmonary insufficiency.

Doppler Evaluation Assessment of pulmonary regurgitation is commonly performed qualitatively and semiquantitatively (Table 12-4).34 Color flow Doppler imaging yields information regarding jet width, length, and area (Fig. 12-20B). A ratio of the jet width to the right ventricular outflow tract diameter of no greater than 38% indicates mild to moderate pulmonary regurgitation, a ratio of 39% to 74% indicates moderate to severe regurgitation, and a ratio of at least 75% indicates severe regurgitation. 35 A jet length shorter than 10 mm has been found in normal subjects with no cardiopulmonary disease, whereas a jet length longer than 20 mm has been associated with pulmonic insufficiency murmur:'.16 As with aortic regurgitation, it should be remembered that jet length is dependent on loading conditions and ventricular compliance. Figure 12-20B displays the color Doppler signal of moderate to severe regurgitation in a patient with carcinoid syndrome. Continuous wave Doppler interrogation of the pulmonic regurgitation jet in either the upper esophageal aortic arch short-axis view, the transgastric right ventricular inflow-outflow view, or the deep transgastric right ventricular outflow view allows estimation of the end-diastolic flow velocity, and therefore the end-diastolic gradient (using the simplified Bernoulli equation) between the pulmonary artery and the right ventricle. This gradient can be used to estimate the pulmonary artery diastolic pressure by adding an estimate of the right atrial pressure,37 and is equal to that of the right ventricle at end diastole, if there is no pulmonic valve stenosis (see Chapter 5). Furthermore,

PULMONIC STENOSIS Common Pathophysiology Pulmonic stenosis is mostly a congenital lesion, with the abnormal valve having abnormal leaflet number or morphology. Sometimes, associated abnormalities of the right ventricular outflow tract are noted. In the adult population, pulmonic stenosis can result from rheumatic heart disease or carcinoid syndrome wherein involvement of other valves is usually evident.23 Right ventricular outflow tract obstruction can result from hypertrophy of the infundibular septum, protrusion of the right sinus of Valsalva of the aortic valve into the right ventricular outflow tract, aneurysm of membranous ventricular septum, and the presence of mass lesions such as sarcoma. Congenital conditions such as tetralogy of Fallot can be recognized from the presence of associated malformations (see Chapter 19). The presence of pulmonic stenosis and/or right ventricular outflow tract obstruction leads to increased afterload and consequently hypertrophy of the right ventricle. In advanced cases, right ventricular failure and dilatation may ensue, leading to the development of tricuspid regurgitation.

Two-Dimensional Evaluation Examination of the leaflets and their mobility in the long axis can be performed in most of the views defined earlier. The presence of thickening, calcifications, and doming in systole should be noted. Abnormalities of the outflow tract can he detected in the midesophageal views, whereas the upper esophageal aortic short-axis view provides good imaging of the proximal part of the pulmonary artery. Direct planimetry of the pulmonic valve cannot be performed because the valve is not imaged well in cross-section by TEE. Examination of the right ventricular chamber size and function is helpful for the assessment of the severity of the stenosis.

Doppler Evaluation Using color-flow Doppler, the pattern of flow across the valve can be assessed; the presence of aliasing indicating turbulent flow should alert the examiner to the

A

8

FIGURE 12-.20. (A) Upper esophageal aortic aKh short-axis view showing malcoaptation (aflow) of the pulmonicvalve leaflets in a patient with carcinoid heart disease. (BJ Color flow Doppler In the same vtew shows severe pulmonlc regurgltatton. (C} Conttnuous-wave Doppler In the same view shows a dense envelope of pulmonlc regurgitation (arrow) with a steep deceleratlon slope as well as significant pulmonlc stenosls (flow above the baseline) with a peak

c

velocity of approximately 2 m/s. PA, pulmonary artery; RVOT, right ventricular outflow tract.

322 I CHAPTER 12

Table J2-f. Echocardlographlc and Doppler parameters useful In grading PR severity

Pulmonlc valve

Normal

Nonnal or abnonnal

RV size Jet size, color Doppler*

Normar Thin (usually 0.7' Soft

Slightly Increased

RF'"'

Dense

Dense; earty termination of diastolic flow Short, 30% (stage DJ MV repair may be considered in patients with rheumatic mitral valve disease when surgical treatment is indicated if a durable and successful repair is likely or if the reliability of long-term anticoagulation management is questionable Transcatheter MV repair may be considered for severely symptomatic patients (NYHA class llVIV) with chronic severe primary MR (stage DJ who have a reasonable life expectancy but a prohibitive surgical risk because of severe comorbidities MVR should not be performed for treatment of isolated severe primary MR limited to less than one half of the posterior leaflet unless MV repair has been attempted and was unsuccessful

LOE

B B B B B Ila

B

Ila

B

Ila llb

c c

llb

B

llb

B

Ill: Harm

B

Reproduced with permission from Nishimura RA, Otto CM, Bonow RO, et al. 2014 AHA/ACC guideline fur the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines,J Am Coll Cardiol 2014 Jun 10;63(22):e57-e185.

preoperative echocardiography to determine the severity of the MR. More recently, Song et al36 used realtime 3D echocardiography to show that geometrical determinants of ischemic MR depend on the location of the prior myocardial infarction, implying that MV repair differs between ischemic and dilated MR Although intraoperative TEE can be very hdpful in more precisdy assessing anatomical details, the severity of MR will be underestimated in most patients, and provocative testing with increased preload and afterload may be necessary. In a prospective, randomized trial through the Cardiothoracic Surgical Trials Network (CTSN), 301 patients with moderate ischemic mitral regurgitation were randomized to undergo coronary artery bypass graft (CABG) alone or CABG plus mitral valve repair. At 2 years, there was no difference in left

ventricular reverse remodding or survival between the two groups. Also, at 2 years the rate of moderate and severe MR was more in the CABG-alone group compared to the combined group. Although there was no difference in survival, the patients without moderate or severe MR, independent of the treatment group, had more reverse remodeling and more im,rovement in global and regional wall motion scores. 3 In another CTSN trial, 251 patients with severe ischemic MR were randomly assigned to undergo either repair or replacement. At 2 years, there was no difference in left ventricular reverse remodeling and survival between groups. Recurrent moderate or severe MR was found to be more frequent in the repair group (58.8% vs. 3.8%). Also, the patients in the repair group had more bean failure-related adverse events and cardiovascular readmissions. However, in the

352 I CHAPTER 14 Table 14-2. Recommendations for secondary MR intervention COR

LOE

Recommendations

Ila

c

Ila

B-R

llb

B

llb

B-R

Mitral valve surgery is reasonable for patients with chronic severe secondary MR (stages Cand D) who are undergoing CABG or AYR. It is reasonable to choose chordal-sparing MVR over downsized an nuloplasty repair if operation is considered for severely symptomatic patients (NYHA class Ill to IV) and persistent symptoms despite GDMT for HF. Mitral valve repair or replacement may be considered for severely symptomatic patients (NYHA class Ill to IV) with chronic severe secondary MR (stage D) who have persistent symptoms despite optimal GDMT for HF. In patients with chronic, moderate, ischemic MR (stage B) undergoing CABG, the usefulness of mitral valve repair is uncertain.

Reproduced with permission from Nishimura RA, Otto CM, Bonow RO, et al. 2017 AHA/ACC focused update of the 2014 AHA/ ACC guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/ American Heart Association Task Force on Clinical Practice Guidelines, J Am Coll Cardiol 2017 Jui 11;70(2):252-289.

repair group the patients who did not have recurrent MR experienced si~ificant reverse remodeling and better quality of life. 3B The authors therefore raise the question of patient sdection for MV repair based on echocardiographic predictors of regurgitation recurrence. One of the mechanisms for recurrent mitral regurgitation that has emerged from subsequent studies is severity of mitral valve leaflet tethering. 39 The 2014 AHA/ACC valvular heart disease guidelines35 and 2017 update recommendations40 for the treatment of chronic secondary MR (including ischemic MR) are summarized in Table 14-2.

REPAIR DURABILITY Since the introduction of standardized techniques for mitral valve reconstruction, mitral valve repair has become the surgical treatment of choice for MR Numerous retrospective studies have demonstrated important advantages of mitral valve repair over mitral valve replacement. Mitra! valve repair is most applicable to patients with degenerative mitral valve disease, with successful valvuloplasty in more than 95% of these patients. Further, it is in patients with degenerative mitral valve disease that repair has been shown to have the greatest durability. With the longest followup to date, Ddoche, Braunberger, and associates41,42 found that 93% of patients with degenerative disease did not require reoperation 15 years after their initial mitral valve repair. In the Cleveland Clinic series of 3383 patients with isolated posterior leaflet prolapse, repair could be performed in 97% with a 15-year survival of 76%, su£erior to the age- and sex-matched U.S. population. 3 At 10 years, freedom from mitral reoperation was 97%. Repair durability was negativdy influenced by failure to use a prosthetic annuloplasty,

left atrial enlargement, and left ventricular remodding and d}'5function. UsingJropensity score adjustment, Jokinen and colleagues confirmed once more the superiority of MV repair over replacement. Despite these excellent results in patients with degenerative disease, some patients may require reoperation for recurrent mitral valve dysfunction. Causes of failed mitral valve repair may be classified as related to procedure (rupture of previously shortened chordae, suture dehiscence, or incomplete initial operation) or to the valve (progressive disease or endocarditis). Other risk factors for failure of mitral valve repair include advanced myxomatous changes of leaflets, chordal shortening procedures, failure to perform an annuloplasty, residual MR at the completion of repair, New York Heart Association functional class III or IY, and performance of concomitant cardiac procedures. Patients with the most common pathological finding, namdy posterior leaflet prolapse caused by chordal rupture, have the lowest risk of late reoperation. Failure to add an annuloplasty to posterior leaflet resection or performing an annuloplasty alone increases the risk of late reoperation. 45 Of interest, the type of annuloplasty ring used (Cosgrove-Edwards, Carpentier-Edwards, or ~ericardial band) did not influence repair durability. 6 lntraoperative TEE guidance also decreases the risk of reoperation. In a recent review on mitral valve repair, some of the echocardiographic predictors for failed repair for degenerative MR identified were prolapse or flail in three or more segments, bileaflet pathology, and atrialization of the posterior leaflet insertion.47 Other measurements that predict a difficult repair are a small posterior leaflet ( < 17 mm), a smaller anterior leaflet (ansion of the prosthesis leading to central aortic insufficiency. A short distance ttom the coronary ostia to annulus (less than 10 to 12 mm), as well as long native leaflet length, predisposes the patient fur increased risk of coronary ocdusion.78 Although 2D imaging is sufficient fur measurement of the distance between the aortic annulus and right coronary ostium, imaging with 3D echo using multiplana.r reconstruction is very helpful in the measurements of the distance between the annulus and left main coronary ostium (Fig. 15-30). Wire placement and particularly balloon valvuloplasty arc important surgical stages that should be monitored by echocazdiography. Migration of the wire or balloon is possible if sudden movement or an «topic beat dwing pacing is encountered, and is appreciated easily on TEE. After valvuloplasty, TEE can fu:ilitate diagnosis of complications quickly in the setting of hemodynamic compromise (e.g., pcrfura· tion, tamponadc, dissection, root rupture, left vcntric· ular dilation, wall motion abnormality).74.79 During the positioning of the valve, TEE can be used to monitor advancement of guidewires and the delivery device and to evaluate the location of the pro.tthes.is.74 For first- and second-generation

Transcatheter Mttral Valve Implantation RAnoNAl.E

The need for complete n:placcmcnt of the mitral valve using transcathcter techniques arises from two principal concerns. First. a vast nwnbcr of disease configuration& lead to some degree of mittal regurgitation (MR) or mitral stenosis (MS) and a correspondingly high number of available techniques to repair these lesions. The transcathetcr mitral repair device mar· kct is dominated by the Mitra-Clip device (Abbott Laboratories, Irvine, CA), although there arc several other devices with a variety of approaches to percutaneously treat MR. These devices arc designed principally for the treatment of MR, and percutaneous treatment of a heavily c:alcified mitral valve or a malfunctioning biological valve is lacking. Transcatheter

388 I CHAPTER 15

FIGURE I 5-30. Measurement of the distance from the aortic annulus to the left main coronary artery (LMCA) ostlum using multlplanar reconstruction ofa three-dimensional dataset. This measurement can only be made In the coronal plane (lower left panel; DJ, green arrow). The top left panel shows the long-axis view (green plane). The short axis (red plane) Is positioned In the aortic root (white arrowIn the top le~ panel) untll It Intersects the l.MCA ostlum as seen in the in the top right panel. The coronal (blue) plane has been tilted so that it intersects the origin of the LMCA (yellow arrow).

mitral valve implantation (TMVI) with a prosthesis is likely to be a single solution for a variety of mitral lesions. Second, with an aging population, the rjsks of open surgery can be potentially mitigated with a percutaneous approach that could be more acceptable to those at prohibitive surgical risk. CHAWNGES

However attractive as these rationales seem, the mitral valve is a large and complex: structwe, and the traditional mechanisms of percutaneous valve placement may not apply. Challenges to 'ThM deployment

include (I) complex valve anatomy, (2) device anchoring, (3) sealing the pro.tthesis, and (4) changes to surrounding structures. The mitral annulus is large and asymmetric, as are the leaflets, with a complex: subvalvular support structure that not only requires preservation, but also avoidance during deployment. The ventricular walls play a major role in supporting the mitral valve substructure and can be involved in the mitral valve pathology, complicating device deployment. .& with the Mittadip system, the uaiu-septal tech.nique for a TMVI prosthesis requires a steerable and fle:x:ible

PROSTHETICVALVES I 389

CENTRAL ILLUSTRATION:Transatheter Mltral Valve Replacement for Native Mltral Ragurgltatlon

• Mltral Valve Position • Valve Sealing • Proximity of LVOT • Patient Selection

• Complex Anatomy • Dellvery System • Valve Thrombogenicity, Long-term Durability • Prosthesis Anchoring and Annular Retention

Apical Tether

AnnularWinglets LA

Native Leaflet Engagement

Radial Force

Mltral Annulus Clamping

External Anchor LA

FIGURE JS-31. Summary of challenges and anchoring mechanisms for transcatheter mltral prostheses In cllnlcal trials. (Reproduced with pennlsslon from Reguelro A, Granada JF, Dagenais F, et al: Transcatheter mltral valve replacement: Insights from early cllnlcal experience and future challenges, J Am Coll Cordlol 2017 May 2;69(17):2175-2192.)

delivery system to navigate an acute angle armed with a larg= prosthesis. In contrast to the TAVR technique,. the landing :zone,. fur a TMVI prosthesis is dynamic and irregular, Wlles.s it is being placed in a calci6ed valve or a sten~d ring or bioprosthesis.

Anchoring of the TMVI device is the major chal-

lenge for all types of prosthesis, and a variety of techniques have been developed to address this challenge (Fig. 15-31). These include (1) tethering the prosthesis to the LV apex: to provide counterttaction for stability

390 I CHAPTER 15 of the prosthesis (Tendyne, Tendyne Holdings LLC, Roseville, MN); (2) annular winglets that provide friction with radial interference through a series of annular anchors (NaviGate Atrioventricular Valved Stent, NaviGate Cardiac Structures, Inc., Lake Forest, CA); (3) native leaflet engagement with ventricular anchors that grasp leaflet-free margins (Tiara, NeoVasc, Inc., BC, Canada); (4) use of radial force to produce a "champagne cork" effect (Intrepid, Medtronic, Minneapolis, MN); (S) clamping the mitral leaflets and chords by engaging the annulus with flanges (CardiAQ-Edwards, Edwards Llfesciences, Irvine, CA); and (6) creation of an external dock or landing zone (Caisson, LivaNova, UK). No device is currently approved for use in the United States, but several clinical trials are underway (Tendyne, NCT02321514; CardiAQ, NCT02718001 and NCT02722551; Caisson, NCT02768402; Tiara, NCT02276S47 and NCT030398SS). In addition to the listed devices, there are several others in preclinical trials worldwide. It is also likely that as therapies evolve, products and companies will coalesce as the few successful devices emerge for clinical use. Seating the TMVI prosthesis can also be a challenge, given the irregular nature of the valve itself. A unique feature of prostheses in the mitral position is the need to withstand high systolic pressure to prevent a leak, unlike devices in other valve locations that do not have to face similar pressures to assure competence. However, recent data suggest that less than 2% of cases have significant paravalvular regurgitation. 81 Perhaps the most common "collateral damage" that may occur following a TMVI procedure is obstruction of the LVOT. Although some narrowing of the aortic annulus is common after surgical placement of mitral rings or prosthetic valves, obstruction of the LVOT is a less common but serious complication. With TMVI procedures, it is more common in calcified valves or following a valve-in-ring placement. 82-84 The most common reasons for LVOT obstruction include an obtuse annulo-mitral angle, septa! hypertrophy, small LV cavity, and flaring of device into the LVOT. PROCEDURE

The TMVI prosthesis can be deployed using a variety of approaches, including a direct surgical technique involving a transapical or transatrial approach, or a percutaneous, transfemoral vein approach using a trans-septal technique. As technology evolves, the eventual goal is to be able to introduce all TMVI prostheses using a percutaneous approach. Most procedures are performed in dedicated hybrid operating

rooms with multiple imaging modalities and availability of cardiopulmonary bypass. INTRAOPERATIVE IMAGING

Most patients will receive extensive preoperative imaging, including 3D CT imaging, which is a preferred modality for sizing of the prosthesis. However, 3D TEE also offers accurate imaging and can especially help with determination of planar irregularities that may affect deployment or predict complications, such as paravalvular leaks or LVOT obstruction. lntraoperatively, 30 TEE can be invaluable for guiding the delivery system through the trans-septal technique as described with the MitraClip S}'litem. As cumulative experience with TMVI procedures is still limited, imaging protocols are being developed as more information is gathered. In the procedural room, TEE plays a complementary role to cine-fluoroscopy to guide placement and detection of postdeployment complications. Prior to the procedure, it is important to document the severity of the lesion in addition to assessment of predictors of LVOT obstruction outlined earlier. In addition to 30 TEE, multiplane imaging can be valuable in determining the appropriate placement of the prosthesis within the delivery system (Fig. 15-32). An example of a TMVI procedure using a Sapien valve (Edwards Lifesciences) designed for aortic valve replacement for an obstructed mitral ring is shown in Fig. 15-32 and for a stenosed bioprosthesis in Figs. 15-33 to 15-37 and Video 8. OUTCOMES

The cumulative experience with this technique is limited, but some data have emerged with respect to outcomes and challenges. Procedural success is relatively high, and technical issues have mainly related to valve stability prompting open surgical repair. Surgical bleeding from apical access and LVOT obstruction have also been reported. The complication rates for valve-in-valve or valve-inring procedures seems to be lower than TMVI for secondary MR Anticoagulation therapy is generally recommended for at least 3 months following implantation. At least one device complication due to thrombosis has been reported resulting in temporary cessation of the program. 85

Transcatheter Replacement for Other Valves There is only one valve approved for transcatheter delivery to replace diseased pulmonary valves: the Melody valve (Medtronic, Inc., Minneapolis, MN).

A

B

FIGURE 15-32. 'Three-dimensional {30) TEE imaging of a transcatheter valve deployment for replacing a dysfunctional mitral ring. Both panels dlsplay a llve 30 Image above two corresponding orthogonal two-dimensional planes. Panel Ademonstrates a valve delivery system In place prior to deployment, and panel Bshows Imaging Immediately following deployment of the prosthesis. 'The delivery catheter Is Indicated by the solld arrow, and the dysfunctional mttral ring Is Indicated by the hatched arrow.

.w

392 I CHAPTER 15 Introduced in 2007. the Mdody valve was approved by the U.S. FDA in 2010 under a hwna.nitaria.n device exemption and indications subsequently expanded to include failed s~y placed prostheses in the pulmonic position.86• Since its introduction, more than 10,000 patients worldwide have received the Mdody wlve. Introduced through a transfcmoral vein approach, the procedure is generally conducted under sedation with fluoroscopy or general ancsthcsia in younger patients or those .requiring TEE. Transcatheter therapies for tricuspid valve disease are dominated by newer devices designed to treat

functional tricuspid regurgitation. Most cases of percutaneous tricuspid valve replacement have focused on treatment of dysfunctional surgically placed bi~ prostheses. Given the high risk of adverse outcome in patients with failed uicuspid bioprostheses, tricuspid wlve-in-wlve implantation is considered a feasible approach with acceptable procedural risk. Although limited data are available at this time, a multi.centcr rcgistty has reported Kood results in 152 cases that received either a Melody or Sapien prostb.esia to treat bioprosthetic uicuspid valve dysfunction. 88 Imaging protocols have not been devdoped for intraprocedural TEE. SUMMARY

With an increasingly aging population, low tolerance for surgical risk, improved survival. and improvemenu in technology, percutaneous techniques for rep.lacing diseased native or surgically placed valves with tra.nscatheter delivery will become more common. Inuaoperative echocardiographers will need to be knowledgeable about procedural requirements and common complications that need to be predicted prior to and ruled out following device deployment. STEHTWS VALVES

FIGURE 15-33. Continuous-wave spectral Doppler tracing showing high transmitral diastolicflowvelocities indicating severe stenosis in a patient with a dysfunctional bioprosthesis.

FIGURE 15-.34. Full volume gated three-dimensional 'TEE dataset showing an en-face view of a stenosed bioprosthesis in the mitral position in diastole for the same patient shown in Fig. 15-33.

These valves are usually difficult to distinguish from native wives, except for an increase in cchogenic signals ttom the annulus and around the base of the leaflets. Other 2D findings depend on the surgi· al technique wed to implant the valve. When the

PROSTHETIC VALVES I 393

FIGURE 1S-35. Live threedimensional imaging of the mitral valve in the en-face view with the transcatheter delivery system In place followlng a balloon valvuloplasty.

FIGURE 15-3'- Threedimensional imaging of the mitral valve in the en-face view with the transcatheter dellvery system In placelmmedlatelyfollowlng deployment of a Sapien valve across the stenosed bloprosthesls shown In Ag. 1S-34.

root inclusion technique is used, the ascending aorta often can appear to be thicker in the aortic root and proximal ascending aorta, as the will now con· tains layers from the prosthesis and the native aorta (a tube within a tube; Fig. 15-38). In the immediate postoperative period, blood, fluid, or thrombus may occupy the potential space between these two layers, and ve.r:y rarely can lead to valve malfunction. This potential space usually di&appeats within the first few

postoperative months.7•8lt Color flow and spectral Doppler signals from stendess prostheses are similar to those from native valves.!~ HOMOGRAFTS AND AUTOGRAm

These valves can also be very difficult to distinguish from native valves. A small-to-moderate increase in echogenicity is frequently noted at the annulus from suture material and accelerated calcification. Doppler

394 I CHAPTER 15

FIGURE 15-37. Contlnuouswave spectral Doppler tracing showing reduced transmitral diastolic flow velocities indicating resolution of stenosis in the same patient shown in Figs. 15-33 to 15-36 following a transcatheter valve lmplantatlon.

equation, modined Bernoulli equation, mean gradients, vn ratios, pressure balf..times (PHTs), and specinc flow characteristics are also applicable tD prosthetic valves. Readers are e.n.cowagcd to refer to the aforementioned chapters for a complete discussion on the qualitative and quantitative assessments of regurgitant or stenotic lesions.

Mltral Position

FIGURE 15-38. Stentless aortic valve. The area of the aortic root and proximal ascending aorta appear thicker (arrows) because the wall now contains layers from the prosthesis and the native aorta. LVOT, left ventricular outflow tract; AO, aorta.

signal& are comparable to stentless prostheses and should be similar to that of native valves.

SITE-SPECIFIC QUALITATIVE AND QUANTITATIVE ANALYSES The various techniques fur assessment of stenotic or regurgitant native valves dcsaibed in Chapters 10, 11, and 12 can be used or modified to evaluate prosthetic valves. The physical principles of the continuity

Transesophageal echocardiography is ideal for viewing and interrogating a mitral prosthesis. Midesopbageal views allow for unobstructed imaging of the left atrial side for assessment of intravalvular or paravalvular Il!gurgitation and mechanical occluder motion.S7,90 Transga.stric and deep ttansga.stric views generally afford views of the ventricular aspects of prostheses and can confum information obtained from midesophageal views. Transgastric views also allow for better evaluation of ventricular wall motion free from acoustic artifacts from the prosthesis. Peak vdocity, mean pressure gradient, and vdocity·time integral should be Il!corded in addition to hemodynamic data. EOA is derived fur a prosthetic mitral valve as the stroke volume through the valve divided by the vn of the ttanamiual flow: EOA (cm1)

= StTo~~olume

-

where sttoke volume (cm') is measured through a reference site proximal or distal to the prosthesis.

PROSTHETICVALVES I 395 This is typically measured at the LVOT or the right ventricular outflow tract (RVOT). However, this does not account for the presence of significant mitral regurgitation. VTI refers to the velocity-time integral of the CWD envelope, or "stroke distance" (cm), of blood flowing through the prosthesis. For a bileaflet mechanical valve, the peak velocity measured with CWD includes the higher-velocity jet in the smaller central orifice, which overestimates the pressure gradient and therefore underestimates the calculated EOA. Due to their design, the monoleaflet and biological prostheses do not exhibit this phenomenon. For a stenotic prosthetic valve, use of the pressure half-time formula to calculate area (using the constant of 220 ms) overestimates the EOA. This constant was derived from studies in native stenotic valves and is not validated in prosthetic valves.9 1 However, a pressure half-time more than 130 ms suggests possible stenosis, and a pressure half-time greater than 200 ms suggests significant stenosis and should ~rompt integrated evaluation with other parameters. When interpreting velocities across prosthetic valves in the mitral position, an increase in transvalvular velocity may be observed and raise suspicion for pathological stenosis. This must be differentiated from high flow across the prosthesis due to concomitant mitral regurgitation or other high-output states. To differentiate between a true stenosis or regurgitation from a high-output state, the ratio of VTI across the mitral valve to the VTI across the LVOT (VTIMv!VI'ILVOT) can he calculated. A normal ratio ( 0.7 cm}, qualitative signs suggestive of prosthetic regurgitation include a dilated right atrium and holosystolic flow reversal in the hepatic veins. Calculation of the EOA should not be performed using the pressure half-time algorithm applied to the mitral valve because this technique has not been validated in the tricuspid position. However, estimation of EOA using a combination of Doppler techniques such as transtricuspid Vfl and LVOT stroke volume is reasonable in the absence of significant concomitant aortic and tricuspid regurgitation. The pulmonic valve position can be difficult to examine even in the absence of a prosthetic valve because it is usually in the far field during TEE. Nevertheless, the type of prosthetic valve and any associated pathology can usually be identified. The optimal views for assessing the pulmonic valve include the upper esophageal aortic arch short-axis view (approximately 70 degrees) with the depth adjusted to 10 to 12 cm, which shows the valve and the main pulmonary artery trunk and allows for measurement of transvalvular gradients and CFD assessment; and the right ventricular inflow-outflow view at approximately 60 degrees, which provides satisfactory windows for valve identification and qualitative assessment of regurgitant jets. Color flow Doppler will usually indicate turbulent flows in prosthesis regurgitation or stenosis, and 2D examination will reveal leaflet thickening or obstructive lesions. Peak velocities greater than 3 m/s for prosthetic valves or 2 m/s for homografts are considered suspicious for prosthetic stenosis, and a prosthetic pulmonary valve regurgitant jet that exceeds 50% of the pulmonary annulus diameter is suggestive of severe regurgitation.57 There are limited data validating these techniques with TEE, and careful inspection of the valve using all available modalities is mandatory for a complete assessment.

MULTIVALVE REPLACEMENT It is not uncommon for surgeons to have to replace more than one valve, either at the same time or sequentially. Diseases such as rheumatic fever and myxomatous degeneration frequently affect more than one valve in the same individual. Surgical implantation of multiple prosthetic valves is an added technical challenge. Combined aortic and mitral valve replacement carries a 70% higher risk and poorer survival rate than replacement of either valve alone. The Society of Thoracic Surgeons national database committee repon indicates an operative monality of 8.2%

for all multiple valve surgeries, compared with 2.2% and 4.8% for aonic and mitral valves alone, respectively.4 Long-term survival depends on preoperative functional status. TEE evaluation of prosthetic valve structure and function with multiple valves in situ also provides a challenge to the echocardiographer. Imaging artifacts from one valve frequently obscure the examination of the other, sometimes making a complete examination difficult, if not impossible. Epicardial echocardiography can sometimes provide valuable information if TEE assessment is inconclusive.

PROSTHETIC MITRAL RINGS See Chapter 14 for a full discussion of mitral valve repair. One method of repairing a regurgitant mitral valve uses prosthetic materials to reestablish anatomical coaptation of the anterior and posterior leaflets. Rings also are used frequently to rectify mitral regurgitation secondary to annular dilation (cardiomyopathy or end-stage coronary heart failure) or leaflet prolapse. A variety of prosthetic rings are available with different amounts of flexibility and overall shapes that are tailored for specific mitral pathologies. Many are complete D-shaped rings, whereas others are shaped like a C or even attempt to reproduce the 30 saddle shape of the mitral annulus. Surgical preference usually dictates the type of prosthesis placed. The ring itself is visible around the periphery of the native mitral valve, as are the sutures used to secure it in place (Fig. 15-43). Prosthetic mitral rings do not require long-term anticoagulation.

PROSTHETIC VALVE PATHOLOGY Patient-Prosthesis Mismatch Patient-prosthesis mismatch {PPM) is present when the EOA is insufficient for the patient's body surface area (BSA), and is associated with worse hemodynamic function, less regression of LV h~ertrophy, more cardiac events, and lower survival. The presence of PPM can be determined by indexing the EOA of the prosthesis to the patient's BSA. Each valve type and size have a normal reference value for EOA. PPM in the aortic position is considered to be hemodynamically insignificant if EOA is greater than 0.85 cm2 /m2 , moderately significant at 0.65 to 0.85 cm2/m2, and severe at less than 0.65 cm2/m 2•94 In the mitral position, PPM leads to insufficient regression of functional TR and systolic pulmonary arterial pressure.95 ·96 An EOA less than 1.2 cm2/m2 strongly suggests PPM and will likdy lead to deterioration in long-term hemodynamics. Overall, PPM is associated with reduced short- and long-term survival.57,94

PROSTHETIC VALVES I 40 I

A

B FIGURE 75-43. (A) Prosthetic mltral ring white arrows ls easily seen after mltral valve repair In the mldesophageal

'TEE views. (8) Three-dimensional image after a mitral repair demonstrating the prosthetic ring which has dehisced from the native mitral annulus (red arrow).

Endocarditis Endocarditis should be suspected in all patients with prosthetic valves who develop scpticemia. Perivalvular abscess formation should be considered in those who do not respond to aggressive antibiotic therapy.. Other clinical indicators prompting a thorough TEE "hunt" for an abscess include new conduction abnormalities

and worsening heart failure (possible fistula formation). Although TfE is the first screening test fi>r suspected endocarditis, when endocarditis is presumed to be present in a patient with a bioprosthcsis, TEE should be perfonned to assess the degree of pathology.'TI Bacterial infections of implanted prosthetic materials are problematic, rcgardl.ess of their location, and

402 I CHAPTER 15

FIGURE 15-44. Endocardltls (arrow) on a porcine blologlcal valve In the mitred position. The acoustic shadow cast by the stTUts of the prosthesis Is seen extending Into the left ventricle. LA, left atrium; LV, left ventricle.

FIGURE 15-45. Echolucent abscess cavity (arrow) at the aortfc root In a patient wtth a prosthetic aonlc valve. AO, aona; LVOT, left ventTlcular outflow tract.

infection of prosthetic heart valves can lead to significant mortality, with reported rates as high as 70% for acute (6 months) endoc:arditis.3 1,32 Prosthetic valves are at an increased risk for endoc:arditis for two reasons: abnormal flow patterns and the pWience of foreign material. The annual rate for late endocarditis is approximately 0.5%, with no significant dif. fcrcncc between mechanical and stcntcd biological valves.31.'2 Compared to native valves, prosthetic valves arc more likely to have ring absc:csscs, conduction abnormalities, and fistulac and have a worse prognosis. Endocatditis has two common appearances on mechanical valve&: vegetations on leaflets, ocduders, or support material and ecbolucent ring absce&Ses with or without fistulae. Tissue valves most frequently develop new stenotic or regurgitant lesions but also can dcvdop vegetations (Fig. 1544) and/or abscesses. New or worsening paravalvular leaks arc highly suggestive of cndocarditis and arc a particularly ominous sign. Transesoph~ cchocardiography is vastly superior to TTE for the evaluation and diagn~is of prosthetic end.ocarditis, with significantly greater sensitivity and specificity (TfE sensitivity is 60% to 80% and specificity is 98%; TEE sensitivities arc l 00% for native valves and 86% to 94% for p~thctic valves, with a spccmcity of 88% to 100%).32 It also better characterizes vegetations, abscesses (Fig. 15-45), and fistulac, thereby providing important diagnostic information related to m.edicafver&us surgical intervention. Imaging with 3D echocardiography is helpful in identifying the location and point of attachment of the

vegetation, sizing of the valve and lesion, and assisting in identifying perforations.9l-93 This can allow the operator to generate views that may not be fea. sible using conventional 20 imaging. Echo findings commonly associated with abscess furmation inclucle dehisccncc manifested as a "rocking" of the valvc98 (Fig. 15-46; Video 9), pcrivalvular luc:ency, and periaortic root thwning.8·31.32 Abnormal color Sow patterns can be suggestive of fistula& and blood Sow into abscess cavities. Abscesses may also ruptwe into the LVOT, right atrium, left atrium, ascending aorta, pcric:ardial space, and main pulmonary artery with catastrophic consequences.

Thrombosis and Hemonhage Thrombosis and hemonbage account for more than 50% of all reported complications for biological pro~ theses and nearly 75% of all mechanical prostheses implanted in left heart ,POSitions.S.99 Maintenance of therapeutic anticoagulation levels continues to be one of the most dauntin} challenges to successful valve replacement. Even perfect.. anticoagulation level& are guiddin~ and do not guarantee l'reedom from these serious and potentially deadly complications. The early detection of periprosthetic thrombosis has been improved significantly with TEE, which can help guide medical (tbrombolysis) and surgical management. However, previously described imaging art.ifac:ts and limitations can interfere with the proper diagnosis. me> Furthermore, differentiating a thrombus from a pannus can be difficult but is often aitical to guiding therapy. In general, pannus formation is more

PROSTHETIC VALVES I 403

A

FIGURE 15-46. (A) Midesophageal long-axis view of a dehisced mechanical prosthesis In the mltral position. The valve has a•rocking* motion. The area of dehlscence Is marked by the yellow arrow. LA, left atTlum; Ao,

B

common in the aonic position and is characterized by a small, dense mass, whereas thrombi are larger, have lower echo density similar to myocardium, and arc more likely to be associated. with abnormal prosthetic valve motion. 57 All mechanical valves catty approximately the same incidence of thrombosis and require long-term

aorta. (8) Three-dlmenslonal en-face view of the same valve with the dehisced area marked by the yellow arrow. MV, mitral valve; AV, aortic valve. anticoagulation to hdp prevent dot formation, with the greatest risk during the first 6 months after implant2tion. Even when anticoagulation levels arc therapeutic, the rate of thrombosis is 0.6% to 1.8% per patien~year for bileaflet valves.69,IOl The risk of spontaneous thromboembolism ia three to six times higher if anticoagulation is subtherapeutic.

404 I CHAPTER 15 mitral compared tn aortic positions (32% w. 13%, reapectivcly).102. 103 These strands arc composed of fibrin and arc usually a few millimeters in length. Their motion is unrelated to that of the valvt: itself, and they can be distinguished from vegetations and thrombi by their movement in and out of the imaging plane. They can also be distinguished from surgical sutures, which arc shorter, have a higher echo density, and have a regularly spaced appearance on the sewing ring. Studies suggest higher rates of systemic embollzation associated with the&e strands.S

Primary Prosthesis Failure FIGURE '5-47. Thrombus (arrow) occluding a prosthetic mltral valve and extending Into the left atrium. In this case, the thrombus ls grossly visible, but sometimes the only Indication of thrombosis Is Inappropriate oc.cluder motion with failure to completely open or dose. LA, left atTfum; MV, mltral valve.

When placed in the tricwpid position, tluombosis of a mechanical valve is seen in more than 20% of patients because of the lower pressures in the right heart. Thrombus adherent to prosthetic materials wu· ally can be visualized, but sometimes the only indication of thrombosis is inappropriate occluder motion with failure to completely open or close (Fig. 15-47). Faulty occluder motion can be visualized directly with 2D echo or 3D echo. New obstructive or regucgitant lesions on CFD and/or specaaJ Doppler strongly suppon a thrombodc complication.

lbromboembollsm TEE is an appropriate initial or supplemental teat for evaluation for any cardiovascular source of embolus with no identified. noncardiac sowce, particularly in the setting of a prosthetic valvc.97 Embolic events in patients with mechanical valves have been reduced to 1% to 4% per patient-year with strict anticoagufation protocols. However, the risk of a scriow bleed while on anticoagulants is l % to 5% per patient-year.101

Fibrin Strands Thin filamentous strands can appear to be attached to the auiaJ side of mittal prostheses, and to the vcntticular side of aortic prostheses. Strands arc fairly common on prosthetic valves (26% to 38%) and are more frequent on mechanical compared to biological prostheses (27% vs. 8%, rcspectivdy) and in

Fonunatcly, a primary failure of mechanicaifrosthctic valves is a rare occurrence. Case reports o occludct device and strut emboli7.ation have been publ.i.shed for most available valves. An uncommon but often fatal complication with the Statr-Edw:ud.s valve in the aortic position was "ball variance," in which small cracks would develop in the Silastic occludcr ball, leading to thrombosis within the utdlite cage and subsequent valve obstruction. 1°"- 105 Prosthesis failure in tissue valves wually is related to calciAc degeneration of the leaflets themselves. Th.is leads to restricted cusp motion (stcnoai&) and, more commonly, .regurgitation secondary to tears and malocclwion. All nonautograft tissue valves will evt:ntually degenerate to the point of requiring replacement in the long term. However, the n~r stcndcss bia. logical valves appear to have a much slower degeneration rate.

P•ravalvular Regurgitation In the case of surgical AYR, crittria used for native valves may be reasonably applied to prostheses, especially spectral Doppler parameters such as the pressure half-time of the rcgurgitantf·et (sec Chapter 11).57 The qualitative evaluation o the nature of rcgurgi· tant jets with CFD and 2D examination is more valuable, as the pressure half-time is heavily dependent on hemodynamia and alignment of the Doppler interrogation angle with blood flow. Identification of the origin of the regucgitant jet with CFO may hdp determine pathology such as pannw, cndocarditis, or prosthetic valve leaflet dysfunction. New transcathctcr aortic valves should be imaged in sbon and long axis using CFO in the annular and subannular regions to assess central or paravalvular aortic insufficiency. Assessing and quantifying paravalvuJar leak from multiple TEE planes and views i& recommended. For transcatheter valves, continuouswave Doppler parameters such as jet density and

PROSTHETIC VALVES I 405 LVOT Obstrudlon

FIGURE 15-48. Paravalvular regurgitation in a patient with a bileaftet tilting disk mitral valve. The jet is seen originating lateral to the sewing ring (arrow) and "hugging•the wall of the left atrium. LA, left atrium; MV, mltral valve.

Although quite rare, obstruction of the LVOT has been described after implantation of prosthetic mitral valves or mitral annular rings.90 Obstruction c:an he cawed by preserved mitral valvular apparatus, the valve strut or tissue leaflets in the case of stented bioprostheses,107,l08 or the native leaflets in the case of mittal valve ring annuloplasty (see Chapter 14). In the latter, the surgical. team may try to mitigate this by performing an edge-to-edge, or ".Alfieri," stitch that drastically reduces the risk of obstruction, but persistent obstruction rarely has been described. tO!) The presence of LVOT obstruction should be considered in all cases, especially in situations of poor hemod.ynamics after cessation of CPB in a previously normal ventricle. This is most easily ass~sed from the transgasttic long-axis or deep transgastric five-chamber view. Residual subvalvulu tissues also may interfere with the valve function, resulting in mittal regurgitation rather than outflow tract obstruction. 110

Uncommon Secondary Obstruction pressure half-time arc less reliable due to the cc-64 l. 102. Kiavar M, Sadeghpour A, Bakhshandeh H, et al. Are prosthetic heart valve fibrin strands negligible? The associations and significance. J Am Soc &hoctiwliogr. 2009;22(8): 890-894. 103. Orsinelli DA, Pearson AC. Detection of prosthetic valve strands by transesophageal echocanliography: clinical significance in

412 I CHAPTER 15 patients with suspecral. cardiac source of embolism. J Am Coll OmiioL 1995;26(7):1713-1718. 104. Grunkcmeier GL, Starr A. Late ball variance with the Modd 1000 Starr-Edwards aortic valve prosthesis. Risk analysis and strategy of operative management. J Thorac Cartiwvasc Surg. 1986;91(6):918-923. 105. Hylen JC, Kloster FE, Hert RH, et al. Phonocardiographic diagnosis ofaortic ball variance. CimJation. 1968;38(1):90-102. l 06. Kappetein AP, Head SJ, Genereux P, et al. Updated standardized endpoint definitions for ttanscatheter aortic valve implantation: the Valve Academic Research Consortium-2 consensus document. J Am Coll CtmJioL 2012;60(15): 1438--1454. 107. Guler N, Ozkara C, Akyol A. Left ventricular outflow tract obstruction after bioprosthctic mitral valve replacement with posterior mitral !call.et preservation. Ta Heart Inst f. 2006;33(3):399--401. 108. Patd H, Antoine SM, Funk M, et al. Left ventricular outflow tract obstruction after bioprosthetic mitral valve replacement with preservation of the anterior leaflet. Rev Cartliovtm: Meti. 2011;12(1):48-51.

109. Bhudia SK, McCarthy PM, Smcdira NG, et al. Edge-to-edge (Alfieri) mitral repair: results in diverse clinical settings. Ann Thorac Sllrg. 2004;77(5):1598-1606. 110. Thomson LE, Chen X. G~ves SC. Entrapment of mitral chonl.al apparatus causing early postoperative dysfunction of a St. Jude mitral prosthesis. J Am Soc Echocttrriiogr. 2002;15(8):843-844. 111. Matsuno Y, Mori Y, Umeda Y, et al. Bioprosthctic mitral valve dysfunction due to native valve preserving procedure. AsUrn Ca~vasc Thl1Tlfc Ann. 2016;24(3):276-279. 112. Sidhu S, Goyer C, Hattakonian R, et al. Transcsophagcal cchocardiographic detection of intracanl.iac BioG!uc postmitral valve replacement. Anesth A~. 2007;105{6): 1572-1573. 113. Otto CM, Kumbhani DJ, Alexander KP, et al. 2017 ACC expert consensus decision pathway for transcatheter aortic valve replacement in the management of adults with aortic stenosis: a report of the American College of Cardiology Task Force on Clinical Expert Consensus Documents. J Am Coll Ca~L 2017;69(10):1313-1346.

Aortic Surgery and Atheroma Assessment Madhav Swaminathan and Joseph P. Mathew

INTRODUCTION Aortic diseases can range from apparently innocuous atherosclerosis to complex aneurysmal pathology. Regardless of the type of disease, the involvement of aortic pathology in any surgical plan can present a challenge to both surgeons and anesthesiologists. Whereas significant atherosclerosis at critical locations can alter surgical plans, aortic dissections can rupture and are life threatening, require rapid and accurate diagnosis, and need definitive medical and/or surgical management due to their high risk of morbidity and mortality. 1•2 A key ingredient in the efficient management of these patients is imaging of the thoracic aorta. The anatomical juxtaposition of the esophagus and aorta makes transesophageal echocardiography (TEE) an attractive imaging tool. It is now recognized as an essential noninvasive diagnostic modality for acute thoracic aortic pathologies, and is a standard part of the echocardiographer's armamentarium in the operating room.3--6 In emergent situations, TEE may be the only imaging modality available. It is therefore important for the echocardiographer to quickly and accurately verify the diagnosis, distinguish true pathology from the many common confounding artifacts, and clearly communicate precise echocardiographic findings of the aorta and related cardiac anatomy to the surgeon to guide intervention. The following text reviews aortic anatomy and pathology and associated echocardiographic features that assist with imaging during aortic surgery.

ANATOMY OF THE AORTA In order to truly appreciate the invaluable role that TEE plays in the assessment for diseases of the aorta, a detailed understanding of the aorta and surrounding anatomical structures is important. The geometrically complex thoracic aorta can be divided into three segments: ascending thoracic aorta, aortic arch, and descending thoracic aorta (Fig. 16-1). The ascending thoracic aorta originates at the level of the aortic valve annulus. As previously described in Chapter 4, the

aortic valve comprises three crescent-shaped leaflets that coapt to form three commissures. Immediately distal to the aortic valve apparatus is a short and dilated aortic segment-the sinus ofValsalva-which is subdivided into the noncoronary, left coronary, and right coronary sinuses. As the nomenclature suggests, the left and right coronary arteries each originate from their respectively named sinus. Distal to the sinus of Valsalva, the aorta slightly narrows, forming the sinotubular junction (STJ). From this point, the ascending aorta crosses beneath the main pulmonary artery, then courses in an anterior, cranial, and rightward direction over the origin of the right pulmonary artery. The ascending aorta terminates and continues as the aortic arch at the origin of the brachiocephalic (innominate) artery. The aortic arch then proceeds to curve in a posterior and leftward direction with cranial convexity. Three arteries arise from the aortic arch: the brachiocephalic, left common carotid, and left subclavian arteries. It is often difficult to visualize the distal ascending thoracic aorta and proximal aortic arch with TEE because the trachea is positioned between the esophagus and aorta, effectively preventing ultrasound transmission. Immediately beyond the origin of the left subclavian artery, at the point of attachment of the ligamentum arteriosum (remnant of the fetal ductus arteriosus), is a second narrowing called the aortic isthmus. Unlike the heart and proximal part of the aorta, the aortic isthmus and descending thoracic aorta are relatively fixed. Consequently, deceleration injury secondary to trauma is most often confined to this level. Distal to the aortic isthmus, the descending aorta follows a caudal, slightly anterior, and rightward trajectory toward the aortic diaphragmatic hiatus. Along its intrathoracic course, the descending thoracic aorta and the esophagus are in close proximity. Whereas the esophagus courses almost straight downward, anterior to the midline of the vertebral bodies, the aorta travels in a smooth, curved direction from the anterolateral side of the 4th thoracic vertebral body to the anterior side of the 11 th vertebral body. During its thoracic descent, multiple intercostal arteries branch off the aorta and may occasionally be

'414 I CHAPTER 16 Trachea

Subdav1an a.

large cavity that is highly deformable, the position of the abdominal aorta in relation to the int.ragastric TEE probe is somewhat variable. The cdiac artery and mesenteric arteries originate from the anterior side of the abdominal aorta. The renal arteries arise from the left and right sides of the aorta. slightly below the mcsenteric vessels. The wall of the aorta is composed of three runicae, or layer:s: the inti.ma, media, and adventitia. The inner layer, the intima. consists of simple squamous epithelium and wulerlying connective tissue and is most susceptible to injury. The twtica media accowus for 80% of aortic wall thickness, consists of circularly arranged smooth muscle and dastic tissue, and is responsible fur its strcn~ and elasticity. TLSSUC disorders of this layer often fead to weakening of the wall and ' The left main and right coronary arteries can often be rdiably visualU:.ed in the ME AV SAX view.25 Direct evidence of coronary involvement is the presence of a dissection Bap enending into the ostium of the ooronary vessel. Indirect evidence includes dectrocardiographic (ECG) changes, cardiovascular instability, and echocardiographic findings of regional wall motion abnormalities. Although branch aneries of the aortic arch can be reliably visuali2'.ed with TEE,55,56 the use of additional modalities including epiaortic scanning and surface Doppler directly over the carotid arteries to assess dissection extent into the arch vessels is highly rccommended.S 7 The remaining side branches, including the renal, intestinal, and spinal cord vessels, are more difficult to examine with TEE. Other important ochocard.iographic findings include the presence of pericardia! and left pleural effusions. Although pericardia! effilsions can .re&ult from the rupture of the dissection through the wall of the aortic root, the most common cause is from the transudation of ftuid across the false Iumen.3·S8 The development of left pleural effusion is similar except for the fact that the rupture occurs in the descending thoracic aona.59.60 A pericardial effusion appears as an ccholw:cnt space between the parietal and visceral pericardium on TEE. Ech.ocardiographic signs suggesting tamponade include early diastolic collapse of the right ventricle, late dia&tolic/early systolic collapse of the right or left atrium, decreased size of the cardiac chambers, and abnormal ventricular septa! wall motion with inspiration. A left pleural effusion is best seen in the descending aorta SAX view as an ocholu· cent space that resembles a "claw" (Fig. 16-10). Following surgical repair, the aorta should be assessed to ensure that the entry tear and false lwucn have been excluded and that flow has been re&torcd to the true lumen.14 The aortic valve should also be evaluated for new aortic insufficiency.1' New regional wall motion abnormalities may suggest mechanical ocdu.sion of a coronary ostium and indicate the need for funher coronary intervention, either via bypass ~ or percutaneous coronary revascular~ i%ation.-Global' assessment of right and left ventricular function is important to assess for the need for more aggressive pharmacological support, since poor ventricular function is associated with a poor outcome.61

AORTIC SURGERY AND AlHEROMA ASSESSMENT I 423 Table 16-3. Grading of thoracic aortic atheroma

,

FIGURE 16-10. Mldesophageal short-axis view of the descending aorta demonstrating a crescent-shaped echolucent space that suggests a significant left pleural effusion.

AORTIC ATHEROSCLEROSIS St.rob: continues to be a significant cause of morbidity and mortality after cardiac surgery. Strokes occur in approximately 1% to 6% of patients following cardiac surgery and account for nearly 20% of deaths. 62-" The association between aortic atheromatous disease and suoke has been dearly deAned.65-67 The high risk of neumlogical dysfunction associated with aortic atherosclerosis is a compelling argument fur routine inttaopcrative atheroma assessment of the thoracic aorta when surgical manipulation is anticipated. Techniques for detecting the presence of aortic atheromas include manual palpation, x:-ray. magnetic resonance and tomographic scans, and cardiac cathetcrization. However, TEE and epiaortic ultrasound arc generally considered to be superior imaging modalitics.68•69 TEE is considered the first-line choice of imaging modality fur the diagnosis of aortic atherosclerosis by the 2015 co.nse.n&us statement on multimodality ~g of diseases of the thoracic aorta from the ASE.1 Several clas.iification syst'CIDS fur grading the severity of aortic athcromas have been proposed. A c:ommonly used system is that of Katt and colieagues, who divided die severity of atherosclerosis into 6.vc gradrs ~ from normal aorta (grade 1) to mobile adieroma. (grade 5).66 In the absence of a unified clas.sification system, the .ASE bas su.gguted grading aortic atherosclerotic disease based on increasing thickness of the lesion from grade 1 through 4. Complex lesions that include ulceration or mobile dcmcnts arc classified as grade 5 because they are sttongly associated with adverse neurological

2

Nonnal Mild

3

Moderate

4

Severe

5

Complex

Intimal thickness ' erative TEE can assist with the trans-scptal puncture,

confirmation of ad.equate placement of the transseptal cannula. and diagnosj& of complications related to implantation of this device. During placement of the device, after obtaining femoral venous access, the presence of the guidewire in the RA can be confumed in the midcsophagcal bicaval view. A zoomed view of the intcrauial septum in the midcso,rhagcal AV short-axis view allows observation of the tenting" of the foua ovalis by the nccdlc during traru~scptal puncture. Can:ful visuali7.a.tion of the needle tip during tranHeptal a.cceu prevent& inadvertent puncture of the aortic root. coronary sinus, right atrium, or left atrium.s• The ~scptal nccdlc is exchanged for a guidewirc, and after dilation of the _puncture sit.e, the inflow cannula is advanced through the &moral vein, across the septum, and into the LA. All the inflow holes of the trans-scptal cannula should be confirmed. within the LA. Al. the in8ow cannula can migrate into the pulmonary veins, the LA appendage, across the MY, or backward into the RA, correct positioning of the inflow cannula should be confirmed again with the pump at full performance.

TEE for Evaluation of the LVAD patient The use of echocardiograpby, and in particular TEE, is essential for the management of patients with LVAD therapy, including confirming the indication for implantation, preplacement evaluation of cardiac structure and function, evaluation immediately post· implantation, and assisting decision making during shon- and long-term. follow-up. The American Society of Ecbocardiography (ASE) consensus statement fur the we of echocardiography in the management of LVAD patients addresses the use of this imaging modality during the different phases of care of these

paticncs.5'

Prelmplantatlon Evaluatlon The preoperative TEE examination must focus on determining the effects of end-atage heart f.ailure on cardiac morphology and physiology, as well as identifying possible determinants of postoperative complications. The most important dements of such assessment arc depicted in Table 17-1. The assessment of left hean anatomy and function intends to confirm the presence of cnd~stage hcan disease and to establish a baseline for post.operative comparison. Another purpose is to detect associated changes in the geometry and function of the MV and papillary muscle& due to LV dilation. Of particular importance, patients with advanced heart f.tllure have decreased blood flow velocity, which predisposes them to blood stasis and LA and LV intracavitary thrombus

ASSESSMENT OF MECHANICAL CIRCULATORY SUPPORT DEVICES I 445 Table 17-1. Pre-LVAD implantation TEE evaluation 1. Eva Iuation of left atrium and left ventride anatomy 2. Assessment of left ventricular systolic and diastolic function 3. Mitral valve anatomy and pathology (mitral stenosis and regurgitation) 4. Aortic valve anatomy and pathology (aortic insufficiency and its severity) 5. Presence of ascending aortic pathology 6. Determination ofintracardiac shunts 7. Tricuspld valve anatomy and pathology (tricuspid regurgitation and its severity) 8. Assessment of right ventricular function 9. Presence of left heart intracardiac thrombus

formation and systemic embolism. Prior myocardial infarctions may result in LY wall aneurysm formation with intramural thrombus accumulation.60 Mitral Valve Stenosis (MS). The presence of MS is not a contraindication for LVAD placement. Nonethele~, a significant trans-MV gradient will lead to impaired LVAD filling, persistence of pulmonary venous pressure elevation, and symptoms of heart failure. Therefore, patients with MS with a mean pressure gradient > 10 mm Hg should be considered for MY replacement at the time of LVAD implantation. It is important to note that in this patient population, previous MY repair or replacement is common. It is essential to evaluate for the presence of severe MS across a native, repaired, or prosthetic MY. MS is optimally assessed by TEE in the midesophageal four-chamber view using CFD and spectral Doppler to measure peak and mean transvalvular gradients and pressure half-time (PHT). However, these measurements should be used cautiously in the setting of decreased left ventricular compliance and lowflow states, which may result in decreased PHT and decreased transvalvular gradients with underestimation of MS severity.61 Mitral Valve Regurgitation (MR). Similarly, the presence of MR is not a contraindication for LVAD placement. In fact, the severity of MR is significantly reduced after LVAD implantation. 18•62 However, if present, severe MR should be repaired when there is expectation of myocardial recovery and subsequent LVAD removal.63 The mechanism of MR improvement involves LY decompression and reverse remodeling with a decrease in LY dimension and improved leaflet coaptation. The optimal level of decompression to reduce MR may limit AV opening, thereby increasing the risk of AI.

Aortic Valve Inmfficiency (AI). The presence of AI results in chronic LY volume overload with ensuing ventricular dilatation and dysfunction. The hemodynamic consequence is a reduction of the pressure gradient across the AV secondary to elevated LY enddiastolic pressure and reduced aortic diastolic pressure. In patients with advanced heart failure, such circumstance may lead to underestimation of AI severity.64•65 The significance of AI in LVAD patients is a consequence of the fact that LVAD therapy can exacerbate preexisting AI or prompt development of de novo AI.66-68 Of significance, up to 25% to 30% ofLVAD recipients will develop mild or moderate AI within 1 year after device implantation.f>Wi8 The proposed pathophysiological mechanism for AI in this situation is the presence of a continuous transvalvular pressure gradient aero~ the AV between the aortic root and the decompressed LV, preventing the AV from opening. The lack of AV opening in turn promotes leaflet fibrosis, thrombus formation, and collagen deposition leading to leaflet fusion and deterioration. Ultimately, there is retraction of the leaflet tips and formation of a central orifice, resulting in development of continuous AI.69,70 This process appears to be more common with continuous-flow devices than with pulsatile ones.71 A possible explanation is that in pulsatile-flow LVADs, blood is ejected each time the device is full; therefore, AI in these patients increases the pump rate. 65 The hemodynamic consequence of significant AI in LVAD patients is the generation of a closed loop of circulation from the LVAD into the aorta and back into the LY. This recirculation reduces LVAD efficiency, worsens heart failure symptoms, and perpetuates AI deterioration.66·72 As AI is likely to progress in the long term and may affect the durability of the device, the International Society of Heart Lung Transplantation recommends correction of moderate or higher degrees of preexisting AI at the time of LVAD placement. 63 There are several possibilities for AI correction in LVAD patients. One option is AV replacement. Mechanical valves are not typically used because of the potential for thrombus formation on the valve as a consequence of the immobility of the leaflets during most LVAD cycles. Furthermore, intermittent opening of the AV renders the patient at risk for embolization.65,73 Thus, if the valve requires replacement, most surgeons recommended the use of a bioprosthesis. However, biological valves may be exposed to similar risk of deterioration after LVAD implantation as native valves. The preferred strategy on OT patients is LY outflow tract closure via AV suture closure or repair, which avoids the increased morbidity associated with valve replacement.74 Another option in patients without the possibility for native heart recovery and subsequent removal of the device is placement of an

446 I CHAPTER 17 occlusive LV outflow tract patch graft with polytetrafluoroethylene. 75 In this situation, all blood must be delivered from the LV to the LVAD, and pump failure may result in severe hemodynamic instability, as the native heart would not be able to eject through the AV.72,73 Altemativdy, there are reports of minimally invasive and percutaneous strategies for management of AI after LVAD implantation.76-78 If the LVAD is being used as BTT therapy and a relativdy short period of support is anticipated, then moderate AI may be better tolerated, anticipating that LVAD speeds/rates may be higher than normal. Aortic insufficiency can be assessed in the midesophageal AV short- and long-axis views using CFO for qualitative evaluation. Quantification of AI severity can be assessed by continuous-wave (CW) Doppler interrogation of the AV regurgitant flow at the deep transgastric or transgastric LY long-axis view in order to measure pressure half-time. Important considerations include the degree of AV calcification and the characteristics of the regurgitant jet. An eccentric regurgitant jet in a heavily calcified valve may be more likely to worsen with ventricular assist device (VAD) support and usually warrants surgical correction. Of particular importance, there are no specific guidelines to grade AI severity in continuousflow LVAD patients. The accepted guidelines for AI quantification are not validated in this setting. As mentioned before, the use of traditional echocardiographic parameters (e.g., AI jet width/LVOT diameter and vena contracta) underestimate AI severity in 33% of patients with continuous-flow LVAD.79•80 Importantly, AI grading does not predict development of heart failure or need for AV closure or repair. 81 Several parameters that intend to quantify AI in this patient population have been described. Such parameters are peak to peak systolic/diastolic (SID) vdocity ratio and diastolic acceleration at the LVAD outflow cannula. These parameters provide better discrimination of AI severity and can be predictive of hospital admission due to heart failure, need for AV interventions, urgent transplantation, and death. Asc:ending Aortic Pathology. The LVAD outflow cannula is typically placed in the right anterior-lateral portion of the ascending aorta (except for the Jarvik 2000, which may be attached to the descending aorta). Thus, a thorough examination of the ascending aorta is an essential component of the intraoperative TEE evaluation. The ascending aorta is optimally viewed in the midesophageal ascending aortic short- and longaxis views. Protruding or mobile atheroma significantly increase the risk of stroke. Given the fact that these plaques can be difficult to palpate, epiaortic scanning will assist the surgeon in selecting appropriate places

for cardiopulmonary bypass (CPB) and LVAD outflow cannulation sites.60•82 An ascending aortic aneurysm may require repair prior to LVAD placement.64 lntracardiac Shunts. After LVAD implantation, the primary physiological effect is LY unloading with reduction of LV diastolic pressures. Thus, LA pressures are reduced but RA pressure can remain elevated or increase as a result of increased venous return from an augmented systemic cardiac output. Therefore, the presence of an intracardiac shunt can result in a rightto-left shunt with hypoxemia and possible paradoxical embolism. Although it is possible to flnd an atrial or ventricular septal defect, the most common cause of an intracardiac shunt is the presence of a PFO. In fact, the f revalence of PFO in the adult population is 25%. 3 In the presence of a PFO, hypoxemia can occur immediately after LVAD pump activation or at any point after implantation when RA pressure exceeds LA pressure. Otherwise, a PFO causing paradoxical embolism can result in LVAO pump malfunction or thrombosis at the time of implantation or later on. The search for a PFO during the LVAD preimplantation period must therefore be exhaustive. TEE examination required for PFO identification includes two-dimensional assessment for foramen ovale flap movement and CFO interrogation, optimized for detection of low-vdocity flow across the PFO. Agitated saline injection along with a Valsalva release maneuver is used to unmask right-to-left shunting.64 For appropriate performance of this technique, the agitated saline should be injected after the Valsalva maneuver produces a decrease in RA volume, and the Valsalva should be released-transiently increasing RA pressure over LA pressure-when the microbubbles are first seen entering the RA. Bowing of the septum to the left upon release of Valsalva confirms the transient increase in RA pressures. Admixture of agitated saline with small quantities of blood has been reported to improve the acoustic signal of the microbubbles. The bubble study is positive if bubbles arpear in the left atrium within three cardiac cycles. 8 TEE examination with CFO and agitated saline injection can detect PFO with high sensitivity and specificity.85 Unfonunately, several pathophysiological events can make PFO identification difficult. First of all, patients with advanced biventricular heart failure can have elevated bi-atrial pressures, which can reduce the RA-LA gradient and thus alter detection with CFO and agitated saline techniques.75 In patients with severe LV failure, LA pressure may be higher than RA pressure. This can result in a left-to-right shunt-a situation in which a Valsalva release maneuver can be insufficient to demonstrate the shunt. In

ASSESSMENT OF MECHANICAL CIRCULATORY SUPPORT DEVICES I 447 such cases, an alternative method involves partial obstruction of the pulmonary artery by the surgeon after the aortic cannula is placed. 86 Tricuapid Regurgitation (TR). Approximately 50% of patients considered for LVAD implantation have significant TR. Importantly, patients with TR at time of LVAD placement have worse outcomes, including decreased survival.87-89 LVAD support reduces LY end-diastolic and pulmonary venous pressures, which then decreases RV afterload, improving RV performance and central venous pressure. This can eventually lead to decreased RV end-diastolic diameter and decreased TR. However, such changes are delayed, and TR can initially increase due to limited change in pulmonary vascular resistance. Postoperative fluid resuscitation can also further dilate the RV and exacerbate TR. A contributing factor is the leftward displacement of the interventricular septum caused by LY decompression, which alters the geometry of the TV and worsens TR.9°-92 Thus, the possibility of improving outcomes, including decreasing the incidence of RV failure by correcting TR, justifies recommending its repair at time of LVAD implantation.63 Careful evaluation of TR, including the presence of hepatic vein systolic flow reversal, is necessary. The TV is optimally viewed in the midesophageal fourchamber and the midesophageal RV inflow-outflow views. It is particularly useful to perform adequate TV spectral Doppler interrogations in the midesophageal modified bicaval view where parallel alignment with trans-TV flow can be achieved.

Right Ventricular Function. The development of RV failure in LVAD recipients is consistently associated with significant poor outcomes, including short-term and long-term mortality. 93 The incidence is highly variable, but it can be estimated between 15% and 25%.94,95 Optimal LVAD performance depends on an adequately functional RV to provide effective preload to the pump. At the same time that LVAD support may enhance RV performance by decreasing pulmonary hypertension and its afterload, the presence of the LVAD may also worsen RV function by increasing its preload. There are also less predictable changes in RV contractility as a consequence ofLVAD support.93 The complete description of RV function assessment is beyond the scope of this review and can be found in chapter 9. The available methods used to evaluate RV function in LVAD recipients are in Table 17-2. The calculation of the global RV fractional area change (FAC) is one of the most commonly used quantitative parameters for RV function determination. It is easy to obtain and it represents a surrogate of RV ejection fraction. A global RV FAC greater than 40% is considered normal. Most patients receiving an

Table 17-2. Methods of right ventricular function TEE evaluation • QUALITATIVE Right ventricular dimensional changes and free-wall longitudinal and radial motions in midesophageal four-chamber, right ventricle inflow-outflow, transgastric right ventricular long-axis, and short-axis views. • SEMI-QUANTITATIVE 1. Global right ventricular fractional area change 2. Tricuspid annular plane systolic excursion 3. nssue Doppler-derived lateral annular systolic velocity (51 4. Myocardial performance index S. Right ventricular outflow tract fractional shortening 6. Longitudinal strain and strain rate

LVAD have a global RV FAC between 20% and 30%. Patients with a global RV FAC less than 20% are at high risk for RV failure following LVAD support.75 The RV systolic and diastolic areas are commonly traced in the midesophageal four-chamber view. Tricuspid annular plane systolic excursion (TAPSE) is another widdy used quantitative parameter for RV function determination, where the distance of systolic displacement of the TV lateral annular segment is measured along the longitudinal plane from a deep transgastric view. The main disadvantage is that this method assumes that the lateral annulus is representative of the entire RV. Otherwise, this method is highly specific; for example, a TAPSE value less than 17 mm can identify abnormal RV systolic function.96 The RV systolic velocity (S') is obtained by tissue Doppler interrogation of the basal free wall in the midesophageal four-chamber view. This measurement is a reproducible and reliable method for evaluation of RV performance. An RV S' less than 10 emfs indicates RV systolic dysfunction.75 The myocardial performance index utilizes tissue Doppler interrogation of the TV lateral annulus in the midesophageal four-chamber view. This quantitative method seems to be independent of preload, heart rate, and RV geometry. 97 This index cannot be measured in patients with first-degree atrioventricular block. There are additional quantitative methods to measure RV systolic function, including right ventricular outflow tract (RVOT) fractional shortening, longitudinal strain and strain rate, and myocardial acceleration during isovolumetric contraction. However, such methods are still in development at this point.75,98 lntracardiac: Thrombus. Patients with advanced heart failure are at high risk of intracardiac thrombus

448 I CHAPTER 17

FIGURE 17-8. Midesophagealfour-chamberview obtained prior to left ventricular assist device (LVAD)

implantation showing a large, elongated, and pedunculated thrombus attached to the left ventrlcular apex. LV, left ventrlde. formation, particulaily in the LA and LV. In general, the incidence of thrombus formation in LVAD recipients is approximatdy 16%.99 Potential risk factors are prior acute myocardial infuction, post-LVAD imr,Iantation bleeding, and LA inflow cannulation site.9 The most common sites of left heart thrombus formation in LVAD recipients at the time ofimplantation are the LA appendage and the LV apex.100:101 Significantly, the presence of LV thrombosis in LVAD patients is associated with a four-fold increase in risk of stroke. A thorough TEE examination must be performed to rule out the presence of left heart thrombus, in particular of LV apical thrombus, prior to the ventticulotomy for placement of the LVAD inflow cannula (Fig. 17-6, Video 5). The use of intravenous ec:hoc:ardiographic contrast increase& the sensitivity and specificity for thrombus detection.7S,l02 When the apex cannot be visualized with TEE, epieatdial examination at the time of implantation is an alternative. In LVAD patients with a surgically dosed AV or with an AV that docs not open intermittently, there is significantly increased risk of thrombus formation due to low or static blood flow in the aortic root and ascending aorta with a consequent high risk of stroke (Fig. 17-7. Video 6).

Immediate Postimplantation TEE Evaluation The objectives of the TEE cu.minatlon in the postLVAD implantation period arc to assess the results of the surgical procedure and to detect any actual or potential problems that require intervention upon

FIGURE 17-7. Midesophageal aortic valve long-axis

view showing a large aortic root thrombus extending into the proximal ascending aorta in a patient on left ventricular assist device (LVAD) support. (LA left atrium, LVOT left ventricular outflow tract). CPB separation or before termination of the surgical procedure. The specific requirements of the immediate post-LVAD implantation TEE evaluation are summarized in Table 17·3. De-airing. The presence of intracardiac air is evidenced as highly hypercchogcnic, white, punctuated rcfi:actors inside the cardiac chambers. Such air bubbles must be dctcctcd prior to activation of the LVAD pump in order to decrease the possibility of air embolism. Following open h.e:.ut surgery. ambient air can be retained in multiple locations of the hean, including the pulmonary veins, left atrial appendage, LV apex, the right coronary sinus of Valsalva, and the pulmonary artery.64.103 In addition, air can be retained inside the LVAD cannulas and the pump, as well as in the

Table 17-3. Immediate post-left ventricular assist device implantation transesophageal echocardiographic evaluation 1. De-airing prior to separation from cardiopulmonary bypass 2. Determination of presence of le~ atrial and ventricular

thrombus 3. Detection of lnteratrlal shunt5 4. Evaluation of right ventricular function S. Determination of tricuspid regurgitation and its severity 6. Assessment ofaortic valve and aortic lnsuftldency 7. Assessment of left ventrlcular assist device Inflow and outflow cannulae posltlon/allgnment and flow velocity

ASSESSMENT OF MECHANICAL CIRCULATORY SUPPORT DEVICES I 449 space between the LVAD inflow cannula oriflce and the inferior wall portion of the interventricular septum.64·104 The de-airing process is more complicated for LVAD implantation compared to valvular heart surgeries. LVADs are able to generate negative intraventricular pressure with a suction effect that can lead to entrainment of air. This is most commonly seen when the pump speed is inappropriatdy increased during a time when the delivery of blood into the LY is reduced. Thus, the de-airing process after LVADs implantation includes removal of intracardiac air as wdl as vigilance to avoid air entrainment. Probably one of the most significant negative effects is when entrained air is embolized into the right coronary artery with subsequent RV dysfunction, leading to a cycle of reduced LY filling, and further entrainment of air. In this situation, TEE interrogation will demonstrate a distended RV, a collapsed LV, and significant air in the aortic root. In order to avoid this scenario, RV function must be preserved during separation from CPB, maintaining LY preload during the period of reduced LVAD flows and until protamine reversal. Most importantly, use of TEE for detection of air should be conducted continually during this period of time. lntracardiac Thrombus. After LVAD placement, the presence of thrombus should be evaluated in all cardiac chambers, in particular the LA and LV. The presence of low blood flow conditions predisposes to thrombus formation, especially in the left atrial appendage, the space around the LVAD inflow cannula insertion site, the LVOT, and the aortic root. 100 lntcratrial Shunu. On occasion, a PFO becomes apparent only after LVAD implantation. This can occur in 20% of cases where a PFO was undetectable in the pre-implantation examination. 105 As discussed before, the hemodynamic effects of a functioning LVAD increase the likelihood of right-to-left shunting due to reduction in LY end-diastolic pressure and LA pressure, makin~ it rcossible to unmask a previously unrecognized PFO. o5, 06 Similarly, previously unrecognized interventricular septa! defects or iatrogenic interatrial septa! perforations (e.g., in patients who have undergone the trans-septal approach for ablation procedures) can become apparent only after LVAD activation.75 RV Function and TR Severity. The devdopment of RV failure after LVAD implantation increases the incidence of poor outcomes, including in-hospital and intensive care unit length of stays and end-organ failure. More importantly, it increases LVAD recipient risk of mortality six-fold. 1o7,to3 There are factors that predispose the LVAD recipient to increased possibility of RV failure. In particular, a functional LVAD

provides a normal cardiac output with a significant increase in the preload to the right heart. Patients with pre-LVAD placement RV dysfunction may be unable to tolerate such increase and can develop overt RV failure. Another factor that can determine the occurrence of RV failure after LVAD placement is due to ventricular interdependence. Thus, rapid reductions in LY end-diastolic pressure result in leftward displacement of the interventricular septum (Fig. 17-8, Video 6). This results in an alteration in RV size and geometry and can also increase the severity of TR If identified, the most effective short-term treatment is to reduce the LVAD speed, which subsequently increases the LY end-diastolic pressure and returns the septum to a more normal anatomical position. The possible acute consequences of RV failure include acute severe TR due to acute severe RV distention, increase in pulmonary pressures, and low LVAD flow secondary to low preload to the left heart. 101 In the long term, LVAD support can significantly improve RV function as evidenced by both hemodynamic and echocardiographic parameters, as well as reduction in TR90 As already discussed in the pre-LVAD implantation section of this chapter, the presence of TV annular dilatation and signiflcant TR should he assessed at the time of LVAD implantation. It is important to note again that patients with significant TR at the time of LVAD placement can benefit from a concomitant TV repair in order to reduce the incidence of post-LVAD implantation RV failure.109 Aortic Valve and AI. A normally functioning LVAD completdy unloads and decompresses the left heart, keeping the AV closed. This occurs because when the LY end-diastolic pressure is low enough, the retrograde aortic-to-LY pressure gradient is high.75 Conversely, if the LVAD provides only partial or variable support, the AV opens intermittently. Another consequence of LVAD support physiology is that after separation from CPB, the severity of preexisting AI worsens and the continuously closed AV is subject to high pressure, making it more susceptible to mechanical damage. As mentioned before, the severity of AI should be determined preoperativdy to allow for correction during LVAD placement, and if the severity of AI is worse than mild, the AV may need to be surgically addressed at this time. 110 Of particular importance, there are no speciflc guidelines to grade AI severity in continuousflow LVAD patients. The accepted guidelines for AI quantification are not validated in this setting. As mentioned before, the use of traditional echocardiographic parameters (e.g., AI jet width/LVOT diameter and vena contracta) underestimate AI severity in 33% of patients with continuous-flow LVAD.79·80 Importantly, AI grading does not predict devdopment of heart failure or need for AV closure or repair. 81 Several

450 I CHAPTER 17

FIGURE17-& Midesophageal four-chamber view demonstrating excessive left ventricular decompression In a patient under left ventricular assist device (LVAD) support. As a consequence. the interventricular septum is deviated toward the left, altering right ventricular performance and tricuspid valve competence. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

parameters that intend to quantify AI in this patient population have been described. Such parameters are peak to peak systolicid.iastolic (SID) velocity ratio and diastolic acceleration at the LVAD outflow cannula. These par.unetcrs provide better discrimination of AI severity and can be predictive of hospital admission due to heart f.Wure, need fur AV interventioM, urgent ttamplantation, and death.

InSow Cannula. Due to diverse LVAD designs, the inflow cannula can be placed in the pulmonary veins, I.A, RA. or LV apex. However, most commonly the inflow cannula is placed in the LV apc:x.60 Adequate positioning of the inflow cannula should be evaluated in at least the midesophageal four-chamber view and the midesophageal long·axis view, or any orthogonal views (Fig. 17·9, Video 7). When the LVAD inflow cannula is placed in the LV apex, it is often directed anteroscptally, aligned with the MV opening but away from the interventricular septum and lateral wall (Fig. 17-10, Videos 8 and 9). If the inflow cannula is misaligned, obstruction of blood flow into the LVAD can occur, causing clinical symptoms in the patient.101 Misalignment of the cannula with inflow obstruction is shown in Fig. 17-11 (Videos 10, 11, and 12). At time of implantation, if the cannula is misdirected, withdrawal and inferior displacement by the surgeon will generally rectify the situation. Color flow Doppler interrogation at the inflow cannula opening should demonstrate low-flow velocity and unidirectional and nonturbulent flow. In

addition, unobstructed flow should be demonstrated using continuous- or pulsed-wave Doppler of the inflow cannula with measured peak vdodties less than 1.5 m/s.':>9 The continuous- or pulsed-wave Doppler interrogation of the inflow cannula in a continuousflow LVAD shows a pulsatile waveform. synchronous with the patient's cc:hocardiogram (ECG) superim· posed on a baseline continuous-flow pattern throughout the device cycle, which is present even when i:he AV is closed (Fig. 17-12). Other findin~ suggesting inflow cannula malposition are abnormal highvelocity £low acrO&S the AV, abnormal hiJ!;;elocity flow within the LV cavity, ina~uate LV mpression, and frequent AV opening. The cannula position should be assessed again after chest closure to ensure that it remains correctly positioned. In the postoperative period, the 6nding of turbulent flow suggests inflow cannula obstruction, whereas reguwtant flow indicates LVAD pump malfunotion. Inflow cannula obsuuction can be continuous or intermittent, and can be caused by a variety of events, including misalignment, thrombus or pannus formation, or papillary muscle or subvalvular apparatus.64,I04,ll I Color flow Doppler across the i.nftow cannula opening demonstrating turbulent flow and continuous-wave Doppler demonstrating a peak velocity greater than 1.5 m/s are suggestive of cannula obsttuction.64•104•111- 113 Three-dimensional TEE image& have also been used to visualhe thrombus in the inflow cannula {Video 13).

ASSESSMENT OF MECHANICAL CIRCULATORY SUPPORT DEVICES I 451

A

B

Outflow Cannula. The outflow cannula of most LVADs is positioned in the ascending aorta. This cannula can be seen in the midesophagcil ascending a.ortl. short-axis or long-axis view at the level of the right pulmonary artery (Fig. 17-13.A. Video 14). In order to assess the blood Bow at the cannula anastomotic site. pulsed- or continuous-wave Doppler can be used. The

FIGURE 77-9. (A) Mldesophageal four-chamber color flow Doppler Interrogation allows confinnation of unobstructed flow across the left ventricle, from the mitral valve, and into the inflow cannula. The cannula is seen in proper position awayfrom the left ventricular walls. (B} Midesophageal twochamber color flow Doppler Interrogation allows conftrmatlon of unobstructed flow across the Inflow cannula. LVAD, left ventricular assist device.

normal peak velocity in the outflow graft should he less than 2.0 m/s 64.!04 The usual ffow pattern of an LVAD outflow graft is demonstrated in Fig. 17-13B. LVAD outflow cannula obstruction can alSo present with a decreased or absent Doppler signal at the anastomotic site in the aorta if the obstruction is located upstream from the anastomotic site (e.g., in the pump).102,1M

452 I CHAPTER 17

A

FIGURE 77-10. CA)Threedtmenslonal transesophageal echocardlographtc Imaging of a left ventrtcular assist device Inflow cannula.The cannula orifice can be seen directed toward the antero-septal wall in alignment with the direction of transmitral flow. The cannula is seen located at the apex; the inlet has no contact with the surrounding left ventricular walls. (B) Color flow Doppler interrogation allows conflrmatlon of unobsttucted flow across the left ventrlcle Into the Inflow cannula. LVAD, left ventrtcular assist B

Tbe outflow cannula. can be obstructed by thrombus or vegetations in the lwnen or by sternal compression at chest closure. Other complications of the outflow cannulac include perforation, kin~ or external compression and malposition.7S.l12,1l 4 Presence of air in the ascending aorta near the outflow cannula anastomosis suggests cannula pcrforation.64

device.

Left Ventricle. The evaluation fur regional wall motion abnormalities and determination of ejec-

tion fraction are unreliable with a functional LVAD because preload reduction alters normal contractility.64 Otherwise, post-LVAD implantation TEE examination must confirm adequate LV unloading. An adequately functioning LVAD reduces the LV

ASSESSMENT OF MECHANICAL CIRCULATORY SUPPORT DEVICES I 453

A

B

diameter. with the interventriculu septum .remaining in neuual position. As explained previoualy. a continuous leftward deviation of the interventticular septwn indicates excessive LV unloading, which will adversely affect RV function. Conversely, intcrventricular septum displacement toward the RV cavity is indicative of insufficient LV unloading. and increased LVAD pump speed is warranted.

FIGURE17-n. (A)Twodlmenslonal transesophageal echocardlographlc Imaging of a misaligned left ventricular assist device (LVAD) inflow cannula: Mldesophageal five-chamber view shows the inlet of the inflow cannula directed against the interventricular septum. (8) Midesophageal aortic valve long-axis view confirms that the inlet of the cannula is positioned against the lnterventrlcular septum.

Postoperative TEE Examination for LVAD Malfunction TEE can be used to evaluate patients with altered LVAD function in order to confirm a clinical diagnosis or. more frequently, to provide an accurate diagnosis in the setting of a difficult clinical scenario, as well as to assist in appropriate management. The potential

454 I CHAPTER 17

FIGURE J7- 12. Pulsed-wave Doppler interrogation of the left ventricular assist device (LVAD) inflow reveals the pattern typical of a normally functioning device. The waveform shows lowveloctty laminar pulsatlle flow (conespondlng to flow across the device due to the native left ventricular contractions) superimposed on the flow produced by a continuous-flow device (LV, left ventricle).

A

8

FIGURE 17-13. UU Mldesophageal ascending aorta long-axis color flow Doppler Interrogation of a left ventrlcular outflow cannula In a patient with a normally functioning device. (8) Continuous-wave Doppler Interrogation of a left ventricular assist device (LVAD) outflow waveform tn a patient with a nonnally functioning device displays a pul,satlle waveform (corresponding to flow aaoss the pump due to the native left ventricular contractions) that Is superimposed to the characteristic wavefonn of a continuous-flow device. The nonnal peak flow veloctty Is 1.0 to 2.0 rn/s.

clinical situations where TEE examination can be useful to determine the cawe of LVAD malfunction are summarized in Table 17-4. Pump Failure. The possible causes of LVAD pump f.ailure are pump thrombosis or mechanical malfunction. The clinical pictwe is characte.rized by decreased

LVAD flow and high LVAD power utilization. The TEE examination demonstrates LV distension/lack of proper unloading., rightward deviation of the interventricular septum, functional MR. AV opening during each caidiac cycle. spontaneous echocardiographic contrast in the LVILA, and regurgitant flow through

ASSESSMENT OF MECHANICAL CIRCULATORY SUPPORT DEVICES I 455

Table 17-4. Postoperative transesophageal echocardlographlc examination for left ventricular assist device malfunction 1. Pump fa!lure 2. Cardlactampcnade

3. Right ventricular failure/pulmonary embolism 4. Hypovolemia

5. Presence of severe aortic insufficiency 6. Inflow cannula obstruction 7. Outflow cannula obstruction

both cannulas.75 A study by Fine et al characterized the presence of reduced diastolic flow velocity and increased systolic/diastolic (SID) flow vdocity ratio as echocardiographic pazameters capable of diagnosing LVAD dysfunction due to suspected pump thrombosis better than other indicators.115 Cardiac Tamponade. The clinical diagnosis of cardiac wnpon.ade after LVAD placement is difficult. Most commonly the fluid collections may be loculated and isolated to discrete regions in the heart, making them difficult to identify. Locations of sw:h .regional tamponade that are particularly problematic to identify are the posterior chambers, posterior or anterior LA, or lateral RA. Normal LVAD physiology, which reduces left heart filling pressures, also confounds this asscs:sment.101 TEE examination is cs.scntial to provide diagnosis of cardiac tamponade in an accurate and timely fuhion (Fig. 17-14).

FIGURE I 7-14. Transgastric midpapillary short-axis

view demonstrating large anterior and posterior pericardia! effusions (marked with *) causing significant extrinsic compression of both right and left ventricular cavities RV, right ventricle; LV, left ventricle.

Hypovolcmia. The diagnosis of hypovolemia is primarily a clinical one. However, the combination of low LVAD pump flow with nonnal LVAD power utilization and the presence of low filling pressures and hypotension constitute a highly suggestive diagnosis. TEE examination will demonstrate the presence of small RV and LV cavities, helping to rule out other potential diffcrential diagnoses (Fig. 17-15, Videos 15 and 16). Pulmonary Embolism. Patients with pulmonary embolism share the same TEE findings as RV failure patients, which include RV dilat2tion, significant RV dysfunction, severe TR, and decreased left heart filling or prdoad. However, patients with pulmonary embolism can have elevated pulmonary artery pressures, whereas those with isolated severe RV failure may have low pulmonary artery pressures. It is important to note that echocardiography currently provides only indirect evidence of pulmonary embolism. However, if there is suspicion of a central or saddle pulmonary embolus, TEE examination can provide direct visualization ofsuch thrombus.101

RIGHT VENTRICULAR ASSIST DEVICE Right hean failure is less common than left bean failure. This f.act m.ab:s the use of RVADs less frequent than LVADs. In &.et. at this time RVADs arc available only as temporary mechanical support modalities. In many cases, RVADs are used in combination with a device for support of the left heart. The indications for RVAD implantation include RV failure after LVAD implantation or heart transplantation, RV failure due to pulmonary hypertension and cecum:nt pulmonary arterial embolism, anhythmogenic RV card.iomyopatliy, and large RV myocardial infucti.ons.60,ll6 R4tbt heart failure after cardiac surgery is more frequently. caused by poor RV myocardial. protection dwing CPB or right coronary artery embolism. In this case most RVADs are placed due to failure to separate from CPB.117-119 The RVAD inflow cannula is usually placed at the level of the RA appendage but it can also be placed in the RV outflow tract. This cannula can be easily visualiud wing the midesophageal bicaval view. The RVAD outtlow cannula is most commonly attached to the main pulmonary artery (PA). It also can be sewn to the right PA or placed across the RV through the pulmonic valve into the main PA. This cannula can be seen in the upper esophageal ascending aortic shon·axis view or occasionally in the midcsophageal RV inflow-outflow view. Color flow and pulsed-wave Doppler cx:amination should reveal laminar, and unidirectional low velocity flow, respectively.60.64 The most common loca· tion and typical appearance of both inflow and outflow RVAD cannulae are depicted in Fig. 17-16 (Video 17).

456 I CHAPTER 17

A

FIGURE'l7-1S. (A)Two-

8

BIVENTRICULARVENTRICULAR ASSIST DEVICES Biventricular mechanical replacement may be indicated for a variety of conditions, including severe biventricular dysfunction not remedied by LV support alone, severe diastolic dysfunction from restrictive or

dlmenslonal transesophageal echocardlographlc Imaging of a patient with left ventricular assist device (LVAD) and severe hypovolemia: 'The transgastric midpapillary short-axis view demonstrates the left ventricle (LV) cavity collapsed around the Inflow cannula due to slgnlflcant decrease In LV preload. (8) 'The transgastrtc mldpaplllary longaxis view In the same patient depicted In panel Ashows the Inflow cannula Inlet obstructed by the left ventricular anteroseptal wall as a consequence of severe hypovolemia. infiltrative myopathy, and bivcntricular dysfunction with persistent ventricular dysrhythmias. Another potential indication for the total artincial heart product is postinfuct VSD and biventricular failure. In these instances, several VADs can be applied in a biventricular mode. These include the Tboratec PVAD, a paracorporeal VAD that can be configured

ASSESSMENT OF MECHANICAL CIRCULATORY SUPPORT DEVICES I 457

A

FIGURE 17-16. (A) Mldesophageal bicaval colorflow Doppler interrogation of a right ventricular assist device (RVAD) inflow cannula at the level of the right atrial appendage. The color flow Doppler pattern visualized is characteristic. (8) Upper-esophageal orthogonal views with color flow Doppler of a right ventricular assist device (RVAD) outflow cannula In the right pulmonary artery. SVC, superior vena cava.

8

to

replace both the RV and the LV. In addition, newer

continuous Row implantable devices can be used for either biventricular support or as a total artificial heart configuration. The most popular product currently

for this application is the HeanWare HVAD ventticular assist device. There have been numerous cases of biventricular application for the HVAD. The HVAD

can be used as a bivcntric:ular assist device (BiVADs) or as a total artificial heart replacement in instances where the ventticular chambers are removed and the devices drain the atrial chambers directly. Paramount in su.ccessfuJ. biventticular mechanical replacement is the process of balancing the right and left ventticular circulations. All currently utilized

458 I CHAPTER 17 VADs have a variety of settings which can be altered to provide increased or decreased mechanical suppon. Excessive support of the RV can lead to a variety of pulmonary complications, including pulmonary edema and hemoptysis caused by pulmonary circulation overload due to excessive flow. On the other hand, inadequate RV mechanical support can lead to underfllling of the left-sided mechanical device and subsequent reduced systemic output and reduced end-organ perfusion. Therefore, proper balancing of the right and left ventricular mechanical replacement is critical. TEE, in addition to previously described utilizations, can be critical in assessing the degree of right and left heart unloading. For patients supported with biventricular assist devices, TEE can examine the relative right and left ventricular chamber size. In addition, the degree of ventricular unloading can be evaluated with TEE by assessing the degree of AV and pulmonic valve opening, respectively. Finally, interatrial and interventricular septa! position can be gauged by TEE to provide further evaluation of the relative degrees of right- and left-sided unloading. Scenarios where one side is maximally unloaded while the other side remains incompletely unloaded should be avoided. TEE examination can be particularly valuable for these patients since invasive catheter monitoring is often difficult in BiVAD patients. Evidence of disparity with regard to unloading should lead to pump speed or other setting changes to rectify the situation. Finally, for BiVAD support, as is the case for isolated RVAD or LVAD, TEE can be valuable in determining the proper inflow cannula position.

TEE Evaluation for the Total Artificial Heart Echocardiography of the TAH requires a detailed knowledge of the device and its components, as well as an understanding of the implantation procedure. The SynCardia-TAH consists of two pneumatic pumping chambers representing the left and right ventricles. Each chamber has an inlet valve representing the mitral and tricuspid valve, respectively, and an outlet valve representing the aortic and pulmonary valves, respectively. The inlet and outlet valves are MedtronicHall (Medtronic-Hall, Medtronic, Minneapolis, MN) single tilting disk valve prostheses. The inlet valves of the pneumatic chambers are sutured to a rim of ventricular myocardium close to the atrioventricular grooves, and the outlet valves are connected to the native aorta and pulmonary artery. 120 Before placement of the TAH, intraoperative TEE examination should evaluate the (1) presence of defects across the interatrial septum such as a PFO, which could lead to hypoxemia due to shunting of

venous blood into the systemic circulation or paradoxical systemic embolization; (2) presence of thrombi in the LA or RA; (3) presence of pulmonary venous return abnormality; and (4) size of inferior vena cava and superior vena cava to establish a baseline size for comparison after placement of the device.120,121 After implantation of the device, electrocardiographic gating during examination cannot be used for image acquisition or three-dimensional gated full-volume acquisition since the ventricles have been removed and no R wave is generated. The pneumatic pumping chambers will generate significant acoustic shadowing precluding imaging at the transgastric level; however, retention of the native atria allows imaging at the mid- and upper esophageal level. Before separation from CPB, adequate de-airing should be assessed by TEE. Generally, there is significant acoustic shadowing from the inlet and outlet valves, from the pumping chambers, and from the compressed air used to drive the pumping chambers. Therefore, adequate de-airing is evaluated by assessment of air in the atria, pulmonary veins, or pulmonary artery and aorta.121 After device placement a comprehensive evaluation of the inlet and outlet valves should be performed. The prosthetic valves should be evaluated by color flow Doppler and continuous-wave Doppler. The inlet valves can be evaluated in the midesophageal views generally used for evaluation of prosthetic valves in the mitral and tricuspid position. The outlet valve in the "pulmonary position" can be evaluated in the midesophageal RV inflow-outflow view as well as upper esophageal aortic arch short-axis view for Doppler measurement of transvalvular gradients. Measurement of the Doppler gradients across the outlet valve in the "aortic" position will be challenging due to limited imaging at the transgastric level; however, the valve can be assessed for adequate functioning by twodimensional imaging and color flow Doppler at the midesophageal level. The connections of the inferior and superior venae cavae to the RA and of the pulmonary veins to the LA should be evaluated for kinking, obstruction, and compression by color flow Doppler and pulsed-wave Doppler after device implantation and after chest closure. Similar evaluation of the aortic and pulmonary connections should be made, although they are less likely to kink.120 Before chest closure and in the immediate postoperative period the pericardia! space should be evaluated for the presence of effusion or thrombus, especially in the presence of low flow generated by the device. While the rigid pumping chambers are not susceptible to compression, decreased device output can still occur due to compression and tamponade of the atria, pulmonary veins, and venae cavae.

ASSESSMENT OF MECHANICAL CIRCULATORY SUPPORT DEVICES I 459

FUTURE DIRECTIONS

b. Post-CPB increase in pulmonary vascular resis-

Transesophageal echocardiography has an established role as a monitoring modality for the patient with advanced heart failure. It is especially instrumental in assisting safe placement and use of mechanical circulatory support devices in the acute settings of the operating room and the intensive care unit. The use of TEE has also become essential in the early detection and troubleshooting of patient- or device-related complications. The significance and application of echocardiography in general, and TEE in particular, are evolving as rapidly as the advances in the field of mechanical circulatory support. Echocardiographic data are effectively used not only as an integral part of risk stratification for proper patient and device selection, but also for outcome prediction when clinically derived data are not conclusive. For example, in patients with ECMO support, there is recent evidence that echocardiographically derived performance data could be used to evaluate the possibility of successful decannulation and its tirning. 53 •122 Similarly, LVAD support can be optimized by the use of specific echocardiographic protocols that have the potential to minimize future complications. The application of such protocols and their derived data can promote early detection of significant and life-threatening complications, potentially altering outcome as in the early diagnosis of LVAD pump thrombosis. Notably, the Columbia ramp study showed the ability of an echocardiographically guided protocol that combines progressive increments of pump speed with lactate dehydrogenase blood values to provide early identification of LVAD pump thromhosis. 123•124 Thus, TEE has a role not just in intraoperative monitoring hut also in outcome prediction and long-term management of patients with MCSDs.

c. Increase in PA pressure and RV dysfunction due the systemic inflammatory response d. Leftward shift of the interventricular septum caused by LV unloading e. All of the above

REVIEW QUESTIONS 1. The most probable mechanism implicated in the development of significant AI after institution of full LVAD support is: a. Presence of endocarditis b. Aortic dissection c. Exposure of closed valve to continuous systolic rather than diastolic pressure d. Aortic leaflet perforation e. Aortic leaflet prolapse 2. Which factors are associated with possible worsening in TR severity after LVAD implantation? a. Increased preload to the RV due to an increased in left-sided cardiac output

tance

3. What is the average peak filling velocity in the inflow cannula of an axial flow device? a. 2.3 m/s e. Inadequate LY cavity decompression 20. Which of the following statements regarding LVAD inflow cannula obstruction is false? a. It can occur intermittently. b. There is usually evidence of turbulent flow upon CFD examination of the inflow cannula inlet. c. It can be assessed in the midesophageal long-axis view. d. Peale blood flow velocity at the inflow cannula inlet is 1 to 2 m/s. 21. Which of the following findings during post-LVAD implantation transesophageal echocardiographic examination should prompt considering further intervention? Please select all that apply. a. Evidence of PFO with left-to-right intracardiac shunt b. Evidence of PFO with right-to-left intracardiac shunt c. Presence of continuous mild AI d. Presence of continuous moderate AI e. Absence ofAV opening evident upon 20 examination f. Intermittent AV opening evident upon 20 examination 22. Regarding the transesophageal echocardiographic evaluation of the LVAD recipient patient, what the anatomical locations most likely to be affected by thrombus formation? Please select all that apply. a. Left ventricular apex b. Right ventricle c. Right atrial appendage d. Main pulmonary artery e. Left atrial appendage 23. Which anatomical locations are most commonly affected by the presence of intracardiac air during LVAD implantation? Please select all that apply. a. LY apex around LVAD inflow cannula b. Right ventricle

c. Right atrium d. Left atrium e. Left atrial appendage 24. What are the most clinically relevant findings during immediate post-LVAD implantation TEE examination? Please select all that apply. a. Evidence of PFO upon CFD examination b. Presence of air in the left ventricle c. Evidence of moderate-to-severe mitral regurgitation d. Evidence of moderate aortic insufficiency e. Evidence of left atrial appendage thrombus f. Evidence of moderate-to-severe tricuspid regurgitation g. Presence of air in the pulmonary artery 25. Regarding RV function and performance in LVAD recipient patients, which of the following statement are true? Please select all that apply. a. Long-term LVAD support can improve RV function. b. After LVAD implantation, RV preload increases. c. After LVAD implantation, pulmonary vascular resistance increases. d. Development of RV failure after LVAD implantation increases recipient mortality. e. Rapid reduction in LY end-diastolic pressure after LVAD implantation can result in increased RV dysfunction. £ Development of RV dysfunction after LVAD implantation is uncommon. 26. Which one of the following transesophageal echocardiographic views is most appropriate to perform TV spectral Doppler assessment? a. Midesophageal four-chamber view b. Midesophageal RV inflow-outflow view c. Midesophageal modified bicaval view d. Transgastric RV inflow-outflow view e. Transgastric RV basal view 27. Regarding the presence ofTR in LVAD recipients, which of the following statements are true? Please select all that apply a. Presence ofTR is associated with worse outcomes. b. TR is present in 15% of patients considered for LVAD implantation. c. Pre-implantation assessment of hepatic vein flow is not necessary to determine TR severity. d. Leftward displacement of the interventricular septum after LVAD implantation decreases TR severity. e. Long-term LVAD support can result in decreased TR severity.

462 I CHAPTER 17 28. Regarding evaluation of AV in the LVAD recipient patient, what is the MOST clinically significant finding during transesophageal examination? a. Pre-implantation presence of mild AS b. Pre-implantation presence of mild AI c. Pre-implantation presence of moderate-to-severe AI d. Post-implantation presence of mild AI e. Post-implantation presence of mild AS. 29. Which of the following conditions MOST LIKELY requires intervention prior to (or during) LVAD implantation? Please select all that apply. a. MildTR b. Moderate TR c. Severe MR d. Severe MS e. MildAI f. Moderate AI 30. Which of the following is most likely seen in a patient with pump thrombosis? a. Aortic valve not opening b. Inflow cannula velocities > 1.5 m/s c. Outflow cannula velocities >2 m/s d. Severe MR e. Leftward shift of the interventricular septum

REFERENCES l. Writing Committee M, Yancy CW, Jessup M, et al. 2013 ACCF/AHA guiddine for the management of heart failure: a report of the American College of Cardiology Foundation/ American Heart Association Task Force on practice guiddines. Cirru/4mn. 2013;128(16):e240-327. 2. Patel CB, Alexander KM, Rogers JG. Mechanical circulatory support for advanced heart failure. Ctm Trtat Op#om CarJWIJfl!C Med. 2010;12(6):549-565. 3. Trost JC, Hillis LD. Intra-aortic balloon counterpulsation. Am ] UirJWL 2006;97(9):1391-1398. 4. Stub D, Bernard S, Pellegrino V, et al. Refractory cardiac arrest treated with mechanical CPR. hypothermia, ECMO and early repcrfusion (the CHEER trial). Resruritation. 2015;86: 88-94. 5. Abram& D, Brodie D. Novel Uses ofExtracorporeal Membrane Oxygenation in Adulu. C/in Chest Med. 2015;36(3):373-384. 6. Garatti A, Colombo T, Russo C, et al. Different applications for left venuicular mechanical support with the Impdla Recover 100 microaxial blood pump. J Heart Lung Transplant. 2005;24(4):481-485. 7. Reesink KD, Dekker AL, Van Ommen V, et al. Miniature intracardiac assist device provides more effective cardiac unloading and circulatory support during severe left heart failure than inuaaortic balloon pumping. Chen. 2004;126(3): 896-902. 8. Ouwened DM, Eriksen E, Sjauw KD, et al. Percutaneous mechanical circulatory support versus intra-aortic balloon pump in cardiogenic shock after acute myocardial infarction. f Am Coll Cardiol. 2017;69(3):278-287.

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ASSESSMENT OF MECHANICAL CIRCULATORY SUPPORT DEVICES I 463 26. Kirklin JK, N aftd DC, Kormos RL, et al. The Founh INTERMACS Annual Report: 4,000 implana and counting. J Heart Lung Transplant. 2012;31(2):117-126. 27. Griffith BP, Kormos RL, Borovel7. HS, et al. HeartMate II left ventricular assist system: from concept to first clinical use. Ann ThoraJ: Surg. 2001;71(3 suppl):S116-120; discussion Sl 14-116. 28. Miller LW, Pagani FD, Russell SD, et al. Use of a continuousftow device in patients awaiting hean transplantation. New Engl] Med. 2007;357(9):885-896. 29. Thoratec. HeartMate II Left Ventricular Assist Device (LVAD) Fact Sheet. 2013. Available at http://www.thoratcc.com/down loads/ HcartMatc II Fact Shcct-Bl0()..0713.pdf. .Accessed November 1, 2013. 30. Frazier OH, Gemmato C, Myers 1J, et al. Initial clinical experience with the HcartMatc II axial-Row left ventricular assist device. Tex Heat Inst]. 2007;34(3):275-281. 31. HeanWarc. HeanWarc Ventricular Assist System Instructions for Use. 2012. Available at http://www.hcartware.com/ sites/de&.ult/files/uploads/docs/ifuOOOOl_rcv_lS.pd£ Accessed November l, 2013. 32. Larose JA, Tamez D, Ashenuga M, et al. Design concepts and principle of operation of the HcartWarc ventricular assist system. ASAIO ]. 2010;56(4):285-289. 33. Necuka I, Sood P, Pya Y, et al. Fully magnetically levitated left ventricular assist system for treating advanced HF: a multicenter study. j Am Colt Card;qL 2015;66(23) :2579-2589. 34. Aaronson KD, Slaughter MS, Miller LW, et al. Use of an intrapericardial, continuous-flow, centrifugal pump in patients awaiting bean transplantation. Ciw:ulanon. 2012;125(25): 3191-3200. 35. Rogers JG, Pagani FD, Tatooles AJ, et al. lntrapcricardial Left Ventricular Assist Device for Advanced Hean Failure. New Engl] Med. 2017;376(5):451-460. 36. Slaughter MS, Pagani FD, McGee EC, et al. HeanWarc ventricular assist system for bridge to transplant: combined resula of the bridge to transplant and continued access protocol trial. J Heart Lung Transplant. 2013;32(7):675--683. 37. Mchra MR. Naka Y, Urid N, et al. A fully magnetically levitated circulatory pump for advanced hcan failure. New Engl] Med. 2017;376(5):440--450. 38. Frazier OH, Myers 1J, Jarvik RI(, et al. Research and dcvdopment of an implantable, axial-flow left ventricular assist device: the Jarvik 2000 Heart. Ann ThflTlll: Surg. 2001;71 (3 suppl):Sl25-132; discussion S144-126. 39. Villa CR. Morales DLS. The total artiflcial heart in end-stage congenital heart disease. Front PhyswL 2017;8: 131. 40. Sale SM, Smcdira NG. Total artificial heart. Best Pract Rn Clin A.naesthtsioL 2012;26(2):147-165. 41. SynCardia Systems, Inc. Total Artificial Hean Faces. 2015. Available at http://www.syncardia.com/total-facrs/total-artifl cial-hean-fu:ts.hcml. Accessed November, 2015. 42. Shekar K, Gregory SD, Fraser JF. Mechanical circulatory support in the new era: an ovenricw. Crit Care. 2016;20:66. 43. de Waha S, Desch S, Eitd I, et al. Intra-aortic balloon counterpulsation - basic principles and clinical evidence. Vase Pharmacol. 2014;60(2):52-56. 44. Kucukcr A, Cetin L, Kucukcr SA, et al. Single-centre experience with pcriopcrativc use of intraaortic balloon pump in cardiac surgery. Heart Lung Circ. 2014;23(5):475-481.

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464 I CHAPTER 17 62. Morgan JA, Brewer RJ, Nemeh Hw, et al. Left ventricular reverse remodding with a continuous flow left ventricular assist device measured by left ventricular end-diastolic dimensions and severity of mittal regurgitation. ASAIO ]. 2012;58(6): 574-577. 63. Fddman D, Pamboukian SY, Teuteberg JJ, et al. The 2013 International Society for Heart and Lung Transplantation Guidelines for mechanical circulatory support: CRCUtive summary.] Heart Lung Transp/ant. 2013;32(2):157-187. 64. Chumnanvej S, Wood MJ, MacGillivray TE, et al. Perioperative echocardiographic examination for ventricular assist device implantation. AnesthAnidg. 2007;105(3):583--601. 65. Rao V, Slater JP. Edwards NM, et al. Surgical management of valvular disease in patients requiring left ventricular assist device support.Ann ThoTllJ:Surg. 2001;71(5):1448-1453. 66. Cowger J, Pagani FD, Haft Jw. et al. The development of aortic insufficiency in left ventricular assist device-supported patients. Circulation Heart Fail. 2010;3(6):668-674. 67. Pak SW, Urid N, Takayama H, et al. Prevalence of de novo aortic insufficiency during long-term support with left ventricular assi&t devices.] Heart Lung Transplant. 2010;29(10):1172-1176. 68. Soleimani B, Haouzi A, Manoskey A, et al. Devdopment of aortic insufficiency in patients supported with continuous flow left ventricular assist devices. ASAIO ]. 2012;58(4):326-329. 69. John R, Mantz K, Eckman P, et al. Aortic valve pathophysiology during left ventricular assi&t device support. J Heart Lung TTlllUplant. 2010;29(12):1321-1329. 70. Conndly JH, Abrams J, Klima T, et al. Acquired commissural fusion of aortic valves in patients with left ventricular assist devices.] Heart Lung Transplant. 2003;22(12):1291-1295. 71. Rajagopal K, Daneshmand MA, Patel CB, et al. Natural history and clinical effect of aortic valve regurgitation after left ventricular assist device implantation. J 'ThoTllf: CzrdimJasc Surg. 2013;145(5): 1373-1379. 72. Savage EB, d'Amato TA, Magovern JA. Aortic valve patch closure: an alternative to ttplacement with HeartMate LYAS insertion. Eur] Gm/;othorac Surg. 1999;16(3):359-361. 73. Bryant AS, Holman WL, Nanda NC, et al. Native aortic valve insufficiency in patients with left ventricular assist devices. Ann ThoTllf: Su1f:. 2006;8 l (2):e6-8. 74. Adamson RM, Dcmbitsk:y WP, Baradarian S, et al. Aortic valve closure associated with HeartMatc left ventricular device support: technical considerations and long-term results. ] Heart Lung Transplant. 2011;30(5):576-582. 75. Ammar KA, Umland MM, Kramer C, et al. The ABCs of left ventricular assist device echocardiography: a systematic approach. Eur Hem] Cmiiovmc Imaging. 2012;13(11):885-899. 76. Santini F, Forni A, Dandale R, et al. First successful management of aortic valve insufficiency associated with HeartMate II left ventricular assist device support by transfemoral CoreValve implantation: the Columbus's egg? JACC Gm/;olJIZJ lnterv. 2012;5(1):114-115. 77. D'Ancona G, Pasic M, Buz S, et al. TAVl for pure aortic valve insufficiency in a patient with a left ventricular assist device. Ann Thorac Surg. 2012;93(4):e89-91. 78. Parikh KS, Mehrotra AK, Russo MJ, et al. Percutaneous uanscathetcr aortic valve closure successfully treats left ventricular assist device-associated aortic insufficiency and improves cardiac hcmodynamics. ]ACC CartJUwasc lnterv. 2013;6{1): 84-89.

79. Grinscein J, Kruse E, Sayer G, et al. Accurate quantiflcation methods for aortic insufficiency severity in patients with LVAD: role of diastolic flaw acceleration and systolic-todiastolic peak velocity ratio of outflow cannula. J Am Coll Car-

diol CardimJasc Imaging.

2016;9(6):641~51.

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widergoing implantation of a continuous-flow left ventricular device.]ThortU Ctml;ovascSurg. 2012;144(5):1217-1221. 110. Horton SC, Khodavenl.ian R, Powers A, et al. Left ventricular assist device malfunction: a systematic approach to diagnosis. ] Am Coll Gm/;o/. 2004;43(9):1574-1583.

97. Rudski LG, Lai WW, Afilalo J, et al. Guidelines for the cchocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography endorsed by the European Association of Echocardiography, a registered branch of the European Society of Cardiology, and the Canadian Society of Echocardiography. ] Am Sac EchoazwJiogr. 2010;23(7):685-713; quiz 786-688.

111. Szymanski P, Religa G, Klisiewicz A, et al. Diagnosis ofbiventricular assist device inflow cannula obstruction. Echocardiogrttphy. 2007;24(4):420-424.

98. Lytrivi ID, Lai WW, Ko HH, et al. Color Doppler tissue imaging for evaluation of right ventricular systolic function in patients with congcnical heart disease. ] Am Soc Echoctm;/;ogr. 2005;18(10):1099-1104. 99. Rcilly MP, Wiegers SE, Cucchiara AJ, et al. Frequency, risk factors, and clinical outcomes of left venuicular assist device-associated ventricular thrombus. Am ] Cardiol. 2000;86(10):1156-1159, Al 110. 100. Miyake Y, Sugioka K, Bussey CD, et al. Left ventricular mobile thrombus a.ssociaced with ventricular assist device: diagnosis by transesophageal echocardiography. Circ]. 2004;68(4):383-384. 101. Scalia GM, McCarthy PM, Sawge RM, et al. Clinical utility of echocardiography in the management of implantable ventricular assist devices. JAm Soc F.choazrd;ogr. 2000; 13(8):754-763. 102. Hamilton A, Huang SL, Warnick D, et al. Left venuicular thrombus enhancement after intravenous injection of echogenic immwioliposomes: studies in a new aperimental modd. Circulation. 2002; 105 (23) :2772-2778. 103. Orihashi K. Matsuura Y, Hamanaka Y, et al. Retained intracardiac air in open heart operations examined by transcsophageal cchocardiography.Ann ThortU Surg. 1993;55(6):1467-1471. 104. Catena E, Milazzo F, Montorsi E, et al. Left ventricular support by axial Row pump: the cchocardiographic approach to device malfunction.]Am SocEchoazrdiogr. 2005;18(12):1422. 105. Liao KK, Miller L, Toher C, et al. Tuning of uansesophagcal cchocardiography in diagnosing patent foramen ovale in patients supported with left ventricular assist device. Ann Tho1"11c S14rg. 2003;75(5):1624-1626. 106. Loyalka P, Iddchik GM, Kar B. Percutaneous left ventricular assist device complicated by a patent foramen ovale: importance of identification and management. Catheter Carriiwmc lntmJ. 2007;70(3):383-386. 107. Matthews JC, Koelling TM, Pagani FD, ec al. The right ventricular failure risk score a pre-operative tool for assessing the risk of right ventricular failure in left ventricular assist device candidates.]Am CoU CarJkJL 2008;51(22):2163-2172. 108. Dang NC, Topkara VK. Mercando M, et al. Right heart failure after left ventricular assist device implantation in patients with chronic congestive heart failure.] Heart Lung Transplant. 2006;25(1):1-6. 109. Piacentino V3rd, Ganapathi AM, Stafford-Smith M, et al. Utility of concomitant tricuspid valve procedures fur patients

112. Horton SC, Khodavenl.ian R. Chatelain P, et al. Left ventricular assist device malfunction: an approach to diagnosis by cchocardiography. J Am Coll CardioL 2005;45(9):1435-1440. 113. Pu M, Stephenson ERJr., Davidson WRJr., et al. An wiexpected surgical complication of ventricular assist device implantation identified by transesophageal echocardiography: a case report.] Am Sac &hor:arJ;qgr. 2003;16(11):1194-1197. 114. Weiael N, Puskas F, Qeveland J, et al. Left ventricular assist device oucflow cannula ob.muction by the rare environmental fungw Mycdiophthora thermophila. Anath Ana{f. 2009; 108(1):73-75. 115. Fine NM, Topilsky Y, Oh JK, et al. Role of cchocardiography in patients with intravascular hernolysis due to suspected continuous-flow LVAO thrombosis. ]ACC Cardiovasc Imaging. 2013;6(11):1129-1140. 116. Christiansen S, Klocke A, Autschbach R. Past, present, and future of long-term mechanical cardiac suppon in adults. ] CarJ Surg. 2008;23(6):664-676. 117. Ochiai Y, McCarthy PM, Smedira NG, et al. Predictors of seven: right ventricular failure after implantable left ventricular assist device insertion: analysis of 245 patients. Circulation. 2002;106(12 suppl 1):1198-202. 118. Osaki S, Edwards NM, Johnson MR, et al. A novd use of the implantable ventricular assist device fur isolated right heart failure. lntmzct Cardiouasc ThOt"ill Surg. 2008;7(4):651-653. 119. Moazami N, Pasque MK, Moon MR, et al. Mechanical support for isolated right ventricular failure in patients after cardiotomy. J Heart Lung Trrmsplant. 2004;23(12): 1371-1375. 120. Fine NM, Gopalan RS, Arabia FA, et al. Intraoperative transcsophageal cchocardiographic guidance of total artificial heart implantation.] Heart Lung Transplant. 2014;33(4):454-457. 121. Mizuguchi KA, Padera RFJr., KowalC"L)'kA. et al. Transesophagcal cchocardiography imaging of the total artificial heart. Anerth Ana{f. 2013;117(4):780-784. 122. Firstenberg MS, Orsinelli DA. ECMO and ECHO: the evolving role of quantitative cchocardiography in the management of patients requiring extracorporcal membrane oxygenation.] Am Soc EchoctZrdi4gr. 2012;25(6):641-643. 123. Rogers JG, Milano CA. Ramping up evidence-based ventricular assist device care.] Am Coll CardioL 2012;60(18):1776-

lm. 124. Urie! N, Morrison KA, Garan AR, et al. Development of a novel cchocardiography ramp test for speed optimization and diagnosis of device thrombosis in continuous-Row left ventricular assist devices: the Columbia ramp study. ] Am Coll CardioL 2012;60(18):1764-1775.

Thoracic Transplantation Sharon McCartney, Susan M. Martinel/ii and Priya A. Kumar

INTRODUCTION Orthotopic organ transplantation for end-stage heart and lung failure is a modality of treatment that is increasingly applied. With experience spanning multiple decades, we have now expanded thoracic transplantation to include higher-risk recipients and donors. Currently, over 4000 heart transplants, over 3000 lung transplants, and between 60 and 100 combined heartlung transplants are performed annually worldwide. l.2 Transesophageal echocardiography (TEE) plays an essential role in the perioperative care of patients presenting for thoracic organ transplantation. In heart transplantation, TEE assists in the donor organ selection process, perioperative management, and post-transplant evaluation of recipients. Patients undergoing lung transplantation may demonstrate sequelae of respiratory failure, most commonly pulmonary hypertension and right ventricular dysfunction. TEE is utili7.ed during lung transplantation to assess preprocedure cardiac function, assess intraopera~ve ~emo­ dynamic changes, and evaluate the anastomotic sites.

HEART TRANSPLANTATION As a result of continued organ shortages, the rate of heart transplantation has remained relatively constant over the past decade.3 The most common indications for heart transplantation include nonischemic (54%) and ischemic cardiomyopathy (37%). 1 Transplantation in high-risk recipients with comorbid diseases such as diabetes with end-organ dysfunction, renal dysfunction, and advanced age (>65 years old) is common. Median survival after heart transplantation is 11 years, although recipients that survive the first year posttransplant have a median survival of 13 years. 1

Surgical Technique In order to accurately assess cardiac allograft anatomy and physiology, the echocardiographer needs to understand the surgical procedure and appreciate the changes that normally occur in the transplanted heart. Two techniques are typically used for heart transplantation, biatrial or bicaval, named according to the location of the anastomoses. The standard, or biatrial, technique, originally described by Lower and Shumway,4 was the

primary method for nearly 30 years. In this technique, the recipient's right atrium (RA) is divided through the body, leaving its posterior aspect in situ. Additionally, most of the native left atrium (LA) and interatrial septum are left in situ. The inferior vena cava (NC), superior vena cava (SVC), and pulmonary venous inflow tracts are left undisturbed. In the donor heart, an LA cuff is created by incising around the pulmonary vein orifices, whereas the RA cuff is created by incising through the NC orifice and extending the incision up toward the base of the RA appendage. The donor RA and LA cuffs are then attached to the recipient's RA and LA, respectively. In the bicaval technique, the recipient's entire RA is removed by dividing both the NC and SVC proximal to the RA, creating NC and SVC cuffs. The posterior aspect of the LA is left in situ, leaving the native pulmonary vein inflow sites intact. The donor heart is then attached via the NC and SVC cuffs and LA suture line. For both biatrial and bicaval techniques, the donor's pulmonary artery and ascending aorta are anastomosed similarly. The bicaval technique was first described in the 1990s5 and has since become the method of choice. There are multiple advantages with this technique. The geometry and function of the atria are better preserved as compared to the biatrial technique.6·~ A well-functioning LA leads to less thrombus formation in the LA appendage8•9 and to improved left ventricular filling and thus improved cardiac output (C0). 10 Less disruption in the geometry of the atrioventricular valves results in reduced valvular regurgitation. There are fewer conduction abnormalities, an increased freedom from permanent pacemaker implantation, and . . mona1·1ty. 11 ' 12 an overall decrease .m penoperat1ve Although the bicaval technique has shown superio.rity to the biatrial technique in short-term outcomes, it is . l ong-term outcomes. 12 equ1·va1ent m

The Role of TEE in Heart Transplantation The application of TEE to the perioperative care of heart transplantation can be divided into five categories: 1. Cardiac donor screening 2. lntraoperative monitoring in the pretransplant period

THORACIC TRANSPLANTATION I 46 7 3. Intraoperative monitoring in the immediate posttransplant period 4. Management of early postoperative hemodynamic abnormalities in the intensive care unit 5. Evaluation beyond the perioperative setting

Cardiac Donor Screening AI> a result of the shortage of available donor hearts, many institutions are now liberalizing their acceptance criteria to include extended-criteria donor hearts (Table 18-1). Additionally, due to a survival benefit in high-risk recipients (alternative list) compared to nonsurgical treatment, many institutions are transplanting this population with extended criteria-hearts.13 The extended-criteria donor organs transplanted in alternative list recipients have shown similar 30-day and I-year mortality and similar primary graft dysfunction when compared to standardcriteria donor hearts and recipients. 13• 14 These data are encouraging, as the heart failure epidemic is projected to increase. Echocardiography plays an important role in the evaluation of potential donor hearts. By ruling out donors with structural abnormalities, severe ventricular dysfunction, or significant wall motion abnormalities (WMAs), the need for costly and timeconsuming cardiac catheterization can be circumvented. Additionally, TEE has proven to be superior to transthoradc echocardiography in the evaluation of potential donors on ventilatory support. 15 Prior to TEE evaluation of the potential donor, hemodynamic and metabolic resuscitation should be optimized. Volume status, acidosis, hypoxemia, hypercarbia. and anemia should be corrected, and inotropic support should be weaned to a minimum while maintaining adequate blood pressure and cardiac output (CO).

Table 18-1. Extended donor criteria Advanced donor age (>55 years) Donor size (donor-recipient size mismatch) lschemia time (>4 hours) Positive viral serologies Donor diabetes mellitus Donor substance abuse Presence of LVH Congenital heart abnormalities High donor inotropic support RV and LV systolic dysfunction Coronary artery disease Valvular abnormalities Abbreviations: LVH, left ventricular hypertrophy; RV, right ventricle, LV, left ventrlcle.

Echocardiographic evaluation of the donor heart should rule out structural abnormalities and assess regional and global function. Historically, valvular abnormalities recognized by echocardiography precluded transplantation; however, expanded criteria may now accept some valvular abnormalities. A donor heart with a normally functioning bicuspid aortic valve may be used for transplantation.16 Additionally, anatomically and hemodynamically abnormal aortic or mitral valves with mild-to-moderate stenosis or regurgitation may undergo bench repair or replacement followed by transplantation. 16 The presence of left ventricular hypertrophy {LVH) in the donor heart is controversial. LVH is defined as an end-diastolic wall thickness greater than 11 mm in the absence of underfilling of the ventricle (pseudohypertrophy). One study showed that LVH is an independent risk factor for primary graft dysfunction.17 However, another study demonstrated that hearts with mild (12 to 13 mm) or moderate (13 to 17 mm) LVH are not associated with increased morbidity.18 A more recent study showed that LVH alone was not an independent predictor of mortality, but LVH combined with donor age ~55 years or ischemic time ~4 hours was associated with increased mortality. 19 Current recommendations state that donor hearts with LVH < 14 mm can he used provided there are no associated dectrocardiographic {ECG) findings suggestive of LVH. 16 Left ventricular (LV) wall thickness is best assessed with the transgastric long-axis {TG-LAX) or transgastric mid-short-axis (TG-SAX) views using M-mode or two-dimensional (20) imaging (Chapter 5). &sessment of WMAs is also a part of the TEE evaluation of potential donors. Presence of WMAs may be the result of myocardial ischemia, myocardial contusion, or ventricular dysfunction after brain injury. Brainstem death is associated with intense sympathetic nervous system activity and catecholamine storm. This sympathetic storm can precipitate myocardial ischemia and an inflammatory reaction with the rdease of cytokines that can exacerbate organ injury. Neurogenic injury frequently causes hypokinesis of the basal septum and basal anterior walls while sparing the apex, corresponding to the distribution of sympathetic nerve endings and catecholamine rdease. This pattern of regional WMAs does not follow a coronary artery distribution and is unlikdy to be caused by myocardial ischemia. There is a poor correlation between the distribution of echocardiographic dysfunction and actual histological evidence of myocardial injury after neurogenic injury. In contrast, contused myocardium will show both histological and echocardiographic evidence of myocardial injury, resembling infarcted tissue. 20 Regional wall motion abnormalities often

468 I CHAPTER 18 improve after traruplantation21 and are not associated with decreased survival in the recipient,21 •22 but they may be associated with early graft fu.ilure. 23 Wall motion analysis is best performed in the TG-SAX view, but ideally requires multiple views that incorporate both midesophageal and trarugastric views for comprehensive assessment {Chapter 4). LV ejection fraction corresponds well to fractional area change (FAC). The lowest acceptable FAC in a donor heart is unknown, but is recommended to be >40%. 16 FAC measurement is detailed in Chapter 7.

lntraoperative Monitoring in the Pre-transplant Period The most common reason for heart transplantation is dilated cardiomyopathy from either an ischemic or nonischemic etiology. These patients may be presenting to the operative arena on inotropic or mechanical support (ventricular assist devices or intra-aortic balloon pumps). They have fixed, low stroke volumes and are extremely sensitive to changes in preload and afterload. They compensate for a low CO by an increase in sympathetic activity, which leads to generalized vasoconstriction and water and sodium retention. The induction of general anesthesia and institution of positive pressure ventilation can alter the delicate balance of prdoad, contractility, and afterload, resulting in a negative hemodynamic impact. TEE monitoring during the pretransplant period is ideally suited to assist in the rapid evaluation and guidance of intraoperative management. Optimization of LV filling volumes is best done with TEE guidance, as the presence of regurgitant valvular lesions, diastolic dysfunction, and positive pressure ventilation leads to poor correlation between measured filling pressures and actual LV volumes. Right ventricular (RV) size and function should be evaluated in the pretransplant period. RV function can be assessed through tricuspid annular plane systolic excursion (TAPSE) or with FAC in the midesophageal four-chamber (ME-4C) view (Chapter 9). The presence of RV hypertrophy is suggestive of longstanding pulmonary hypertension, which may lead to acute RV dysfunction in the transplanted heart. When the pulmonary artery systolic pressure exceeds 60 mm Hg and is not reversible with vasodilator therapy, the risk of right heart fu.ilure and early death is increased in the posttransplant period.24 Pulmonary artery {PA) catheters are commonly utilized during heart transplantation but may be difficult to place in the presence of RV dilatation, tricuspid regurgitation, and low CO. In such scenarios, TEE can help guide the placement of the PA catheter when observing via the midesophageal RV inflow-outflow or midesophageal

ascending aorta short axis view. Alternatively, TEE can determine CO and PA pressures during the precardiopulmonary bypass (CPB) period if PA catheter placement is unsuccessful. Estimation of PA systolic pressure can be performed using continuous-wave Doppler on the tricuspid regurgitant {TR) jet. The peak velocity of the TR jet can be used to calculate the pressure gradient between the RV and right atrium (Chapter 5). TEE is also utilized in the pretransplant period to assess the presence of intracardiac thrombi. Prethrombotic sluggish blood flow is characterized echocardiographically by spontaneous echo contrast, or "smoke." Patients with dilated cardiomyopathy have a high incidence of thrombus formation in the LV apex. The LA appendage should also be assessed for possible thrombi, particularly in patients with atrial fibrillation (midesophageal two-chamber view and midesophageal mitral commissural view focused on the left atrial appendage). When thrombi are present in the left heart, manipulation of the heart prior to aortic cross-clamp should be minimized to avoid systemic thromboembolization. As in all CPB cases, the aorta (ascending, arch, and descending) should be examined for atherosclerotic plaque prior to aortic cannulation. Air entrainment during explantation of a ventricular assist device (VAD) is another potential source of embolization that should be carefully assessed.

lntraoperative Monitoring in the Post-transplantation Period Prior to separation from CPB, TEE is utilized to detect retained air and assist de-airing maneuvers. Retained air is commonly seen in the right and left upper pulmonary veins, the LV apex, the left atrium, and the coronary sinus. The right coronary artery is most susceptible to air embolus because of its more anterior location in the ascending aorta. Air embolus of the right coronary artery leads to a hypocontractile dilated RV, bradycardia, and ST-segment changes in the inferior ECG leads. After separation from CPB, a comprehensive TEE exam should be performed. The function of the newly transplanted heart depends on many factors (Table 18~2). There are several echocardiographic findings that would be considered abnormal in the nontransplanted hean but are characteristic in the cardiac allograft. Because the donor heart is typically smaller than the dilated failing native heart, the allograft tends to be positioned more medially in the mediastinum and rotated clockwise. This results in difficulty in obtaining the standard tomographic views, and nonstandard TEE

THORACICTRANSPLANTATION I 469 probe positions and angles may have to be wed. Characteristics of ea.eh component of the cardiac allograft will be deacribed. ATRIA

Evaluation of the right and left atria should be per· formed in multiple views. Anastomotic atrial suture lines or infolded left atrial tissue at the anastomosis may protrude into the atria and appear eche>-dense. &imilar to .maM lesions or duombi25 (Fig. 18-1, Vldeos 1 and 2). Additionally, the left atrial appendage may have become inverted and appear as a mass in the left anium (Fig. 18-2).26 When the biattial technique is used, difiUcnt-sized portions of the native aaia are left in situ (Fig. 18--3).

Table IB-2. Factors influencing cardiac allograft function Ba5ellne function befcre brain death Degree of myocyte damage before and during haM!st Amount of donor inotropic support lsdiemlc ttme Myocardlal protection

Reperfuslon Injury Cardiac denervation

Donor-recipient size mismatch Donor age Degree of pulmonary hypertension ln the recipient

Tbc composite atria an: en.l.arRed and will have intralwninal protrusion of the atrial anastomosea, giving an hourgla&s configuration. This makes the t:ranspJanted heart appear as a six-chamber structure (Fig. 18-4). Mild constriction at the anastomotic sururc line may cause an increase in inttaatrial Doppler flow velocities. While uncommon, severe LA stenosi& from the suture line prccieitating heart fai.lw:c bas been reported.27 Additionally, the anastomotic prottusioru may occasionally contact the posterior mitral leaflet in systole. Severe C35CS of supramittal valve obstruction, or acquired cor ttiatriatum, have been described after heart transplantation and should be suspected when the LA remnant is markedly enlaxgcd and LY volume is n:duc:ed.28 Turbulent flow by color flow Doppler (CFD), fluttering of the mittal valve leaflets, and cle-vated blood flow velocities by pulsed-wave Doppler may aid in the confumat.ion of this diagnosis. The integrity of the interaaial septum should be evaluated wing CFD and contrast echocardiography (agitated saline or saline microcavitation). In the setting of LY dysfunction, a Valsalva maneuvu may not increase RA p~ enough to overcome LA pressure, preventing a diagnosis of interatrial shunt with conuast ccbocanliography. Shunts can occur ar. the inreratrial anastomotic suture line (biattial tc:cbnique) or through an unrecogniud donor puent for.uncn ovale (PFO). lnteratrial shunting may become hemodynamically

significant postoperativdy, particularly in the setting of pulmanary bypenension, RV dysfunction, or TR. and may present as persistent hypoxcmla. 29 Identification

FIGURE 78-J. Modified midesophageal four-chamber

view showing the left atrial anastomosis suture line (arrow) protruding into the left atrium. LA, left atrium; LV, left ventricle; RV, rightventticle.

470 I CHAPTER 18

FIGURE '18-2. Mldesoph~ geal four-chamber view after orthotoplc heart transplant showing an Inverted left atrial appendage (a"ow) in the left atrium. RA, right atrium; RV, right ventricle; LA, left atrium; LV, left ventricle.

A

B

FIGURE 1B-3. Posttransplantatlon transesophageal echocardtography demonstrating atrial consequences of the blatrlal technique for heart transplantation. (A) Mldesophageal four-chamber view showing the composite atria appearing as a multlchamber structure with two fossa ovale (arrows). (8) Mldesophageal left atrial appendage view showing two atrial appendages (arrows). pv, pulmonary vein; RA, right atrium; RV, right ventricle.

of a left-to-right shunt across the intcratrial anastomosis should prompt surgical cottcaion, as it can contribute to RV volume overload and significant TR. Although the pulmonary veins are anastom~d en bloc with a cuff of recipient LA. part of the LA anastomosis and pulmonary venous inflow sites at the LA should be assessed with color ftow and pulsed-wave Doppler. The left pulmonary veins are imaged from the midesophagcal left atrial appendage and left upper pulmonary vein view. 30 The right pulmonary veins are imaged from the midesophageal right pulmonary vein

view at 0 degrees or turning theJ>robe clockwise from the midcsophageal bic:aval view. VENAE CAVAE ANAsTOMOSES

.Anastomotic stricture& can also occur at the levd of the central veins, SVC. and IVC, with .resultant endorgan dysfunction such as liver and kidney f.Ww:e3 1 or superior vena cava syndrome.32 The SVC and IVC anastomotic sit'CS should be carefully evaluated by 20 imaging and color flow Doppler in the midcsophageal bic:aval view (Fig. 18~5, Videos 3 and 4). A high level of

THORACICTRANSPLANTATION I 471

FIGURE 18-4. Midesophageal two-chamber view showing anastomotic protrusions (a"ow), creating the impression of a multichamber left atrium. LA, left atrium; LV, left ventricle.

suspicion for anastomotic stcno.sis should be ttitzcrcd by the presence ofdis4 hours), poor organ preservation, and development of radical oxygen species. Acute RV f.a.i.lure of the allograft is a predictor of early and late mortality and accounts for 50% of all cardiac complications following cardiac transplant. Timely assessment and aggressive hemodynamic support of the RV is essential. RV systolic function can be aasesaed with v.u:ious cchocardiographic functions, including TAPSE, RV-FAC, and RV myocardial performance index (RV-MPI) (Chapter 9). In the presence of RV dysfunction, TEE should be used to optimir.c RV filling to avoid distcntion of the vcntridc and assess the response to inotropic suppon. TEE should also be utiliu:d to assess stenosis of the PA anastomosis as a possible cause of RV dysfunction. In the setting of maximum inot:ropic support and pulmonary vaaodilator therapy, the prc&ence of a dilated and hypokinetlc RV and a small hyperdynamic LY should prompt the consideration of a mechanical assist device.

PULMONARY ARTERY ANAsTOMOSIS

The PA anastomosis should be examined for possible stcnosis, kinking, or torsion, particularly in the setting of RV dysfunction (Fig. 18-9, Video 9). This anastomosis can sometimes be visualized in the upper esophageal aortic arch short-axis view when increasing the Seid depth, or the midesophageal ascending aorta short-axis view.'° Alternativdy, it may be seen from the midesophageal ascending aorta long-axis view by centcring the image plane on the short axis of the right pulmonary artery and rotating the probe countcrdockwise. This will result in long-axis imaging of the main pulmonary artery. This view will optimize the imaging plane for pulsed~wavc, continuow--wavc, or color flow Doppler evalU2tion of the main PA30 CFO may detect turbulent flow, and the pressure gradient can be measured with continuow.-flow Doppler. Unfortunately, there is not a defined pressure gradient that indicates the need for surgical revision. AoRTIC ANASlOMOSIS

Anastomosis at the aortic sut!UC line is a potential source of early and late complications. Compliance mismatch, technical, and hemodynamic factor& lead to rare but serious complications, including aortic dissection. This anastomosis is best seen in the midcsophagcal ascending aorta long-axis view and the midesophageal ascending aorta shore.axis view.30 As in all CPB cases, aortic evaluation should be performed after CPB and aortic dccannulation.

FIGURE 78-P. Mtdesophageal ascending aorta SAX demonstrating the pulmonary artery anastomosis (arrow) after orth~ topic heart transplantation. PA, main pulmonary artery; RPA, right pulmonary artery.

THORACIC TRANSPLANTATION I 475

Management of Early Postoperative Hemodynamic Abnormalities in the Intensive Care Unit After the operative arena, care of the heart transplant recipient continues in the intensive care unit (ICU). During this time, management of hemodynamics may be largely based on measured values from invasive monitoring. When unexplained changes in hemodynamics are seen or when a patient develops inappropriate responses to escalating therapies, TEE can be an invaluable diagnostic tool. TEE can be used to assess biventricular function, anastomoses, valvular abnormalities, sources of systemic emboli, and the detection of pericardia! tamponade.

Evaluation Beyond the Perioperative Setting Following the perioperative period, TEE of heart transplant recipients may yield several findings not seen in the acute posttransplant period. For one, spontaneous echo contrast can be detected in up to 55% of heart transplant recipients. This is usually confined to the donor atrial component and is associated with thrombi, typically at the LA free wall underneath the protruding suture line. Thrombus formation on a protruding suture line can result in inflow obstruction. Second, pericardia! effusions are present in up to 20% of heart transplant recipients. These effusions typically do not cause hemodynamic chanyes and often resolve by the fourth postoperative week. 6 Finally, the aortic anastomosis is another source of potential pathology after the perioperative period. Reported pathology includes acute aortic rupture at the anastomotic site, infective pseudoaneurysms, true aneurysms on either donor or recipient ascending aorta, and aortic dissections. These pathological events can occur many years after transplantation. Since the allograft is denervated, classic pain symptoms are often absent. All reported cases of aortic dissection have been limited to the donor aorta. The aortic suture line seems to prevent the extension of the dissection to the native aorta, and therefore classic signs of tamponade and limb malperfusion are not seen.39 Diagnosis is often made on routine surveillance. Risk factors for aortic dissection after heart transplantation include hypertension, diabetes mdlitus, unrecognized donor connective tissue disorder, and accderated atherosclerosis due to immunosuppression.

LUNG TRANSPLANTATION Lung transplantation for chronic respiratory failure has been steadily increasing over the past decade. 2 With over 3000 lung transplantations performed annually, both

the median donor and recipient ages have increased.2 The most common indications for lung transplantation currently are chronic obstructive pulmonary disease {34%), interstitial lung disease {24%), and cystic fibrosis (17%).2 Median survival after lung transplantation is 5.6 years; however, patients who survive the first posttransplant year have a median survival rate of7.9 years.2

Surgical Technique To understand the application of TEE during lung transplantation, it is prudent to understand the surgical technique. The surgical procedure commences with a clamshell thoracotomy, median sternotomy, or anterolateral thoracotomies with sternal sparing for bilateral lung transplantation and anterolateral thoracotomy for single lung transplantation. The procedure may be performed with or without CPB support, depending on the patient's tolerance to the hemodynamic disturbances. The first lung to be transplanted is typically the one with the least perfusion on ventilation-perfusion (VIQ) scan. One-lung ventilation is used during this phase, and this may be a time of hypoxemia, hypercarbia, and hemodynamic instability. The pulmonary artery and pulmonary veins are dissected, and the bronchus is divided immediately proximal to the upper lobe take-off. Clamps are applied to the pulmonary veins, and the pericardium is opened to allow exposure to the pulmonary vein inflow sites and left atrium. Next, the pulmonary artery is clamped. Hypoxemia should improve with PA clamping, but RV function may deteriorate. Once the allograft has undergone hilar dissection, the bronchus anastomosis is made proximal to the upper lobe take-off. After the bronchial anastomosis, the PA and then pulmonary veins are anastomosed. The pulmonary veins are anastomosed either individually or en bloc with a LA cuff after a side clamp is applied to the LA. Initially, V/Q mismatch may occur, with ventilation preferentially going to the compliant allograft lungs and perfusion to the native lungs due to donor vasoconstriction. Hypoxemia, hypercarbia, and hemodynamic instability may ensue. The second lung is transplanted in a similar manner.

Application of TEE During Lung Transplantation lntraoperative TEE during lung transplantation has become a routine part of monitoring. The application of TEE during lung transplantation can be divided into four categories: 1. lntraoperative monitoring in the pretransplant period 2. lntraoperative monitoring during lung transplantation

476 I CHAPTER 18 3. In~a°frativc monitoring in the posttransplant pcno 4. Diagnosis ofbemodynamic or oxygenation abnormalities in the ICU

lntraoperative Monitoring in the Pre-transplant Period Induction of ancsthesia in patients presenting for lung transplantation will lead to alterations in respiratory mechanics, and cardiogcnic shock may result, particularly in patients with severe pulmonary hypertension. TEE is particularly useful dwing these hcmodynamic derangements to optimize CO and right heart function. Additionally, patients with severe emphysema can develop hemodynamic collapse from autopositive end-expiratory pressure, decreased venous return, and pulmonary tamponade.40 During pulmonary tam· ponadc:, compression of attial and ventricular chambers of the heart will be present, but pericardia! fluid will be absent. Treatment includes disconnection from the ventilator to allow time for the lungs to ddlate, 1'e&Olving hypotension. Induction of anesthesia may be followed by significant hypoxemia. After assessing for ventilatory causes ofhypoxemia (e.g., inadequate tube position or obstruction, ventilator settings), TEE can be utiliud tD assess for inttacardiac causes of hypoxcmia, including intracudiac shunting (e.g., patent foramen ovale, atrial septa! defect) and RV failure. Even in the absence ofhemodynam.ic derangements, it is important to evaluate baseline RV s.i7.e and function (Fig. 18-lOA. Videos 10 and 11). As with heart transplantation, RV function can be ~cd in the midesopbagcal or transgasttic views by using difkrent pawncn:rs and methods (TAPSE, PAC) (Chapter 9). In the presence of RV dilation and dysfunction, PA catheters may be difficult to position. TEE can be utiliud to e&timate PA pressure by measuring the maximum velocity jet ofTR and applying the simplified Bernoulli equation (Chapter 5). However, Doppkr-derived pressure gtadients of pulmonary artery pressures may be inaccu· rate in patients with advanced lung diseasc.41 TEE can also hdp guide the placement of the PA catheter when obs~ via ~e midesophagcal RV inflow-oudlow or midesophageal ascending aorta sbott.-axis view. Evidence exists that CPB increases perio~rative and I-year mortality in lung t.ransplantation.42 The decision to initiate CPB typically involves acid-base status, oxygenation, ventilation, change in PA pressures, and systemic arterial blood pressure. An already dysfunctional RV may not tolerate these metabolic and hemodynamic changes, and may fuil, leading to the necessity to institute CPB. TEE is useful in determining the need fur initiation of CPB.

A

B

FIGURE 18-10. {A) Midesophageal four-chamber view ofa severely dilated right ventricle in a patient presenting for bilateral orthotopic lung transplantation. (8) Midesophageal four-chamber view of the same patient's rightventrtcle Immediately after transplantation, showing decompression of the rightventrtcle. RA, right atrium; RV, rightventrtcle; LA, left atrium; LV, left ventrlde.

lntraoperative Monitoring During the Transplant Period Clamping of the PA can induce acute RV dilation, tticuspid regurgitation, and paradoxical intcrventticular septal shift. The septa! shift toward the LV occurs in late dia&tole with RV volume overload and at end systole and early diastole with RV pressure overload. Septa! shifting prohibits adequate LV diastolic filling and results in low CO and hypotension. Systemic hypotcnsion and devated. RV pressure will further impair myocardial perfusion and RV contractility. Echocardiographic signs of impending

THORACIC TRANSPLANTATION I 477 Table 18-3. TEE signs of impending RV failure RV dilation with resultant tricuspid regurgitation RV free-wall hypokinesis Systolic and diastolic flattening of the interventricular septum, with D-shaped LV Paradoxical septal motion Dilation of the RA, IVC, and PA Abbreviations: LV, left ventricle; RA, right atrium; IVC, inferior vena cava; PA, pulmonary artery.

RV failure are presented in Table 18-3. In the presence of a PFO or atrial septal defect {ASD), the high right atrial pressure may induce right-to-left intracardiac shunt and hypoxemia. PFOs and ASDs can he detected by pulsed-wave Doppler, color flow Doppler, or contrast echocardiography (agitated saline or saline microcavitation). Hemodynamic derangements not related to PA clamping during lung transplantation are common. Etiologies of such derangements include manipulation of the native or transplanted lung, resulting in compression of cardiac chambers or major vascular structures, and hypovolemia with acute blood loss. Although a rare occurrence, intraoperative hemodynamic instability has been reported with pneumopericardium, resulting in cardiac tamponade, diagnosed withTEE.43

lntraoperative Monitoring in the Post-transplant Period The pulmonary vein anastomosis is the last anastomosis to be completed during lung transplantation. Improper de-airing of the donor pulmonary vein may lead to air entrapment when the anastomosis is made. Air entrapment will lead to systemic air embolization and may result in bradycardia, hypotension, and cardiovascular collapse. TEE should be used to rapidly diagnose air embolization. Multiple views, focusing on the pulmonary vein, LA, LV. and aorta, can be used for this diagnosis. If cardiovascular collapse occurs, rapid institution of CPB or aggressive de-airing maneuvers may be required. LY and RV function should be reassessed to rule out myocardial ischemia. Elevated PA pressures after reperfusion of the lung allograft are concerning for elevated PVR, pulmonary edema, and graft failure. Persistent pulmonary hypertension may be caused by stenosis of pulmonary arterial or venous anastomoses, intrapulmonary thrombi, or primary graft failure. Donor and recipient risk factors for primary graft failure are shown in Table 18-4. TEE is particularly useful in rapidly providing accurate information to complement hemodynamic monitoring for

Table 18-4. Risk factors for primary graft dysfunction in lung allografts Donor Risk Factors: Female donor Donor age ~45 and ::!>21 years lschemia time >7 hours Brain death as cause of death Prolonged mechanical ventilation Bronchial aspiration Pneumonia Trauma Multiple blood transfusions Hemodynamic instability Recipient Risk Factors: Primary pulmonary hypertension Lung reperfusion technique

diagnosing potential problems leading to elevated PA pressures. Complete obstruction of a main pulmonary vein leads to unilateral pulmonary edema and hemorrhagic infarction of the corresponding pulmonary lobe within 4 to 6 hours, limiting the therapeutic options to lobectomy or retransplantation.44 The incidence of pulmonaz vein obstructions is reponed to be 1.8% to 15%4 •46; therefore, intraoperative TEE is recommended to diagnose anastomotic complications. TEE successfully images pulmonary vein anastomoses and the right pulmonary arterial anastomosis; however, it is challenging to visualize the left pulmonary arterial anastomosis due to the echocardiographic blind spot created by the left main bronchus interposing between the esophagus and pulmonary vasculature.47 When difficulty in viewing venous or arterial anastomoses occurs, use of epicardial ultrasound to determine diameter and peak systolic velocities may he appropriate.« The right PA (RPA) can be seen from the midesophageal ascending aorta shon-axis view, while only the initial take-off of the left PA (LPA) can be seen in this window (Fig. 18-11, Video 12). From the ME-4C view, the probe can be turned 180 degrees and withdrawn to image the proximal descending thoracic aorta. From this location, the LPA can be visualized as it passes anterior to the descending aorta. Slight withdrawal of the probe and turninf to the right allows further imaging of the LPA.4 Unfortunately, no echocardiographic criteria are established for the diagnosis of PA stenosis after lung transplantation. The PA anastomosis should be considered normal if the diameter of the anastomosis is at least 75% that of the proximal PA that neighbors the anastomosis.49

478 I CHAPTER 18

FIGURE 18-'l'I. Mldesophageal ascending aorta short-axis view showing colorflow Doppler across the right pulmonary artery anastomosis after bilateral orthotopic lung transplant. RPA, right pulmonary artery;Asc Aorta, ascending aorta.

Table 'IB-5. Criteria for determining pulmonary vein obstruction

Pulmonary vein diameter 1 m/s Pulmonary vein-left atrial pressure gradient~10-12 mm Hg Non-laminar flow through the anastomosis Presence oftht0mbus Color flow Doppler should also show unobstructed flow through the anastomosis. The pulmonary vein flow should be evaluated using both color flow and pulsed-wave Doppler. Criteria to determine pulmonary vein obstruction are shown in Table 18-5. The we of peak systolic flow velocity (PSFV) is confounded by cardiac output, pulmonary blood flow, left atrial presswe, velocity of transmittal flow (affected by systolic or diastolic dysfunction), and whether the lung tram· plantation is unilateral or bilateral. HoWl:Ver, in bilateral procedures, the individual pulmonary resistances tend to be equal, and therefore an increase in PSFV in only one pulmonary vein may indicate stenosi&. In unilateral lung transplants, the PSFV and pulmonary vein diameter are significantly greater than in the native lung.50 The normal PSFV in lung transplant patients is not very well-defined. Jn nor· mal patients or those undergoing coronary ancry bypass grafting, it has been fuund to be 0.41 to 0.63 m/s. In a sm:ill study of patients undergoing lung

uansplantation,!1 1 the PSFV of the native pulm~ nary veins prior to transplant was found to be < 1 m/s, and this is cwrcntly accepted as the value for normal PSFV after lung uansplantation (Figs. 18-12 and 18·13, Vidcos 13 and 14). Additionally, the pul· monary vein anastomosis is not a perfect circle, so measurement of the diameter should be performed with color flow Doppler measwing the "functional" diamctcr.s2 Immediatdy after transplantation, right ven· tricular end·diastolic area decreases and tricuspid regurgitation improves; however, RV-FAC docs not ·

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·c

FIGURE 20-10. Midesophageal four-chamber view of a large, mobile thrombus (arrow) in the left ventricle. LA, left atrium; LV, left ventricle.

FIGURE 20-12. Atrial septal aneurysm bulging into the left atrium. LA, left atrium; RA, right atrium. FIGURE 20-11. Three-dimensional image of a thrombus (atrOW) In the apex of the left ventricle. LA, left atrium.

15 mm (Fig. 2()..12, Video 8). Aneurysmal excursion can be best recorded on M-mode cchocardiography (midcsophagcal bicaval view). It is associated with

atrial septa! defects (often multiple) and conunonly a patent foramen ovale (and higher incidences of cryptogcnic43 and recurrent-" stroke) and mitral valve

prolapse.4s-48 Spontaneous contrast and thrombus

entrapment have been described in the a.neurygmal pocket and may necessitate differentiation from a cardiac twnor.

ENDOCARDITIS Vegetations differ from thrombi and twnors, in that they occur often in patients with normal ventricular function and move in phase with valve motion becawe they are attached to valvular strucrures; they are associated with valvular regurgitation, flail leaflets, ring abscesses, sinus of Valsalva aneurysms, paravalvular

Sl4 I CHAPTER 20 structure. Between these two layers, up to 50 ml

of pericardia! fluid (appearing as a dark space in 2D imaging bca.wc it has eduigenicity similar to the blood) arc di&tributcd moatly over the atrioventricular and interventricular grooves and minimize the friction from the beating heart.so In the resting healthy state, the right and left ventricles have a "serial" (the stroke volume of the ventricles is the same) as well as a direct interaction in diastole (the ventricles share the interventricular septum). In hemodynamically .significant pericardia! pathology (due to a fluid colleaion or constrictive pericardiru), the pericardium becomes nondi.stcnsiblc, compromising diastolic fillin~ and c:xaggcrati.ng the diastolic interaction of the two. 1 FIGURE ~73. Large, heterogeneous vegetation attached to the atrial side of the mitral valve in the midesophageal four-chamber view. LA, left atrium; t.V, left ventricle.

leaks, and clinical sepsis. Vegetations most frequently originm from the atrial side of the atrioventricular wives (Fig. 20-13) and from the ventricular side of the aortic or pulmonic valves. They can be mobile. irregularly shaped, and heterogeneous, and are prone to embolization. For the diagnosis and description of endocarditis, TEE is superior to lTE. TEE is also very accurate in detecting complications of cndocarditis and for monitoring therapy. Vegetations can change in she or, ideally, disappear afu:r ~ to months of antibiotic therapy; thus, repeated cchocardiogtaphy is C&Sential.

PERICARDIAL PATHOLOGY The clinical features of pericardia! diseases may rC$CDl· blc right- or left-sided cardiac failure, but the clinical management may differ signifu:antly from that of ventricular dysfunction or valvular heart d.Ueasc:. TEE is an important imaging tool for the diagnosis and evaluation of pericardia! diseases.

Anatomy The pericardium surrounds the heart (apart from the posterior aspect of the left attiwn, where the four pulmonary veins enter) and its connections with the inflow (vcnae cavae) and outflow vessels (great arteries) and isolates it from the adj~t organs. It consists of a parietal fibrous and a visceral layer; the latter reflects at the origins of the great vessels and forms the inner layer of the parietal pericardium." The two layers are not typically visualized by cchocardiograpby unless thickening exists; it is their interface with the l~ parenchyma that appears as a thin, linear

Cardiac Tlimponade In cardiac tamponadc, there is a signifu:ant rise in inttapericardial prcssure, which resulu in decreased filling gradient.a between the cavae and pulmonary veins to the RV and LV. respcctivdy; increasing, and evenrually equalization, of pericardia! and diastolic intra.cardiac pressures; reduced cardiac chamber dimensions; decreased cardiac output; and an exaggerated inspiratory dc:crcase in systolic anerial pressure (> 10% = pulsus paradoxus). The she of the pcricard.ial dlUsion is not necessarily related to its hemodynamic significance. The parietal pericardium can stretch over time because of the wavy orientation of the collagen fibers,S2 and slowly expanding effusions can become quite large (>I OOO mL) with very little increase in pericardia! pressure or symptomatology. On the other hand. rapid accumulation of smaller (or critically located) volumes (50 to 100 ml), as in post-cardiac surgery patients, can cause hemodynamic instabifity5~ becawc the parietal pericardium does not have the time to stretch and the inttapericardial pressure increases acutdy. In global pericardia! effusion, the total intrapericardial volume (pericardia! fluid and intracardiac volume) becomes fixed and results in 1) compression of cardiac chambers and 2) exaggerated ventricular interdependence as the RV and LV "compete" fur spa.cc. The compressive cffi:cts of a pericardia! fluid collection are seen first on thin-wall chambers at the time of their lower inttac:ardiac pressure, that is, atria during atrial relaxation (ventricular systole) and the RV during diastole. Therefore, systolic atrial inversion will be noticed carlicr5'S.S or more often than diastolic RV comp?C$sion.56 In the presence of pulmonary hypertension and clevarcd ~Mided pressures, left atrial (LA) inversion or co!fapse may pre20 mm..59 Hcmorrhagic or purulent fluid is more echogenic than serous collections, and 6.brin strands are often visible. In the absence of previous surge.ry or pericardia! disease, any pericardia! effi:ision will be diffuse with clear separation between the parietal and visceral pericardia! layer& (Fig. 20-14). The entire heart may

be seen swinging within the pericardia! sac, corp relating with electrical alte.rnans. RA l)'ldOiic ClOllapte. The RA free wall should be imaged in the ME foW'-chamber (4C) and bicawl views (TEE) or apical £Our-chamber and parutemal long-axis (LAX) ('ITE) views (Fig. 20-15). lnver· sion of the RA concavity is a sensitive sign of cardiac wnponade56 and can be appreciated with M-mode (Fig. 2()..16). RV diaseolic collap.se. The RV free wall should be imaged in the ME 4C, ME and TG RV inflowpoutflow, ME LAX, and TG RV inflow views60 (Fig. 20-17). RV collapse may not occur in the presence of RV hypertrophy or when RV end-diastolic pressW'C is devated (pulmonuy hypertension), where a more significant elevation of pericardia! pressure is required before the RV collapses. Dilation of potential spaces. Folds in the pericardium form potential spaces, such as the transverse sinus (Fig. 20p18), found between the posterior ascending aorta and the anterior LA wall. Significant pericardia! effusions may dilate the transverse sinus (ME LAX view) so that the left auium and ascending aorta walls are separated. Ventriculat .interdependence by Doppler. The $alient respiration-induced phasic ventricular filling is exaggerated; an increase in RV filling (in spontaneous inspiration or mechanical cxhap lation) will impede LV filling and vice versa. This reciprocal size change is accompanied by variation of the transtricuspid and transmitral diastolic velocities (vi5ualized by spectral imaging with pulscd·wave Doppler; 30% and shortened isovolumic relaxation time) during spontaneous inspi.rarion (Fig. 20p19). These 6.ndp ings arc less consistently found in mechanical ventilation.61

Constrictive Perlcardltls The symptomatology associated with constrictive pericazditis depends on the cause and severity of preeristing acute pcrica.rdial inflammation, the speed of/rogrcssion to chronic constrictive pericarditis, an resulting limitation to chamber £illing. In the United States and Europe, it primarily occurs after viral inflammation, c:ardiotomy, or radiation treatment; tuberculosis is the primary cause in developing countries. Typical findings in inflammation include retrostcrnal chest pain that is enremdy variable in

FIGURE 20- f 5. Right atrial collapse. 'The left atrium, right atrium, right ventricle. and left ventTicle are seen in a midesophageal four-chamber view with the probe rotated toward the right atrium. There Is pericardia! effusion around the heart (asterisk, outside the free wall of the right ventrlcle). lhe picture Is slgnlftcant because the free wall of the right atrium Is Inverted {white arrow) during systole. Systolic right atrial collapse should always raise the suspicion of hemodynamlcally significant pericardia! fluid collectlon. LA, left atrium; LV, left ventricle; RA. right atrium; RV, right ventrlcle.

FIGURE 20- f 6. M-mode image of right atrial free wall compression in cardiac tamponade. While in the transesophageal echocardlographlc mldesophageal four-chamber view, the cursor llne Is positioned. so that It transects the left atrium, lnteratrlal septum, and the free wall of the right atrium. 'The Inward motion of the right atrial free wall during systole Is apparent. Although this may be normal If short-lived, It Is Indicative ofcardiac tamponade Ifthe duration of the Inward motion lasts longer than one-third of the systolic period (white arrow). /AS, Interatria IseptUm; RA, right atrium.

CARDIAC MASSES AND PERICARDIAL PATHOLOGY I 537

FIGURE 20-17. Right ventricular dlastollc collapse. The left and right ventricles are seen In a transgastrlc short-

axis view with a large pericardia! effusion detected anteriorly and posteriorly. In the left pane~ the right ventricle is seen at end systole; in the right panel, the right ventricle is inverted during diastole (arrow). E, effusion; LV, left ven· tricle; RV, right ventricle.

FIGURE 20-1& In this mldesophageal long-axis

view, pericardia! effusion compresses the free wall of the right ventride and the right ventricular outflow tract. The transverse sinus (o"ow), a potential space created by the pericardia! folds between the left atrium and the ascending aorta, is also filled with pericardia! fluid. In large pericardia! effusions, this space can be markedly dilated and serve as a helpful diagnostic flndlng. AO, ascending aorta; E, effusion; LA, left atrium; RVOT, right ventricular outflow tract intensity and quality and may be suggestive of acute abdomen or myocardial ischemia. It is frequently exacerbated when lying supine, coughing, or with deep breathing. On physical examination, signs of

chronic constrictive pericarditis include a pericardial rub; distant heart sounds; increased jugular venous pressure, which is paradoxically elevated with inspifa.. tion (Kussmaul sign); peripheral edema; and ascites. All of the&e signs may be indistinguishable from those of severe RV dysfunction and tricuspid insufficiency. In the early stages of pericarditis, the electtocardio· gram typically demonstrates diffuse ST-segment concave elevation, without reciprocal ST-segment depression as .s«:n in myocardial ischem.ia, and may have a low~voltagc pattern. In chronic pericarditis, the chest radiograpbs may show calcification of the pericardiwu principally on lateral views with a nor· mal catdiac silhouette, with or without evidence of cazdiomegaly. Large pleural effilsions may also be seen. In constrictive pcricarditis, the total cardiac volume becomes med and gradually dccn:ascs as the disease progresses. The inelaStic, fibrotic pericardium creates a noncompliant space, which limits the diastolic expan· sion of the cardiac chambers. Ventricular and atrial volwne changes are governed by the noncompli· ant pericardium. rather than by the compliance of the chambers. Because of the pericardia! constriction, the atrlovcntricular pressure gradient dissipates rapidly and diastolic 6lling terminates (plateaus) in early diastole (dip antiplatetJU o~nMTJot sign in ventricular trac· in~) (Fig. 20.20). Central venous tracing ahibits the classic "M" or "W" pattern in which the v wave is enhanced secondary to non.compliance of the RA62.63 and there is a .rapid y descent, reflecting abrupt RA emptying with tricuspid valve opening.

538 I CHAPTER 20

FIGURE 20-1'. Regional cardiac tamponade. (A) Right ventricular Inflow velocities recorded with a pulsed-wave Doppler sample volume between the tips oftTlcuspld valve demonstTate a 47% deaease In early (E) velocltywlth mechanical Inspiration. (8} Left ventricular Inflow velocities recorded In a similar manner at the tips of mltral valve show lack of significant respiratory variation. (C} Right ventricular outflow velocities decrease with mechanical inspiration, while left ventricular outflow velocities (D) are unaffected.

ECHOCARDIOGRAPHIC FINDINGS

1. Pericardial thickening. Two-dimensional TEE enmination can identify pericard.ial thiclwting in constrictive pcricarditis in nearly 90% of ca.ses.~ Normally, the pericardium is an echo-dense line,. 1 to 2 mm in thickness, separated from the myocardium by an area oflucency (fluid or pericardia! fat); a pericardium thidw than 3 mm .is considered abnormal."8•6j Multiple measurements in various ME and TG views should be performed to obtain an average thickness because pericardia) thickening may be asymmetric in distribution. Pericardial thickening appears as increased ochogenicity (Fig. 20-21, Video 9) and as multiple parallel reflections on the surface of the LV with M-mode. 2. Dilated 'W:Da am1.C. Examination of the venous inflow to the right and left heart (cavae veins and

pulmonary veins) also may assist in the diagnosis of pericardia! disease. A dilated and nonpulsatile inferior vena cava (IVC) is a nonspecific indica· tor of constrictive pericarditis62: with spontaneous inspiration, a decrease of less than 11 mm thickness) by a ratio > 1.3: 1 rdative to the measured inferolateral wall thickness (Figure 21-6). 35

Pathophysiology The histopathology displays abnormalities ranging from simple hypertrophy of longitudinally directed muscle fibers to a disarray of abnormal-appearing flbers. 36 Microvascular ischemia is likdy to be caused by concentric hypertrophy of the coronary arteries, poor perfusion, increased intracavitary pressures, and reduced coronary artery vasodilatory reserve.37 The disorganized cellular architecture, postinfarction scarring, and interstitial fibrosis are possibly arrhythmogenic. 38 AF is the most common arrhythmia in 20% of patients, and risk factors include age and increase in LA pressure and size.39 Different patterns of hypertrophy have been reported, including isolated septal hypertrophy,40 inferolateral wall hypertrophy,41 concentric or diffuse hypertrophy,42 and RV hypertrophy in a small number of cases (Figure 21-7).43 The mechanism of LVOTO is explained by a narrow LVOT with or without distortion of MV leaflet coaptation and subsequent MR 44

Classification HCM is classified into four types: type I-anterior septal hypertrophy; type II-anterior and posterior septal hypertrophy; type III-diffuse hypertrophy

SUDDEN DEATH

Sudden death after vigorous exercise is often the first clinical manifestation of HOCM. The risk is highest for younger patients with severe LV hypertrophy {~30 mm thickness), LVOT gradient >50 mm Hg, LA dilatation, hypotension during exercise, and a history of syncope. The implantable cardio defibrillator {ICD) has been proven to be the most effective treatment for high-risk patients.30

LVOTO LVOTO is dynamic, variable, and influenced by loading conditions such as dehydration, exercise, and ingestion of alcohol or heavy meals.31 The goals of treatment are to prevent or delay mitral-septal contact and to enlarge the LVOT while maintaining optimum ventricular function and loading conditions. Treatment of LVOTO includes disopyramide and beta blockers.46 Interventions to reduce LVOTO include surgical septectomy of the basal septum or anterior mitral leaflet (AML) repair.47 Percutaneous alcohol septal ablation, which creates a transmural infarct by infusing absolute alcohol into the first major septal perforator artery, is an alternative in surgically unfit patients.48 HEART fAIWRE

Heart failure with preserved systolic function is frequent in middle-aged adults, with 10% to 20% of patients progressing to severe progressive heart failure. 49·50 Women have more severe symptoms occurring later in life that are more frequently associated with LVOT0.51 Heart failure may be caused by myocardial ischemia, LVDD, LVOTO, AF, and MR The only known predictor of end-stage HCM is a family history of end-stage disease. 52 In recent times, CMR has proved to be useful in imaging segmental hypertrophy, thin-walled LV apical aneurysms, end-stage systolic dysfunction, and changes to papillary muscles and mitral valve. Contrast-enhanced CMR with late gadolinium enhancement (LGE) is useful to identify

556 I CHAPTER 21

FIGURE 21-6. Midesophageal long-axis view showing thickened interventricular septum. LA, left atrium; RV, right ventricle; LV, left ventricle.

FIGURE 21-7. Transgastrtc mldpaplllary short-axis view of the left ventricle showing hypertrophied myocardium. RV, right ventricle; LV, le~ ventrlcle.

mar

myocardial fibrosis, which prove to be a novel muker for risk stratification.5 Patients with ESHF may need heart transplantation or MCS as a bridge to transplant.

severity of valve dysfunction. Intra.operative transesophageal echocardiography (TEE) examination hdps to confirm diagnosis, formulate the surgical plan, and assess the results immcdiatdy after cardie>pulmonuy bypass (CPB).>'

Echocardlography

VENIRICULAR 5TRUCl1JRE AND MORPHOLOGY

Echocaldiography is used to assess LV hypenrophy and function, diagnose LVOTO, and quantify the

Ecbocardiographie assessment should be performed at the base, mid, and apical segments to ddineate

VENTRICULAR DISEASES I 557 the pattern of hypertrophy and identify the site of LVOTO. Hypertrophied segments often have slightly increased brightness with wall thickness ranging from normal to greater than 50 mm. Hypertrophy localized to the anterolateral wall or the apex can be difficult to visualize, and LY cavity opacification by intravenous contrast agents may be needed.55 Narrowing of the ventricular cavity ( 1.4 m/s). The risk ofLVOTO is determined by the angle between LVOT outflow and transmittal inflow and the intrusion of septal tissue into the LVOT. Angles greater than 35 and 80 degrees at provocation and rest, respectively, are predictive ofLVOT0.56 ATRIAL STRUCTURE AND VOLUME

Increased LA size is related to increased wall tension and filling pressure caused by LVDD, MR, or atrial myopathy. LA size and volume can be measured using the area-length method, Simpson method, or 3DE and are prognostically significant in patients with HCM.57 Longitudinal LA strain measured by TOI and 20 strain is significantly lower in patients with HCM compared with those with secondary LY hypertrophy.SS VENTRICULAR SYSTOLIC FUNCTION

2DE, and increasingly, 3DE are used to assist in morphological and functional assessment of cardic function, myocardial thickness, chamber size, and valve function. 59 Systolic function is usually preserved or hyperdynamic. TOI at the mitral annulus showing reduced systolic (lateral S', 8.2±2.1 vs. 15±1.2 cm/s) and early diastolic (lateral e 1, 8.1 ±2.3 vs. 16.5±2.8 cm/s) velocities provides a novel and accurate means for early diagnosis before the onset of overt hypertrophy. 60 Strain rate imaging has been useful in differentiating nonobstructive HCM from hypertensive LY hypertrophy but is limited b[, angle dependence and a poor signal-to-noise ratio.61, 2 DIASTOLIC FUNCTION

LVDD is caused by impaired ventricular relaxation and increased myocardial fibrosis and occurs in almost all patients. The correlation between assessment of LVDD using TMDF/PVDF profiles and other invasive catheterization techniques is poor.63 The atrial reversal velocity and duration recorded from the pulmonary veins have a significant correlation with LY end-diastolic pressure (LVEDP). 64 The E/e 1 ratio has been correlated with LY filling pressures across a wide range of annular velocities as well as exercise tolerance in adults.6 5·66 A comprehensive approach to estimating LY filling pressures in patients with HCM should also include measurement of pulmonary artery pressures and LA volume.

SYSTOLIC OUTFLOW OBSTRUCTION

LVOTO may be precipitated by ventricular hypertrophy, systolic anterior motion (SAM) of the mitral valve, and reduced preload resulting in high systolic flow velocities and increased ventricular cavity pressures. Echocardiography is the imaging modality of choice to assess LVOTO. Doppler echocardiography is used for assessment of abnormal and high-flow zones and measure velocities and gradients within the ventricular cavity.(;! In the deep transgastric five-chamber view, it is important to avoid contamination of the signal with the MR jet. Midcavitary obstruction can also occur in hypertrophic and hyperdynamic ventricles, especially in elderly patients with a sigmoid septurn:43 SAM is defined as mechanical impedance to outflow resulting from mitral valve-ventricular septal contact (or near contact) in midsystole causing turbulent flow. Anterior displacement of the coaptation point directs the ventricular inflow toward the septum, causing the blood to move posteriorly while pushing the MY leaflets toward the LVOT (Figure 21-8, Video 3). The displaced leaflets are pulled into the LVOT, creating a funnel composed of the distal ends of the leaflets, thereby generating a gradient. Septal hypertrophy, Venturi forces created as flow enters the narrowed LVOT, and anomalous insertion of the papillary muscles may also contribute to LVOT0.44 A large anterior mitral leaflet (anterior annulus to coaptation point in end diastole, AL >2.0 cm in length), a relatively large posterior leaflet (posterior annulus to coaptation point in systole), anteriorly displaced papillary muscles, and a ratio of AL: PL :5'.; 1.3 all increase the risk of SAM/ LVOTO (Figure 21-9).68•69 In the midesophageal (ME) three- or five-chamber window, the distance between the coaptation point and the ventricular septum (C-Sept) less than or equal to 2.5 cm increases the risk of SAM/LVOTO/MR7o Using M-mode, LVOTO can be demonstrated by visualizing the aortic valve from the ME long-axis (LAX) AV views. The valve leaflets open normally and close prematurely in midsystole due to LVOTO, with a second opening as final ejection occurs (Figure 21-lOA). PWD sampling of the ventricular cavity, using the transgastric (TG) views, can be used to identify the location of abnormal systolic outflow. The continuous-wave Doppler (CWD) profile demonstrates midsystolic acceleration and late peaking (> 1.4 m/s) with a "dagger shaped" appearance which is diagnostic of dynamic LVOTO (Figure 21-lOB). In the acceleration phase, an inflection point occurs between a velocity of 1 and 2.5 m/s, which correlates with contact between the mitral leaflets and the septum.71 This marks the start of the dynamic increase in velocity of blood flow due to a decrease in LVOT area caused by

558 I CHAPTER 21

FIGURE 21-& Midesophageal rour~hamber view showing displacement of the mitral valve leaflets into the leftve~ tricular outflow tract predisposing to SAM. RA, right atrium; LA. left atrium; Rv; right venttide; SAM, systolic anterior motion.

the decreasing distance between the anterior mitral leafiet and septum. This amplification of obstruction causes the tra(:ing to curve conc:avc to the left until peak velocity. Color flow Doppler (CFO) imaging of the ME five-chamber and LAX aortic valve views demonstrate& an aliasing. mosaic pattern at the level of the LVOTO consistent with turbulent flow and across the MY .revealing significant MR. This Y-sbaped CFO is consistent with SAM (Figure 21-11, Video 4). MmtAL REGURGmmoN

FIGURE 27-9. Diagram showing the measurements in the midesophageal five-chamber view used to predict systolic anterior motion of the mit.Tal valve. LA, left atrium; RV, rightventride: LV, leftventride;At.. anterior leaflet length; PL. posterior leaflet length; C.OOptAnn, distance from the mitral coaptation point to the annular plane; CSept, distance from the mitral coaptation point to the septum; LV1Ds, left ventricular internal diameter in systole.

The cause of MV enlargement in HCM is currently not well understood, but elongation and thickening of the A.ML, malpositioning of the papillary muscle& and MY, and SAM of the MV leaflets .result in MR and dynamic LVOT0. 72 The excess anterior motion of the larger AML shifts the leaflets toward the LVOT, causing chordal and leaflet laxity, thereby creating a gap, resulting in a posteriorly directed jct of MR. The degree of MR is also dynamic and proportional to the mismatch of anterior to posterior leaflets and can be quantified by measuring the coaptation length between the two leafiets.7' Inttinsic abnormalities such as MV prolapse, leaflet thickening secondary to injury from repetitive septa! contact, or a turbulent regurgitation jct may also lead to MR.74 THREE-DIMENSIONAL ECHOCARDIOGRAPHY

Rtal-time 3DE allows detailed evaluation of the morphological changes in the LV and is comparable to CMR. Rtal-time geometric analysis has demonstrated that SAM is asymmetric and predominantly mediaf .7S

VENTRICULAR DISEASES I 559

ECG

CWD

.._ c:

M-mode A

• Nonnal

HOCM

B

FIGURE 21-10.

(A) Schematic diagram showing left ventricular outflow tract obstTUctlon (LVOTO). Continuous wave Doppler (CWD) profile demonstrates 'dagger shaped'"appearance, and the M-mode demonstrates premature dosing of the aortic valve In mldsystole with a second opening as final ejection occurs due to LVOTO. (B) CWD profile demonstrates mldsystollc acceleration and late peaking, which Is diagnostic of dynamic LVOTO. ECG, electrocardlogram; HOCM, hypertrophlc obstructive cardlomyopathy.

Hyputrophic OL..ttuctive Cardiomyupathy. Intraoperative TEE helps to assess the thickness and c:x:tent of septa! bulge, identify endocardial fibrous plaque (friction or impact lesion), charactet.ize mittal valve abnormalities, and identify complications such as iatrogenic ventricular septa! defects or aortic regurgitation. The primary goal of MV repair is to move the coaptation point posteriorly in order to produce a posteriorly directed ventticular inflow and to keep the MV lcaflets away from the LVOT. For alcohol septa! ablation, myocardial contrast echocardiography with the injection of echocardiographic conttast agent into the target septa! arteries i&

used to delineate the vascular distribution of the individual pcrforamr branches. Typically, MCE produces a demarcated area with increaaed echo density in the basal septum and an acoustic shadowing effect, which can be detected by intraprocedural TI'.E or TEE.

RESTRICTIVE AND INFILTRATIVE CARDIOMYOPATHY Introduction Ratrictive cardiomyopadties (RCMs) are a heterogeneous group of heart muscle disorders which present as

560 I CHAPTER 21

FIGURE 27-7 7. In this mldesophageal long-axis view, left ventricular outflow tract (LVOD obstruction Is demonstrated by the aliasing In the LVOT caused by turbulence due to systolic anterior motion of the mltral valve. LA, left at.rtum; RV, right ventrlde; Llf, left w .ntrlcle; Ao, Ao.rta; MR, mltral regurglt.atton; LI/Ur, left ventricular outflow tract

diasmlic heart f.ailu.re caused by stiffness of the myocar-

dium. Unlike other cardiomyopathiea, which are baaed on morphological classification. RCM is a functional c1assifiau.ion. Restrictive cardiomyopathy ls charactui7.ed by abnormal venttiatlar filling in which increased stiffness of the myocardium causes ~ntricular pressure to rise precipitously with small inaeues in volume.1

Etlology, Pathophyslology, and Classification The classic features of RCM are those of a small ventricle with normal systolic function, LVDD, and marked atrial dilatation in the absence of peric:ardial disease. The diastolic dyafunction leads to pulmonary hypcncnsion and :Anally end-stage systolic dysfunction. Familial RCM is often characterized by autosomal-d.ominant inheritance. Secondary cawea of RCM include infiltrative disease& such a& amyloidosis, sarcoidosis, glycogen storage diseases, d~ (anthracyclines, crgotamine, methysergide, serotonin), and other miscellaneow causes (transplant rejection, radiation, cancers, toxins) (Tables 21-1and2 1-2).

Cllnlcal Presentation and Outcomes The elevated systemic and pulmonary venous pressures present as pulmonary congestion, hepatomegaly; ascites, and peripheral cdcma. Systolic murmurs of mitral and tticwpid regurgitation and a third heart

sound are common. The disproportionate rise in vcntticular pressures to small dwigcs in volume until a maximum is reached leads to a charactcd.stic dip and

plateau (or square root) bemodynamic pattern during diastole. Atrial dilatation is wociated with AF.

Echocardiogr11phy General echocardiographic features of RCM include variable myocardial thickening, small ventricles, biatrial enlargement, normal AV valves, preserved sygtolic function, dia&tolic dyafunction, and pulmonary hypertension.76 As ventricular stiffiiess increases, LVDD causes an increase in ventricular and atrial pressures. The elevated LA pressure drives an early transmittal Bow (d«:rcascd isovolumic relaxation time) and a diminished atrial contraction (high E wave and low A wave) into a stiff LV (dccrca.scd propagation velocity and deceleration time). The incomplete LA emptying lead& to b:ackpreasurc into the pulmonary veins with a blunted systolic flow and accentuated retrograde A wave. This demonstration of restrictive TMDF and PVDF profiles in patients with RCM is an inherent component of the diagnosis and has been shown to correlate with outcome.

Amyloldosls Cardiac amyloidosls is the most common cause of RCM. This disorder of protein metabolism is

VENTRICULAR DISEASES I 561 associated with infiltration of extracellular amyloid protein into the myocardial interstitium, coronary arteries, and conduction tissues leading to a firm and rubbery consistency of the myocardium. In primary amyloidosis, the amyloid protein comes from plasma cells. Secondary amyloidosis is associated with chronic inflammatory diseases such as rheumatoid arthritis and tuberculosis. Four types of amyloidosis have been described: primary, secondary, familial, and agerelated amyloidosis.77 Cardiac involvement is common in primary or age-related amyloidosis. DIAGNOSIS, MANAGEMENT, AND OUTCOME

The clinical manifestations include nonspeciflc symptoms such as fatigue, dyspnea, pedal edema, angina, arrhythmias, and signs such as periorbital ecchymosis, macroglossia, and right upper quadrant pain secondary to hepatomegaly. First-degree AV block, low voltage, and pseudoinfarction are common nonspecific ECG abnormalities.78 Low-voltage ECG with prolonged PR interval in RCM patients helps to differentiate from HOCM, which is diagnosed by the high-voltage signals and normal PR interval. Diagnosis is established by endomyocardial biopsy. CMR and delayed PGE images reveal the characteristic diffuse suhendocardial enhancement of myocardial fibrosis, which may well have important prognostic implications. 79 Prognosis is related to the extent of infiltration, thickness of the ventricular walls, severity of LVDD, presence of systolic dysfunction, and RV involvement.80 The median survival of patients with primary cardiac amyloidosis with and without heart failure is 5 months and 2.3 years, respectively. Cardiac amyloidosis is treated with chemotherapeutic agents, stem cell therapy, and cardiac transplantation. Two-DIMENSIONAL ECHOCARDIOGRAPHIC EVALUATION

Ventticular Systolic Function. There is marked thickening of the atrial and ventricular walls with a small LY. The atria are enlarged with a thickened interatrial septum. The "speckled," ground glass, or "starry skied" echocardiographic appearance of the amyloid myocardium caused by the acoustic interface created by myocytes and amyloid protein is highly sensitive and specific for cardiac amyloidosis (Figure 21-12, Video 5). The presence of LVOTO may mimic HOCM. Valvular thickening with normal leaflet motion due to amyloid infiltration of all valves may be seen in advanced disease. TDI. TDI helps to differentiate between constrictive pericarditis and RCM. TDI is used to measure septal and lateral mitral annular tissue velocities hut is limited by angle dependence. Low mitral annular tissue velocities both in the systolic wave and early diastolic (e' wave) are also diagnostic of a restrictive

pattern. 81 The E/e 1 ratio is consequently high, suggestive of elevated filling pressures. Myocardial strain and strain rate measurements using TDI are more sensitive and accurate than tissue velocities in identifying both systolic and diastolic dysfunction hut are limited by a high signal-to-noise ratio. s2

Idiopathic Restridive Cardiomyopathy Idiopathic restrictive cardiomyopathy is a rare, autosomal-dominant disease caused by mutations in the troponin I or desmin gene and is associated with interstitial myocardial fibrosis and skeletal myopathy. 1 The histology is nonspeciflc with myocyte hypertrophy and interstitial fibrosis.

Endocardial Fibroelastosis Endocardial fibroelastosis is found in children and is characterized by a thick endocardium.83 Inflammation of the endocardium (possibly viral) subsequently results in thickening and thrombus formation, especially at the apex.

Endomyocardial Disorders Endomyocardial disorders can be subclassifled, according to the presence or absence of eosinophilia, into hypereosinophilic syndrome or endomyocardial fibrosis, resfectively, which are a continuum of the same disease. 8 The occurrence is greater in parts of Africa and Asia, accounting for as much as 25% of cardiac deaths.

HypereosinophiJ synJrome (Lo.flier ~)

is associated with an eosinophilic count > 1.5 X 109/L and may be idiopathic or secondary to lymphoma, tumors, vasculitis, or parasitic or infuctious diseases.85 Degranulation of eosinophils and the resultant secretion of toxic products causes cell injury followed by fibrosis in the heart, lun~, and nervous system leading to neurological deficits. 6 EnJomyocartlUdfibro.U devdops into a thick shell with fingerlike extensions into the myocardium. With 2DE, the fibrosis is seen as an echogenic line covering the endocardial surface from the apex to the base of the ventricles consistent with calcium deposition. Echocardiography can also demonstrate hiventricular apical thrombus, AV valve regurgitation with poor mobility, biatrial enlargement, and a restrictive pattern.

Hemochromatosis Hemochromatosis is an infiltrative disease due to excessive storage of iron in a number of organs causing fibrosis and cell death. The causes may be hereditary or transfusion overload. The clinical features include cirrhosis, diabetes, changes in skin pigmentation, endocrine failure, arthropathy, and heart

562 I CHAPTER 21

FIGURE 27-72. Transthoracic echocardiographic apical four-chamber view showing thickened ventricular walls and speckled appearance characteristic ofamyloidosis. RA, right atrium; LA, left atrium; LV, left ventricle.

fulurc, which is the leading ca,usc of death in as many as 40% of patients with primary hemochromatosis.'7 .Echocardiographic kanm:s include nonspecific changes such as increased vcntticular wall thiclmc:§ with po.ssible regional or global hypokinesia.

Sarcoldosls Sarcoidosis is a syswnic diaeaae of unknown ctiol-

ogy in which organs arc infiltrated with nona.scating granuloow caused by CD4+T cells that interact with antigen-presenting cells. Cardiac sarcoidosis manifests as vcntticular dysfunction, tachyarrhythmias, heart block, syncope, and sudden death. Echocard.iographic features also include regional wall motion abnormalities (RWMA), ventricular aneurysm, pcricarclial dfu. sion, and LV thrombus. RV thickness and d}'Jfunction usually develop from w:coid involvement of the lung parcnchyma producing pulmonary hypertension.

Scleroclenna Sclcroderma or systemic sclerosis is caused by autoantibodiell against various cellular antigens and is associated with atensive fibrosis and vascular alterations in the esopbagus, lung, arterial vasculaturc, and myocardium. The disease is often asymptomatic with nonspecific signs and symptoms, but arrhythmias and right heart fulurc an: common.

Miscellaneous Irradiation therapy for malignancies can cawc progressive myocardial damage, including pericard.i.tis,

pericardia! thickening, myocardial fibrosis, valvular abnormalities, and conduction disturbances. Quite often echocardiography may show features of both RCM and corutrictive pcricarditis. Carcinoid infiltration of the heart is associated with fibrous plaques within the AV valves and along the RV free walL Anthracydinc--associated cardiotoxicity is ca,used by generation of reactive free radical species that interact and damage cellular membranes due to the cumulative dosage. Anthracycline (doxorubicin) causes both restrictive and a dilated card.iomyopathy. Glycogen, Upid, and mucopolysaccharide storage diseaaea are uncommon di&eases, and these disorders share features of both HCM/HOCM and with other RCM.

Dlfferentlal Diagnosis D~tiation of constrictive pedcarditis (CP) from RICM is important since pericardial diseases can be treated with surgcry.88 In CP, the pericardial inflammation causes scarring, thickening. fibrosis, and calcifica,tion, which in tum causes dissociation of intrathoracic and intracard.iac prc:sswa and i.nc:rcascd intcrvcntricu· lar intetdepcndcnce (Figun: 21-13, Video 6). Both CP and RICM present with ucitcs, periphcr.a.I cdcma, elevated RA pre.uurea, diastolic dysfunction, and the dip and plateau or square root sign on the RV wavefomt. But other clinical and diagno.nic katures can differentiate between the two pathologies (Table 21-3). Although one singtc fcanuc may not prove to be diagnO'ltic, a systmiatic approach using all the modalities,

including newer echocardiograpbic ~iques such as

VENTRICULAR DISEASES I 563

FIGURE 27-73. Mldesophageal four-chamber view showing eggshell calc!flcatTon of constrictive perlcardltls. RA, right atrium, LA, left atrium; RV, right ventricle; LV, left ventricle.

speckle tracking and velocity vector imaging. help diffCrcntiatc between CP and RICM.119

to

PERIPARTUM CARDIOMYOPATHY Etlology and Pathophyslology Peripartwu cardiomyopath.y (PPCM) causes heart failure associated with pregnancy in women with. no known eatdiovascular disease, usually towud the end of pregnancy or in the months following delivery. The incidence of PPCM is around 1:3,000 to 1:4,000 live

births.90 The clinical cour:sc is highly variable, and rapid deterioration may be associated with mortality rates of 10% to 30%.91 Spontaneous and complete recovery of ventricular function is seen in 23% to 41 % of patients. The exact pathophysiology is unknown, but oxidative stress involving cleavage of prolactin hormone, viral infection, malnutrition, autoimmune, or genetic mechanisms have been suggested.

Diagnosis and Management PPCM is a diagnosis of exclusion after ruling out other causes of heart failure. Early signs and sym~ toms of PPCM often mimic normal physiological findings of pregnancy and may progress to hepatic congestion, postural hypotension, MR, left ventricular thrombosis, and embolic episodes. The diagnosis

is

aided by LV hypertrophy and ST-T wave abnor-

malities on ECG, elevated plasma brain natriuretic peptide (BNP) levels, and ventricular dilatation/dys-

function measured by MRI. Oxygen, diuretics, hydralazine, inottopes, MCS, and transplantation are various treaunent options for heart failure. Bromocriptine is a novel diseascspeciflc treatment for PPCM that needs further investigarion.92

Echocardlography Echocardiography is required to confirm. dilated cardiac chambers and LV systolic dysfunction and to rule out structural causes of heart &nu.re. The cchoc.ardiography c:riteria include a left ventricular ejection 6:ac:rion (LVEF)