Principles of Echocardiography and Intracardiac Echocardiography: Expert Consult - Online and Print [1 ed.] 9781437704037

Table of contents :
Front Cover
Principles of Echocardiography and Intracardiac Echocardiography
Copyright
Dedication
CONTRIBUTORS
PREFACE
WITH ACKNOWLEDGMENT AND SINCERE APPRECIATION
CONTENTS
ONLINE VIDEO CONTENTS
Chapter 1 - The Aortic Valve
NORMAL AORTIC VALVE ANATOMY
IMAGING THE AORTIC VALVE BY ECHOCARDIOGRAPHY
ANATOMIC VARIANTS/MALFORMATIONS OF THE AORTIC VALVE
ECHOCARDIOGRAPHIC RECOGNITION OF BICUSPID AORTIC VALVES
THE VICISSITUDES OF AGING: AGE-RELATED CHANGES OF THE AORTIC VALVE AND ROOT17
SUMMARY
REFERENCES
Chapter 2 - Aortic Stenosis
GOALS OF ECHOCARDIOGRAPHY IN AORTIC STENOSIS
SCANNING ISSUES
EQUATIONS
PATHOPHYSIOLOGY AND FINDINGS OF AORTIC STENOSIS
ROLE OF TRANSESOPHAGEAL ECHOCARDIOGRAPHY IN AORTIC STENOSIS
REPORTING ISSUES
SUMMARY
REFERENCES
Chapter 3 - Aortic Insufficiency
GOALS OF ECHOCARDIOGRAPHY IN AORTIC INSUFFICIENCY
SCANNING ISSUES
DETERMINATION OF THE CAUSE OF AORTIC INSUFFICIENCY
PROBLEMS WITH COLOR DOPPLER FLOW-MAPPING “QUANTIFICATION”
SPECTRAL AND VOLUMETRIC TECHNIQUES
REPORTING ISSUES
NOTES ON ECHOCARDIOGRAPHIC METHODS TO DESCRIBE SEVERITY OF AORTIC INSUFFICIENCY
UTILITY OF TRANSESOPHAGEAL ECHOCARDIOGRAPHY IN AORTIC INSUFFICIENCY
SUMMARY
REFERENCES
Chapter 4 - The Mitral Valve
ANATOMIC COMPONENTS
MITRAL LEAFLETS
THE COMMISSURES
CHORDAE
PAPILLARY MUSCLES
THE MITRAL ANNULUS
REFERENCES
Chapter 5 - Mitral Stenosis
GOALS OF ECHOCARDIOGRAPHY IN MITRAL STENOSIS
SCANNING ISSUES
VALID METHODS FOR MITRAL VALVE AREA DETERMINATION (NEED ≥2 CONCORDANT)
SCANNING NOTES
REPORTING ISSUES
DESCRIPTORS OF MITRAL STENOSIS SEVERITY
SUITABILITY FOR VALVULOPLASTY AND COMMISSUROTOMY ISSUES
SURGICAL ISSUES
PROVOCATIVE TESTING TO ENHANCE TRANSMITRAL GRADIENTS AND RIGHT VENTRICULAR SYSTOLIC PRESSURE
NOTES ON MITRAL STENOSIS
CARDIAC CATHETERIZATION FOR ASSESSMENT OF MITRAL STENOSIS
MITRAL VALVE CATHETER BALLOON VALVULOPLASTY
SUMMARY
REFERENCES
Chapter 6 - Mitral Insufficiency
GOALS OF ECHOCARDIOGRAPHY IN MITRAL INSUFFICIENCY
SCANNING ISSUES
REPORTING ISSUES
ROLE OF TRANSESOPHAGEAL ECHOCARDIOGRAPHY IN MITRAL REGURGITATION
WHEN THE GRADE OF MITRAL REGURGITATION IS DIFFERENT ON SERIAL ECHOCARDIOGRAPHIC STUDIES
NOTES ON SPECIFIC CAUSES OF MITRAL REGURGITATION
NOTES ON THE PATHOPHYSIOLOGY OF MITRAL REGURGITATION
NOTES ON MITRAL REPAIR AND MITRAL REPLACEMENT
WHAT IS THE SINGLE BEST TECHNIQUE TO DESCRIBE MITRAL REGURGITATION SEVERITY?
SELLERS GRADE (CONTRAST VENTRICULOGRAPHY)
NOTES ON TIMING OF SURGICAL INTERVENTION IN MITRAL REGURGITATION
SUMMARY
REFERENCES
Chapter 7 - Tricuspid and Pulmonic Valve Disease
TRICUPSID VALVE APPARATUS ANATOMY
TRICUSPID REGURGITATION
TRICUSPID STENOSIS
PULMONIC STENOSIS
PULMONIC INSUFFICIENCY
SUMMARY
REFERENCES
Chapter 8 - Prosthetic Valves
SCANNING ISSUES
REPORTING ISSUES
DISCORDANCE OF GRADIENT ASSESSMENT WITH CATHETERIZATION
AREA ISSUES
PROSTHETIC VALVE DYSFUNCTION
SUMMARY
REFERENCES
Chapter 9 - Infective Endocarditis
GOALS OF ECHOCARDIOGRAPHY IN INFECTIVE ENDOCARDITIS
SCANNING ISSUES
REPORTING ISSUES
NOTES ON INFECTIVE ENDOCARDITIS
COMPLICATIONS OF INFECTIVE ENDOCARDITIS
NATIVE VALVE INFECTIVE ENDOCARDITIS
PROSTHETIC VALVE INFECTIVE ENDOCARDITIS
RIGHT-HEART INFECTIVE ENDOCARDITIS
NOTES ON VEGETATIONS
INFECTIVE ENDOCARDITIS AND THE ROLE OF TRANSESOPHAGEAL ECHOCARDIOGRAPHY
SUMMARY
REFERENCES
Chapter 10 - Echocardiographic Assessment of the Left Ventricle
LEFT VENTRICULAR ASSESSMENT AND QUANTIFICATION
LEFT VENTRICULAR THICKNESS AND MASS
SYSTOLIC FUNCTION
CARDIAC MAGNETIC RESONANCE
REFERENCES
Chapter 11 - Coronary Artery Disease: Ischemia, Infarction, and Complications
WALL MOTION ABNORMALITIES AND THEIR RELATION TO BLOOD FLOW
ECHOCARDIOGRAPHY FOR WALL ASSESSMENT IN ACUTE MYOCARDIAL INFARCTION
CORONARY CARE UNIT ECHOCARDIOGRAPHIC STUDIES
ECHOCARDIOGRAPHY FOR THE ASSESSMENT OF COMPLICATIONS OF ACUTE MYOCARDIAL INFARCTION
REFERENCES
Chapter 12 - Coronary Artery Disease: Stress Echocardiography
NECESSARY EQUIPMENT
STRESS ECHOCARDIOGRAPHIC IMAGES
SEGMENTAL WALL MOTION ANALYSIS
WALL THICKENING/EJECTION FRACTION RESPONSE
AVAILABLE FORMS OF STRESS
EXERCISE STRESS ECHOCARDIOGRAPHY
DOBUTAMINE STRESS ECHOCARDIOGRAPHY
ADENOSINE AND DIPYRIDAMOLE STRESS ECHOCARDIOGRAPHY
COMPARISON OF EXERCISE, DOBUTAMINE, AND DIPYRIDAMOLE STRESS ECHOCARDIOGRAPHY
TRANSESOPHAGEAL STRESS ECHOCARDIOGRAPHY
LIMITATIONS OF STRESS ECHOCARDIOGRAPHY
REFERENCES
Chapter 13 - Cardiomyopathies
CARDIOMYOPATHY: REQUIRED PARAMETERS TO OBTAIN FROM SCANNING
2006 AMERICAN HEART ASSOCIATION DEFINITIONS AND CLASSIFICATION OF CARDIOMYOPATHIES2
DILATED (CONGESTIVE) CARDIOMYOPATHY
HYPERTROPHIC CARDIOMYOPATHY
APICAL BALLOONING SYNDROME
RESTRICTIVE AND INFILTRATIVE CARDIOMYOPATHY
CARDIAC SARCOIDOSIS
CARDIAC HEMOCHROMATOSIS
CHAGAS DISEASE
MYOCARDITIS
REFERENCES
Chapter 14 - Diastolic Dysfunction and Echocardiographic Hemodynamics
BASIC EQUATIONS AND THEIR ASSUMPTIONS
DIASTOLIC FUNCTION, DYSFUNCTION, AND HEART FAILURE WITH NORMAL EJECTION FRACTION
ECHOCARDIOGRAPHY AS A PULMONARY ARTERY CATHETER
REFERENCES
Chapter 15 - Contrast EchocardiographyHoward leong-poi
OVERVIEW
INDICATIONS
SAFETY ISSUES
PRACTICAL TIPS FOR CONTRAST LEFT VENTRICULAR OPACIFICATION
MYOCARDIAL PERFUSION
REFERENCES
Chapter 16 - Proximal Isovelocity Surface Area and Flow Convergence Methods
PROXIMAL ISOVELOCITY SURFACE AREA SCANNING PARAMETERS
SIMPLIFIED METHODS
TECHNICAL POINTS ON PROXIMAL ISOVELOCITY SURFACE AREA METHOD
PROXIMAL ISOVELOCITY SURFACE AREA: A SUMMARY
REFERENCES
Chapter 17 - Echocardiography and Its Role in Cardiac Resynchronization TherapyGLEN SUMNER
PRECARDIAC RESYNCHRONIZATION THERAPY PATIENT SELECTION USING ECHOCARDIOGRAPHY
QUANTIFICATION OF INTERVENTRICULAR DYSSYNCHRONY
QUANTIFICATION OF INTRAVENTRICULAR DYSSYNCHRONY
DYSSYNCHRONY INDEX USING REAL-TIME THREE-DIMENSIONAL ECHOCARDIOGRAPHY
PACING LEAD PLACEMENT: ROLE OF ECHOCARDIOGRAPHY
LEFT VENTRICULAR DYSSYNCHRONY AND NARROW QRS COMPLEX: ROLE OF ECHOCARDIOGRAPHY
SUMMARY
REFERENCES
Chapter 18 - Stress, Strain, Speckle, and Tissue Doppler Imaging: Practical Applications
THE HEART DEFORMATION COORDINATE SYSTEM
TISSUE DOPPLER IMAGING
STRAIN AND STRAIN RATE IMAGING
SPECKLE TRACKING ECHOCARDIOGRAPHY
REFERENCES
Chapter 19 - Principles of Transesophageal Echocardiography
TRANSESOPHAGEAL ECHOCARDIOGRAPHIC PROCEDURE, EQUIPMENT, AND VIEWS
TRANSESOPHAGEAL ECHOCARDIOGRAPHY: SAFETY AND COMPLICATIONS
TRANSESOPHAGEAL ECHOCARDIOGRAPHY AND AORTIC DISEASE
CONGENITAL HEART DISEASE
TRANSESOPHAGEAL ECHOCARDIOGRAPHY IN CRITICALLY ILL PATIENTS
PERICARDIAL DISEASES
INFECTIVE ENDOCARDITIS
INTRACARDIAC MASSES AND CARDIAC SOURCE OF EMBOLISM
PROSTHETIC VALVE DISEASE
VALVE DISEASE
LEFT VENTRICULAR OUTFLOW TRACT LESIONS
LEFT VENTRICULAR ASSESSMENT
REFERENCES
Chapter 20 - Role of Transesophageal Echocardiography in Mitral Valve Repair
MITRAL VALVE DIAGRAMS
CASE 20-1
CASE 20-2
CASE 20-3
CASE 20-4
CASE 20-5
CASE 20-6
CASE 20-7
CASE 20-8
CASE 20-9
CASE 20-10
CASE 20-11
CASE 20-12
CASE 20-13
CASE 20-14
CASE 20-15
CASE 20-16
CASE 20-17
CASE 20-18
CASE 20-19
CASE 20-20
CASE 20-21
CASE 20-22
CASE 20-23
CASE 20-24
CASE 20-25
CASE 20-26
CASE 20-27
Chapter 21 - Intracardiac Echocardiography
TECHNIQUE
SPECIFIC INDICATIONS
REFERENCES
Chapter 22 - Pericardial Diseases
PERICARDIAL EFFUSIONS
PERICARDIAL TAMPONADE
INTRAPERICARDIAL BLOOD CLOT
PERICARDIAL CONSTRICTION
PERICARDIAL CYST
REFERENCES
Chapter 23 - Right Heart Diseases
ECHOCARDIOGRAPHIC FINDINGS IN RIGHT HEART DISEASE
RIGHT VENTRICULAR HYPERTENSION AND PULMONARY HYPERTENSION
RIGHT VENTRICULAR HYPERTROPHY
INFERIOR VENA CAVA DIMENSIONS AND COLLAPSE
INTERVENTRICULAR SEPTAL SHAPE
RIGHT VENTRICULAR VOLUME
TRICUSPID ANNULAR PLANE EXCURSION
RIGHT VENTRICULAR INFARCTION
RIGHT VENTRICULAR DYSPLASIA
PULMONARY EMBOLISM
PRIMARY PULMONARY HYPERTENSION
REFERENCES
Chapter 24 - Cardiac Masses
THORACIC MASSES
INTRAVASCULAR MASSES
CARDIAC NEOPLASMS
BENIGN PRIMARY CARDIAC TUMORS
PRIMARY MALIGNANT CARDIAC TUMORS
INTRACARDIAC THROMBI
REFERENCES
Chapter 25 - Cardiac Trauma
BLUNT CARDIAC TRAUMA
PENETRATING CARDIAC TRAUMA
MISSILES WITHIN THE HEART
BLUNT AORTIC TRAUMA
INDICATIONS FOR TRANSESOPHAGEAL ECHOCARDIOGRAPHY IN CARDIAC TRAUMA
REFERENCES
Chapter 26 - Echocardiographic Guidance of Procedures
JUGULAR VENOUS CANNULATION
ENDOMYOCARDIAL BIOPSY
PERICARDIOCENTESIS
TRANSSEPTAL PUNCTURE
CATHETER MITRAL BALLOON VALVULOPLASTY
PERCUTANEOUS AORTIC VALVULOPLASTY
INTRA-AORTIC COUNTERPULSATION BALLOON TIP LOCALIZATION
SURGICAL VENTRICULAR ASSIST DEVICE PLACEMENT AND FUNCTION
REFERENCES
Index

Citation preview

PRINCIPLES of ECHOCARDIOGRAPHY and INTRACARDIAC ECHOCARDIOGRAPHY Stuart J. Hutchison, md, frcpc, facc, faha Clinical Professor of Medicine University of Calgary; Departments of Cardiac ­Sciences, Medicine, and Radiology Director of Echocardiography Foothills Medical Center Calgary, Alberta, Canada

1600 John F. Kennedy Blvd. Ste 1800 Philadelphia, PA 19103-2899 PRINCIPLES OF ECHOCARDIOGRAPHY AND INTRACARDIAC ECHOCARDIOGRAPHY Copyright © 2012 by Saunders, an imprint of Elsevier Inc. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance ­Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions. This book and the individual contributions contained in it are protected under copyright by the publisher (other than as may be noted herein).

Notice Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility. With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein.

Library of Congress Cataloging-in-Publication Data Hutchison, Stuart J. Principles of echocardiography and intracardiac echocardiography / Stuart J. Hutchison. — 1st ed. p. ; cm. — (Principles of cardiovascular imaging) Includes bibliographical references and index. ISBN 978-1-4377-0403-7 (pbk. : alk. paper) 1. Echocardiography. I. Title. II. Series: Principles of cardiovascular imaging. [DNLM: 1. Echocardiography—methods. 2. Heart Diseases—ultrasonography. WG 141.5.E2] RC683.5.U5H88 2012 616.1′207543—dc23 2011023886

Content Strategist: Dolores Meloni Content Coordinators: Julia Bartz and Bradley McIlwain Publishing Services Manager: Pat Joiner-Myers Project Manager: Marlene Weeks Design Direction: Steven Stave

Printed in China. Last digit is the print number:  9  8  7  6  5  4  3  2  1

ISBN: 978-1-4377-0403-7

To my Cindy, Noel Keith, and Liam James—your gifts of love, time, and belief can only ever be repaid in kind. To our patients, the center of medicine, and the best teachers.

CONTRIBUTORS Michael M. Brook, MD UCSF Medical Center University of California at San Francisco San Francisco, California

Robert Moss, MD University of British Columbia; St. Paul’s Hospital Vancouver, British Columbia, Canada

Dal Disler, RVT University of Calgary; Alberta Children’s Hospital Calgary, Alberta, Canada

Brad Munt, MD University of British Columbia; Cardiologist Department of Echocardiography Heart Failure/Heart Transplant Service St. Paul’s Hospital Vancouver, British Columbia, Canada

Stuart J. Hutchison, MD Clinical Professor of Medicine University of Calgary; Departments of Cardiac Sciences, Medicine, and Radiology Director of Echocardiography Foothills Medical Center Calgary, Alberta, Canada Deborah Isaac, MD Clinical Professor of Medicine University of Calgary; Director Cardiac Transplant Clinics Foothills Medical Center Calgary, Alberta, Canada Mark Johnson, MD University of British Columbia; St. Paul’s Hospital ­Vancouver, British Columbia, Canada Howard Leong-Poi, MD Associate Professor of Medicine University of Toronto; Head Division of Cardiology St. Michael’s Hospital Toronto, Ontario, Canada

Ahmad S. Omran, MD Head Non-Invasive Laboratory King Abdulaziz Medical City Riyadh, Saudi Arabia Grant L. Peters, MD Clinical Assistant Professor Department of Cardiac Sciences Alberta Health Services Calgary, Alberta, Canada Nazmi Said, BSc, RCTA, RDCS Echocardiography Clinical Instructor Education Coordinator Foothills Medical Center Calgary, Alberta, Canada Glen Sumner, MD Assistant Professor of Medicine ­University of Calgary; Foothills Medical Center; Libin Cardiovascular Institute of Alberta Calgary, Alberta, Canada

Phillip Moore, MD Professor of Clinical Pediatrics Department of Cardiology; Director Pediatric Cardiac Catheterization Laboratory UCSF Medical Center University of California at San Francisco San Francisco, California vii

PREFACE For more than two decades, I have aspired to learn the optimal role and contribution of transthoracic and transesophageal echocardiography toward the management of patients with cardiac and aortic disease. Initially, I approached echocardiography as a lot of younger attendings did, as being the “answer” to all questions. At that time, the use of echocardiography had grown rapidly; CT had little to offer for the assessment of cardiac disease; and cardiac MRI was an exotic diagnostic modality of great complexity but that had little availability and minimal involvement in acute cases. At a later juncture, I endeavored to learn cardiac CT and cardiac MRI because they promised more insofar as cardiac and aortic imaging were concerned. CT has grown spectacularly over the past decade, and cardiac MRI has gained clinically powerful and well-validated pulse sequences. As I came to know the three methods with a more balanced approach, investment of time, and level of awareness, I discovered that I wanted to understand none of them as singular diagnostic entities. Rather, I wanted to understand their individual strengths and weaknesses and how they may together afford the best possible means to satisfy the diagnostic needs of all of our cases, especially the most complicated ones. The greater challenge appears to be establishing the boundaries of the contributions of the different modalities, a matter that continues to evolve as the frontiers of each modality progress. Whilst learning cardiac CT and cardiac MRI I gained, by way of relative comparison, a better understanding of, and a definitely renewed appreciation of, what role echocardiography, my first diagnostic modality of interest, affords patients with cardiovascular disease. When on-call after hours, when the sense of medicine is immediate and real—because the clinical stakes of decisions and their consequences are

real—echocardiography is a wonderful diagnostic test to reach for as a means to contribute to the best of our abilities toward patient care.

WITH ACKNOWLEDGMENT AND SINCERE APPRECIATION Sandeep Aggarwal, MD; Junja Ako, MD; Nanette Alvarez, MD; Monica Attwood; Doris Basic, MD; Jason M. Berstein, MD; Daniel Bonneau, MD; John H. Burgess, MD; Patrick Champagne, MD; Kanu Chatterjeee, MBBS; Anson Cheung, MD; Robert J. Chisholm, MD; Tony M. Chou, MD; Michael S. Connelly, MD; Prakash C. Deedwania, MD; Patrick Disney, MD; Lee E. Errett, MD; Neil P. Fam, MD; Quentin Forrest, PhD, MD; David J. Gilmour; Marko S. Hansen, MD; Bryan Har, MD; Michael C. Hartlieb, MD; John Janevski, MD; Sanjeet J. Jolly, MD; Majo Joseph, MBBS; Michael Kanakos, MD; Han Ho Kim, MD; David A. Latter, MD; Yves LeClerc, MD; Howard Leong-Poi, MD; Mat Lotfi, MD; Naeem Merchant, MD; Brad I. Munt, MD; Stuart F. Nicholson, MD; Christopher B. Overguaard, MD; William W. Parmley, MD; Grant L. Peters, MD; Mark D. Peterson, MD, PhD; Geoffrey S. Puley, MD; ­Shahabuddin H. Rahimtoola, MD; Nazmi Said, BSc, RCTA, RDCS; Gary C. Salicidis, MD; ­Nelson B. Schiller, MD; James A. Stewart, MD; ­Kishnankutty Sudhir, MD, PhD; Glen L. Summer, MD; Lisa Tolton; Inga Tomas; Julio F. Tubau, MD; Atul Verma, MD; Ram Vijayaraghavan, MD; John G. Webb, MD; Joel M. Wolkowicz, MD; Richard W. Wright; and Sayeh Zielke, MBA, MD Stuart J. Hutchison

ix

CONTENTS 1

The Aortic Valve

1

2

Aortic Stenosis

18

3

Aortic Insufficiency

42

4

The Mitral Valve

62

5

Mitral Stenosis

68

6

Mitral Insufficiency

90

7

Tricuspid and Pulmonic Valve Disease

119

8

Prosthetic Valves

137

9

Infective Endocarditis

155

10

Echocardiographic Assessment of the Left Ventricle

173

11

Coronary Artery Disease: Ischemia, Infarction, and Complications

201

12

C  oronary Artery Disease: Stress Echocardiography

213

13

C  ardiomyopathies

225

14

D  iastolic Dysfunction and Echocardiographic Hemodynamics

253

15

C  ontrast Echocardiography

271

16

Proximal Isovelocity Surface Area and Flow Convergence Methods

285

17

Echocardiography and Its Role in Cardiac Resynchronization Therapy

299

18

Stress, Strain, Speckle, and Tissue Doppler Imaging: Practical Applications

317

19

Principles of Transesophageal Echocardiography

323

20

Role of Transesophageal Echocardiography in Mitral Valve Repair

337

21

Intracardiac Echocardiography

371





Howard Leong-Poi

Nazmi Said and Dal Disler Glen Sumner

Grant L. Peters

Ahmad S. Omran

Phillip Moore and Michael M. Brook

xi

xii

Contents

22

Pericardial Diseases

387

23

Right Heart Diseases

415

24

Cardiac Masses

441

25

Cardiac Trauma

453

26

Echocardiographic Guidance of Procedures

463



Index

501



Stuart J. Hutchison, Deborah Isaac, Mark Johnson, Robert Moss, and Brad Munt

ONLINE VIDEO CONTENTS The Aortic Valve See Chapter 1

• Bicuspid aortic valve CMR SSFP • Tricuspid aortic valve—TEE with color Doppler • Bicuspid aortic valve—TTE • Bicuspid aortic valve—TEE • Bicuspid aortic valve AI—TTE suprasternal color Doppler • 3D MRA bicuspid aortic valve and aortopathy • TEE LAX color Doppler coarctation Aortic Stenosis See Chapter 2

• TEE AS SAX 1 • AS CMR SSFP Aortic Insufficiency See Chapter 3

• AI • AI • AI • AI

CMR SSFP TTE PLAX color Doppler TTE PSAX color Doppler TTE A3CV color Doppler

Mitral Insufficiency See Chapter 6

• TEE 2D papillary muscle rupture • TEE color Doppler papillary muscle rupture Tricuspid and Pulmonic Valve Disease See Chapter 7

• TTE 4CV color Doppler • TTE 4CV zoom Right Heart Diseases See Chapter 23

• A4CV McConnell • TTE A4CV ventricular interdependence Echocardiographic Guidance of Procedures Stuart J. Hutchison, Deborah Isaac, Mark Johnson, Robert Moss, and Brad Munt See Chapter 26

• Video supplement • Video supplement • Video supplement • Video supplement • Video supplement • Video supplement • Chat 1

1: 3D TEE cross-plane 2: TEE mid-esophageal 3a.: TEE color Doppler long axis 3b. : TEE color Doppler short axis 4a: TEE color Doppler mid-esophageal long axis 4b: TEE color Doppler mid-esophageal short axis

xiii

xiv Online Video Contents • Chat 2 • Chat 3 • Chat 4 • Chat 5 • SHM1: • SHM2: • SHM3: • SHM4: • SHM5: • SHM6: • SHM7:

TEE LVOT TEE guidewire image TEE image guidewire advance TEE image aortic valve TEE image beyond aortic valve Color Doppler post-insertion Color Doppler device on

1

The Aortic Valve

he aortic valve opens and closes through an average of 105,000 cardiac cycles daily, or about 3.5 billion times in a lifetime. Given the systemic arterial pressures it is subjected to through all phases of the cardiac cycle, it is remarkable that most aortic valves function adequately through life.

T

NORMAL AORTIC VALVE ANATOMY The aortic valve is a complex, three-dimensional (3D) structure. In diastole, its three cusps (pockets) swell (fill) like three apposing parachutes to achieve a competent seal. In systole, the three pockets are pushed aside so that they do not impede ventricular ejection. Because the valve is a 3D structure, it may appear in a variety of ways on tomographic imaging modalities, including echocardiography. Normally, the dimensions of the aortic annulus and of the sinotubular junction are nearly identical. From below the valve, the fibrous aortic annulus provides optimal support for the base of the leaflets as well as optimal apposition of the base of the leaflets at the site of their attachment to the aortic wall. From above the valve, the sinotubular junction maintains optimal support (suspension) of the top of the leaflets, transmitted along their commissures to the body of the leaflets. The sinotubular junction also imparts optimal apposition of the upper part of the leaflets, acting essentially as a “supra-annular” support for the valve. The sinotubular junction, the ring-like union of the top of the aortic root sinuses with the ongoing tubular portion of the ascending aorta, is critically important for correct suspension of the aortic valve leaflets. Dilation of the sinotubular junction exerts radial traction on (tethers) the superior part of the aortic cusps, reducing the length of coaptation surface of the aortic valve leaflets and moving the coaptation point higher into the aorta. Excessive dilation of the sinotubular junction compromises coaptation and renders the valve apparatus insufficient, typically through a central regurgitant orifice. Thus, aortic annular dilation comprises aortic cusp coaptation as mitral annular dilation comprises mitral leaflet coaptation, and sinotubular dilation comprises aortic leaflet coaptation as left ventricular (LV) dilation comprises mitral leaflet

coaptation. Dissection and intramural hematoma of the aortic wall into the sinotubular junction or beneath it results in loss of suspension of the adjacent aortic cusp(s), with development of aortic valve prolapse, and insufficiency. The sinuses allow for (1) sufficient systolic excursion of the aortic valve leaflets and (2) a low-pressure zone that facilitates inflow into the coronary ostia by creating flow vortices. The aortic valve is 1.5 to 2.0 cm tall (about 80% of the height of the sinus), with a circumference of 7 to 9 cm. The normal valve is tricuspid with three equal-size cusps. There are one anterior and two posterior (left and right) cusps. The usual nomenclature alludes to the origins of the coronary arteries; hence, the cusps/sinuses of Valsalva are named right (for right coronary; the anterior cusp/sinus), left (for left coronary; the left posterior cusp/sinus), and the noncoronary (right posterior cusp/sinus). The cusps are normally of equal size. They consist of endocardial folds with thin fibrous sheets with small central nodules at their centers. There is a ventricular surface and an arterial surface. The fibrous center is thicker along the free edges, and particularly along the insertion of  the cusp to the wall, allowing maximal flexibility of the body of the cusp. The ventricular surface has three components: (1) a free edge; (2) a thicker closing surface 1 to 2 mm beneath the free edge (i.e., coaptation occurs not along the free edge but underneath it); and (3) the nodule of Arantius (or Morgangi) along the center of the free edge, which may optimize coaptation at the very center of the curving free edge because otherwise the free edge could not achieve a sharp triangular center. The nodule is seldom apparent by imaging other than transesophageal echocardiography (TEE) or cardiac computed tomography (CT). The arterial surface of the cusp forms a pocket— the sinuses of Valslva. The valve annulus is not planar; it consists of three semicircular arcs (open-upwards) that drape from the level of the sinotubular junction down to the base of the body of the cusp. The annulus inserts in its upper part into the sinus wall of the aorta, and at its base inserts into different structures: the right coronary cusp into the muscular septum, the left coronary cusp into the aortomitral fibrosa (“curtain”) that is contiguous with the anterior mitral leaflet (involvement by 1

2

Chapter 1  |  The Aortic Valve

endocarditis of the aortomitral fibrosa portends major clinical risks), and the noncoronary cusp into the interventricular and atrioventricular portions of the membranous septum (hence annulus abscess and rupture can fistulize into the right atrium via the atrioventricular portion of the septum—a Gerbode defect), as well as the mitral annulus. Normally there are three cusps; hence, normally there are three commissures—the lines of diastolic apposition and systolic separation of the cusps. The normal commissures have the following relationships: (1) the right–left commissure abuts the same commissure of the more anteriorly pulmonic valve; (2) the right–noncoronary commissure lies beneath the membranous septum near the His bundle (hence aortic ring abscesses and surgical trauma from aortic valve replacement surgery may result in heart block); and (3) the left–noncoronary commissure abuts the middle part of the anterior mitral leaflet. Normally the noncoronary cusp abuts the interatrial septum via the posterior trigone of fibrous skeleton.

IMAGING THE AORTIC VALVE BY ECHOCARDIOGRAPHY On transthoracic echocardiography, a normal tricuspid aortic valve in diastole (in the parasternal short axis view) appears as three commissures and three cusps, all of equal size, producing an inverted Y ­configuration, popularly (and longingly) referred to as the ­“MercedesBenz sign.” By TEE, the appearance is rotated 30 degrees counterclockwise. The systolic appearance of a normal tricuspid aortic valve is of a rounded triangle whose three sides are the three free edges of the aortic valve. Some congenitally tricuspid aortic valves are composed of cusps of unequal size, with or without degrees of commissural fusion. Not all tricuspid aortic valves are structurally normal, and not all will function normally through life. The appearance of the valve in systole should be scrutinized to determine whether the valve is tri- or bicuspid (the most common congenital malformation of the aortic valve encountered in adulthood). The systolic appearance of a bicuspid valve is not triangular, but, rather, ellipsoid. An ellipsoid appearance of the aortic valve in systole is, as assessed by somewhat dated transthoracic studies, 96% specific and of 93% diagnostic accuracy1 for the bicuspid aortic valve anomaly. The long axis of the ellipse may lie in several possible orientations, of which left-upper to rightlower is the most common. In adults, the orientation has little or no clinical relevance. If only one or two cusps are present, the cusp(s) are predisposed to restriction of their free edge. This restriction results in the systolic doming motion of bicuspid (and unicuspid) valves.

The diastolic appearance of the aortic valve is of little utility in identifying whether the valve has two or three commissures and cusps, because a raphae of the aortic valve may be indistinguishable in diastole from a commissure. A raphae essentially is a commissure, but one that did not divide. The term raphae derives from the Latin word meaning “seam suture, to sew” and refers to any seamlike line or line of union between two similar parts of the body, or, in this case, of the aortic valve. In children, the right–noncoronary fusion subtype of bicuspid aortic valve appears more prone to valvular dysfunction and provides a shorter time to intervention.2 This subtype is the predominant morphology associated with coarctation of the aorta.3

ANATOMIC VARIANTS/ MALFORMATIONS OF THE AORTIC VALVE r Unicuspid

aortic valves are very rare: 1.5:1) formerly were recognized as signs of a bicuspid valve, but neither was of particular sensitivity or specificity. However, obvious eccentric closure by 2D or M-mode imaging should prompt consideration of a bicuspid valve.

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The true bicuspid aortic valve has one (long) commissure, two cusps, and two sinuses of Valsalva. A “functionally” bicuspid valve has a raphae, an incompletely developed commissure that is still fused over part of its length. The residual fusion tends to be thickened. In diastole it may not be distinguishable from a normal commissure. Occasionally, an acquired disease process—especially rheumatic valve disease, but occasionally endocarditis—may result in fusion of a previously functioning commissure, rendering the valve functionally bicuspid.

THE VICISSITUDES OF AGING: AGE-RELATED CHANGES OF THE AORTIC VALVE AND ROOT17 The aortic valve seldom retains pristine architecture in older adults. Typically, lesser degrees of thickening and a more echogenic appearance develop as the valve scleroses. Most of this thickening is wear-andtear injury and response, and occurs most prominently at the line of closure.17 Bright, thin Lambl’s excrescences (fibrous whiskers) on the free edge and the closure line,18 which invariably are directed upward into the aorta and do not have mobility, may develop at advanced age. They have no functional consequence or clinical relevance, but may be a source of confusion with respect to endocarditis. Lambl’s excrescences differ in appearance from vegetations in that they are on the aortic side of the leaflets, whereas vegetations are most commonly on the underside. Lambl’s excrescences have little motion independent from the valve, whereas longer vegetations usually have independent motion. As a result of gradually rising systolic blood pressure through adult life, the diameters of the aortic root and ascending aorta tend to increase. Elongation of the aorta occurs concurrent with age- and hypertension-related diameter increase of the aorta. This elongation often results in a rightward tilt of the root of the aorta with downward protrusion, angling the interventricular septum into a sigmoid shape. Unfolding of the aorta from its normally tight “candy-cane” curvature displaces the aortic root downward into the superior aspects of the atria. Atheromatous disease may extend into the root and onto the aortic valve, thickening both and often making the appearance more echogenic. Age-related sclerosis and atherosclerosis of the aorta and aortic valve are extremely common by the time patients reach their late 70s and 80s. These processes stiffen the aorta, reducing its compliance, and result in a wide pulse pressure and systolic hypertension. The systolic hypertension imparted by a stiffened sclerotic aorta, often associated with a sclerotic aortic valve, is commonly associated with concentric LV hypertrophy.

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Chapter 1  |  The Aortic Valve

SUMMARY r The

anatomy of the aortic valve involves support from below and above, from the annulus and the sinotubular junction, respectively, and the three cusps. Coaptation occurs along a surface beneath the free edge rather than at the edge. A small nodule commonly occurs along the center of the free edge. The mitral-aortic fibrosa joins the aortic annulus to the mitral annulus. r Congenital variants include uni-, bi-, and quadricuspid malformations, all of which can be recognized by echocardiography using specific views and criteria, as may be the associated functional disturbances and complications. r Bicuspid aortic valves are the most common congenital malformation. These are significant for their tendency to degenerate into stenosis (usually), their heritablility, the association with dilation of the ascending aorta, and other extracardiac and intracardiac lesions. Bicuspid aortic valves may occur with two sinuses and one commissure or three sinuses and three cusps, with the commissure between two ­incompletely divided, leaving a “raphae.” r Age-related changes to the aortic valve are inevitable and are seen most prominently in cases with hypertension and atherosclerosis, both of which thicken the valve and result in sclerosis.

REFERENCES 1. Brandenburg Jr RO, Tajik AJ, Edwards WD, et al. Accuracy of 2-dimensional echocardiographic diagnosis of congenitally bicuspid aortic valve: echocardiographicanatomic correlation in 115 patients. Am J Cardiol. 1983; 51(9):1469–1473. 2. Fernandes SM, Khairy P, Sanders SP, Colan SD. Bicuspid aortic valve morphology and interventions in the young. J Am Coll Cardiol. 2007;49(22):2211–2214. 3. Fernandes SM, Sanders SP, Khairy P, et al. Morphology of bicuspid aortic valve in children and adolescents. J Am Coll Cardiol. 2004;44(8):1648–1651. 4. Herman RL, Cohen IS, Glaser K, Newcomb III EW. Diagnosis of incompetent quadricuspid aortic valve by two-dimensional echocardiography. Am J Cardiol. 1984; 53(7):972. 5. Butany J, Collins MJ, Demellawy DE, et  al. Morphological and clinical findings in 247 surgically excised native aortic valves. Can J Cardiol. 2005;21(9):747–755. 6. Hwang DM, Feindel CM, Butany JW. Quadricuspid semilunar valves: report of two cases. Can J Cardiol. 2003;19(8):938–942. 7. Movahed MR, Hepner AD, Ahmadi-Kashani M. Echocardiographic prevalance of bicuspid aortic valve in the population. Heart Lung Circ. 2006;15(5):297–299.

8. Basso C, Boschello M, Perrone C, et al. An echocardiographic survey of primary school children for bicuspid aortic valve. Am J Cardiol. 2004;93(5):661–663. 9. Cripe L, Andelfinger G, Martin LJ, et al. Bicuspid aortic valve is heritable. J Am Coll Cardiol. 2004;44(1): 138–143. 10. Roberts WC, Morrow AG, McIntosh CL, et  al. Congenitally bicuspid aortic valve causing severe, pure ­aortic regurgitation without superimposed infective endocarditis. Analysis of 13 patients requiring aortic valve replacement. Am J Cardiol. 1981;47(2):206–209. 11. Hahn RT, Roman MJ, Mogtader AH, Devereux RB. Association of aortic dilation with regurgitant, stenotic and functionally normal bicuspid aortic valves. J Am Coll Cardiol. 1992;19(2):283–288. 12. Morgan-Hughes GJ, Roobottom CA, Owens PE, ­Marshall AJ. Dilatation of the aorta in pure, severe, bicuspid aortic valve stenosis. Am Heart J. 2004;147(4):736–740. 13. Lindsay Jr J. Coarctation of the aorta, bicuspid aortic valve and abnormal ascending aortic wall. Am J Cardiol. 1988;61(1):182–184. 14. Januzzi JL, Isselbacher EM, Fattori R, et al. Characterizing the young patient with aortic dissection: results from the International Registry of Aortic Dissection (IRAD). J Am Coll Cardiol. 2004;43(4):665–669. 15. Stewart WJ, King ME, Gillam LD, et  al. Prevalence of aortic valve prolapse with bicuspid aortic valve and its relation to aortic regurgitation: a cross-sectional echocardiographic study. Am J Cardiol. 1984;54(10):1277–1282. 16. Zema MJ, Caccavano M. Two dimensional echocardiographic assessment of aortic valve morphology: feasibility of  bicuspid valve detection. Prospective study of 100 adult patients. Br Heart J. 1982;48(5):428–433. 17. Sahasakul Y, Edwards WD, Naessens JM, Tajik AJ. Age-related changes in aortic and mitral valve thickness: implications for two-dimensional echocardiography based on an autopsy study of 200 normal human hearts. Am J Cardiol. 1988;62(7):424–430. 18. Hurle JM, Garcia-Martinez V, Sanchez-Quintana D. Morphologic characteristics and structure of surface excrescences (Lambl’s excrescences) in the normal aortic valve. Am J Cardiol. 1986;58(13):1223–1227. 19. Douglas PS, Garcia MJ, Haines DE, et  al. ACCF/ ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/ SCCT/SCMR 2011 appropriate use criteria for echocardiography. J Am Coll Cardiol. 2011;57(9):1126–1166. 20. Cheitlin MD, Chair JS, Alpert JS, et  al. ACC/AHA guidelines for the clinical application of echocardiography: a report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines (Committee on Clinical Application of Echocardiography). Circulation. 1997;95:1686–1744. 21. Bonow RO, Blase AC, Chatterjee K, et al. ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2006;114: e84–e231. 22. Taylor AJ, Cerqueira M, Hodgson JM, et  al. ACCF/ SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/ SCMR 2010 appropriate use criteria for cardiac computed tomography. J Am Coll Cardiol. 2010;56(22): 1864–1894.

The Aortic Valve  |  Chapter 1 23. Hendel RC, Manesh PR, Kramer CM, Poon M. ACCF/ACR/SCCT/SCMR/ASNC/NASCI/SCAI/ SIR 2006 appropriateness criteria for cardiac computed tomography and cardiac magnetic resonance imaging. J Am Coll Cardiol. 2006;48(7):1475–1497. 24. Pennell DJ, Sechtem UP, Higgins CB, et  al. Clinical indications for cardiovascular magnetic resonance (CMR): Consensus Panel report. J Cardiovasc Magn Reson. 2004; 6(4):727–765. 25. Hendel RC, Berman DS, Di Carli MF, et  al. ACCF/ ASNC/ACR/AHA/ASE/SCCT/SCMR/SNM

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2009 appropriate use criteria for cardiac radionuclide ­imaging. J Am Coll Cardiol. 2009;53(23):2201–2229. 26. Nishimura RA, Carabello BA, Faxon DP, et al. ACC/ AHA 2008 guideline update on valvular heart disease: focused update on infective endocarditis: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol. 2008;52:676–685.

BOX 1-1  Bicuspid Aortic Valve with Dilated Ascending Aorta: ACC/AHA 2006 Recommendations Class I 1. Patients with known bicuspid aortic valves should undergo an initial transthoracic echocardiogram to assess the diameters of the aortic root and ascending aorta. (Level of evidence: B) 2. Cardiac MRI or cardiac CT scanning is indicated in patients with bicuspid aortic valves when morphology of the aortic root or ascending aorta cannot be assessed accurately by echocardiography. (Level of evidence: C) 3. Patients with bicuspid aortic valves and dilation of the aortic root or ascending aorta (diameter >4.0 cm) should undergo serial evaluation of aortic root/ ascending aorta size and morphology by echocardiography, cardiac MRI, or CT on a yearly basis. (Level of evidence: C) 4. Surgery to repair the aortic root or replace the ascending aorta is indicated in patients with bicuspid aortic valves if the diameter of the aortic root or ascending aorta is greater than 5.0 cm or if the rate of increase in diameter is 0.5 cm per year or more. (Level of evidence: C) 5. In patients with bicuspid valves undergoing AVR because of severe aortic stenosis or aortic ­regurgitation, repair of the aortic root or replacement of the ascending aorta is indicated if the diameter of the aortic root or ascending aorta is greater than 4.5 cm.    (Level of evidence: C) From ACC/AHA 2006 guidelines for the management of patients with valvular heart disease. Circulation. 2006;114(5):e84–e231.

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Chapter 1  |  The Aortic Valve

BOX 1-2  Appropriateness Criteria and Indications for Cardiac Imaging Modalities for the Assessment of Aortic Valve Morphology* TRANSTHORACIC ECHOCARDIOGRAPHY ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/ SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography 19 For Murmur or Click with TTE n Initial evaluation when there is a reasonable suspicion of valvular or structural heart disease Appropriateness criteria: A; median score: 9 n Initial evaluation when there are no other symptoms or signs of valvular or structural heart disease Appropriateness criteria: I; median score: 2 n Re-evaluation in a patient without valvular disease on prior echocardiogram and no change in clinical status or cardiac examination Appropriateness criteria: I; median score: 1 n Re-evaluation of known valvular heart disease with a change in clinical status or cardiac examination or to guide therapy Appropriateness criteria: A; median score: 9 Adult Congenital Heart Disease n No specific mention of bicuspid aortic valves Initial evaluation of known or suspected adult ­congenital heart disease Appropriateness criteria: A; median score: 9 ACC/AHA/ASE 2003 Guideline Update for the Clinical Application of Echocardiography n No specific mention of bicuspid aortic valves Recommendations for Echocardiography in the Evaluation of Patients with a Heart Murmur n Class I • A patient with a murmur and cardiorespiratory symptoms • An asymptomatic patient with a murmur in whom clinical features indicate at least a moderate probability that the murmur is reflective of structural heart disease n Class IIa • A murmur in an asymptomatic patient in whom there is a low probability of heart disease, but in whom the diagnosis of heart disease cannot be reasonably excluded by the standard cardiovascular clinical evaluation n Class III • In an asymptomatic adult, a heart murmur that has been identified by an experienced observer as functional or innocent TRANSESOPHAGEAL ECHOCARDIOGRAPHY ACCF/ASE/ACEP/ASNC/SCAI/SCCT/SCMR 2011 Appropriateness Use Criteria for Echocardiography19 TEE as Initial or Supplemental Test—General Uses n Use of TEE when there is a high likelihood of a nondiagnostic TTE due to patient characteristics or inadequate visualization of relevant structures Appropriateness criteria: A; median score: 8

Recommendations for Echocardiography in the Adult Patient with Congenital Heart Disease n Class I • Patients with clinically suspected congenital heart disease, as evidenced by signs and symptoms such as a murmur, cyanosis, or unexplained arterial desaturation, and an abnormal ECG or radiograph suggesting congenital heart disease • Patients with known congenital heart disease on follow-up when there is a change in clinical findings • Patients with known congenital heart disease for whom there is uncertainty as to the original diagnosis or when the precise nature of the structural abnormalities or hemodynamics is unclear n Class IIb • A follow-up Doppler echocardiographic study, annually or once every 2 years, in patients with known hemodynamically significant congenital heart disease without evident change in clinical condition n Class III • Multiple repeat Doppler echocardiography in patients with repaired patent ductus arteriosus, atrial septal defect, ventricular septal defect, coarctation of the aorta, or bicuspid aortic valve without change in clinical condition ACC/AHA 1997 Guideline Update for the Clinical Application of Echocardiography 20 n No specific mention of evaluation of bicuspid aortic valve malformations ACC/AHA 2006 Guidelines for the Management of Patients with Valvular Heart Disease 21 n With respect specifically to the evaluation of bicuspid aortic valve malformations • Patients with known bicuspid aortic valves should undergo an initial TTE echocardiogram to assess the diameters of the aortic root and ascending aorta. (Class I; level of evidence: B) n Indications for echocardiography in the evaluation of heart murmurs • A murmur in an asymptomatic patient if the clinical features indicate at least a moderate probability that the murmur is reflective of structural heart disease. (Class I)

n Routine use of TEE when a diagnostic TTE is reasonably anticipated to resolve all diagnostic and management concerns Appropriateness criteria: I; median score: 1

  

The Aortic Valve  |  Chapter 1

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BOX 1-2  Appropriateness Criteria and Indications for Cardiac Imaging Modalities for the Assessment of Aortic Valve Morphology*—cont’d CARDIAC COMPUTED TOMOGRAPHY ACCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/SCMR 2010 Appropriate Use Criteria for Cardiac CT 22 n Characterization of native cardiac valves Suspected clinically significant valvular dysfunction Inadequate images from other noninvasive methods Appropriateness criteria: A; median score: 8 ACC/AHA 2006 Guidelines for the Management of Patients with Valvular Heart Disease 23 n With respect specifically to the evaluation of bicuspid aortic valve malformations CARDIAC MAGNETIC RESONANCE IMAGING ACCF/ACR/SCCT/SCMR/ASNC/NASCI/SCAI/SIR 2006 Appropriateness Criteria for Cardiac Magnetic Resonance Imaging 23 n Characterization of native and prosthetic cardiac valves—including planimetry of stenotic disease and quantification of regurgitant disease Patients with technically limited images from echocardio­graphy or TEE Appropriateness criteria: A; median score: 8 SCMR Consensus Panel Report: Indication for Cardiac Magnetic Resonance Imaging 24 n For bicuspid aortic valves (Class II)



• Cardiac MRI or cardiac CT is indicated in patients with bicuspid aortic valves when morphology of the aortic root or ascending aorta cannot be assessed accurately by echocardiography. (Class I; level of evidence: C) n Cardiac MRI or cardiac CT is reasonable in patients with bicuspid aortic valves when aortic root dilation is detected by echocardiography to further quantify severity of dilatation and involvement of the ascending aorta. (Class IIa; level of evidence: B)

ACC/AHA 2006 Guidelines for the Management of Patients with Valvular Heart Disease 21 n With respect specifically to the evaluation of bicuspid aortic valve malformations • Cardiac MRI or cardiac CT is indicated in patients with bicuspid aortic valves when morphology of the aortic root or ascending aorta cannot be assessed accurately by echocardiography. (Class I; level of evidence: C) n Cardiac MRI or cardiac CT is reasonable in patients with bicuspid aortic valves when aortic root dilatation is detected by echocardiography to further quantify severity of dilatation and involvement of the ascending aorta. (Class IIa; level of evidence: B)

NUCLEAR ACCF/ASNC/AHA/ASE/SCCT/SCMR/SNM 2009 Appropriate Use Criteria for Cardiac Radionuclide Imaging 25 n No specific mention of bicuspid aortic valves OTHER ACC/AHA 2008 Guidelines on Valvular Disease: Focused Update on Endocarditis 26 Management of Congenital Valvular Heart Disease in Adolescents and Young Adults n Antibiotic prophylaxis is no longer indicated in the adolescent and young adult with native heart valve disease for prevention of infective endocarditis.

ACC/AHA 2008 Guideline Update on Valvular Heart Disease: Focused Update on Infective Endocarditis 26 n In select circumstances, the committee also understands that some clinicians and some patients may still feel more comfortable continuing with prophylaxis for infective endocarditis, particularly for those with bicuspid aortic valve or coarctation of the aorta, severe mitral valve prolapse, or hypertrophic obstructive cardiomyopathy. In those settings, the clinician should determine that the risks associated with antibiotics are    low before continuing a prophylaxis regimen.

Appropriateness criteria: A, appropriate; I, inappropriate; U, uncertain. TEE, transesophageal echocardiography; TTE, transthoracic echocardiography. *See Chapter 2 for appropriateness of cardiac imaging modalities for the assessment of aortic stenosis and Chapter 3 for the appropriateness of cardiac imaging modalities for the assessment of aortic insufficiency.

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Chapter 1  |  The Aortic Valve

TABLE 1-1  U  tility of Different Imaging Modalities and Cardiac Catheterization in the Assessment of Aortic Valve Morphology and Related Disturbances and Associations MODALITY

PROS

CONS/CAVEATS

Transthoracic Echocardiography

• 2D short-axis imaging in systole, if the images are clear, can detect most bicuspid aortic valves by their elliptical orifice (78% sensitive, 96% specific). • Doppler echocardiography can assess functional disturbance of the aortic valve. • Can depict bicuspid aortic valve associated aortopathy and coarctation

• Inability to sufficiently image the aortic valve occurs (15–20% of adult cases)

Transesophageal Echocardiography

• 2D short-axis imaging (30°–50°) in systole can reliably depict most bicuspid (>95%) aortic valves by their ellipitical orifice. • Doppler echocardiography can assess functional disturbance of the aortic valve. • Can well depict bicuspid aortic valve–associated aortopathy, coarction, and dissection

• Patient discomfort/semiinvasive

Cardiac CT

• ECG-gated contrast-enhanced cardiac CT can yield excellent images of the valve morphology, but the images must include systolic phase. • An excellent means to depict associated aortopathy, coarction, and dissection

• Radiation • Motion sensitive imaging • Calcium is overrepresented, and may “bloom.” • Cannot provide functional assessment

Cardiac MRI

• SSFP sequences are able to depict the aortic valve morphology well (>95%). • SSFP sequences and MR aortography can well depict associated aortopathy, coarctation, and dissection. • Phase contrast sequences can quantify bicuspid aortic valve–associated aortic insufficiency.

• Motion sensitive imaging • Calcium appears as signal voids.

Chest Radiography

Can demonstrate heart failure and some findings of bicuspid aortic–valve associated aortopathy.

—

Cardiac Catheterization

• Cardiac catheterization with left ventriculography can reveal doming of the aortic valve leaflets consistent with bicuspid morphology. • Calcification is readily appreciated by fluoroscopy. • Contrast aortography is a standard and excellent means to identity • Associations of bicuspid aortic valves such as aneurysms and especially coarctation • Complications such as aortic valve stenosis, aortic insufficiency, and aortic dissection

• Not a standard test to assess aortic valve morphology

2D, two dimensional; ECG, electrocardiographic; SSFP, steady-state free precession.

The Aortic Valve  |  Chapter 1

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Figure 1-1.  Examples of bicuspid valves, seen in short-axis echocardiography. Upper left (tranesophageal echocardiography [TEE] view): Bicuspid valve with an elliptical orifice and two sinuses. Upper right (TEE view): Bicuspid valve with a triangular orifice, and two sinuses. Middle left (transthoracic echocardiography [TTE] view): Bicuspid valve with an elliptical orifice and two sinuses. Middle right (TTE view): Bicuspid valve with an elliptical orifice and three sinuses/raphae. Lower left (TTE view): Bicuspid valve with an elliptical orifice with two sinuses. Lower right (TTE view): “Functionally bicuspid” (acquired bicuspid) morphology resulting from rheumatic disease fusing the left posterior commissure creating a left posterior raphae. Note also the dilated left atrium from mitral stenosis, this patient’s predominant disease.

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Chapter 1  |  The Aortic Valve

Figure 1-2.  Neonate with unicuspid aortic valve stenosis. Upper left: Posterior long-axis view shows doming of the aortic valve. Upper right: Posterior shortaxis view demonstrates an eccentric orifice. Lower left: A long-axis view depicting doming of the valve. Lower right: Color Doppler flow mapping reveals proximal isovelocity surface area before the doming valve, consistent with flow acceleration before aortic stenosis.

Figure 1-3.  Transesophageal echocardiography images of a quadricuspid aortic valve in diastole (left) and systole (right).

The Aortic Valve  |  Chapter 1

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Figure 1-4.  Examples of infective complications of bicuspid valves seen on transesophageal echocardiography. Upper left: Long-axis view reveals doming of a bicuspid valve that is not infected. Upper right: Long-axis view shows vegetation on the anterior leaflet of the aortic valve. Lower left: Short-axis view shows vegetations rendering the free edge of the bicuspid valve shaggy in appearance. Lower right: Short-axis (another patient): shows vegetation at the right aspect of the commissure.

Figure 1-5.  Examples of distal aortic associations and complications of bicuspid valves. Upper left: Long-axis transesophageal echocardiography view of the proximal descending aorta shows a “waist-like” narrowing of the aorta, consistent with coarctation. Upper right: Flow convergence and associated jet. Lower left: A very narrow site of coarctation and then a ballooning of the post-coarctation aorta are seen. Lower right: Associated jet emerging from the coarctation.

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Chapter 1  |  The Aortic Valve

Figure 1-6.  Examples of proximal aortic associations of bicuspid valves. Upper left: Long-axis transesophageal echocardiography (TEE) view shows doming of a bicuspid valve and aneurysmal dilation of the sinuses, a less common level of dilation of the aorta (than the ascending aorta) associated with bicuspid aortic valves. Upper right: Parasternal long-axis TEE view shows an aneurysm of the ascending aorta above the sinuses of Valsalva, which is more commonly associated with bicuspid aortic valves. Lower left: Long-axis TEE view of the ascending aorta shows a linear intimal flap in an aneurysmal ascending aorta. Lower right: Aortographic view in the same patient as bottom left image shows an aneurysm of the aorta above the sinuses of Valsalva, with a medial linear intimal flap with vertical orientation.

Figure 1-7.  Lambl’s excrescences on the aortic valve. Fine “whisker-like” excrescences are seen pointing upward and arising from the free edge of the valve.

The Aortic Valve  |  Chapter 1

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Figure 1-8.  Transthoracic (top) and transesophageal (bottom) images of the same patient with a bicuspid valve. The left images are diastolic and the right images are systolic. Despite the use of zoom views of the aortic valve, transthoracic echocardiography is in this case incapable of affording clear enough images to determine the morphology of the valve. Transesophageal images reliably determine the aortic valve morphology by using short-axis images between 30 and 70 degrees rotation.

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Chapter 1  |  The Aortic Valve

Figure 1-9.  Transesophageal images of a tricuspid aortic valve in diastole (top) and systole (bottom). In both systole and diastole the three aortic sinuses are evident. It is only in systole, however, that the triangular orifice of the aortic valve is apparent, establishing its trileaflet morphology.

The Aortic Valve  |  Chapter 1

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Figure 1-10.  Age-related changes. The chest radiograph (left) is notable for extensive calcific plaques in the aorta seen best at the arch level, where they project largely tangentially. The parasternal long-axis echo image (upper right) reveals sclerosis of the aortic and mitral valves, some mitral calcification, and sclerosis or atherosclerosis of the aorta. There is concentric left ventricular hypertrophy (LVH) of the left ventricle. The spectral Doppler image of left ventricular inflow (lower right) reveals summation of the E and A waves, with A wave dominance consistent with the impaired relaxation pattern of diastolic dysfunction, typical of LVH due to hypertension. Calcification of the aorta diminishes the aorta’s compliance, resulting in systolic hypertension, which then incites LVH, with its diastolic dysfunction.

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Chapter 1  |  The Aortic Valve

Figure 1-11.  Transthoracic (top), transesophageal (middle), and cardiac steady-state free precession MRI (bottom) images. Left panels are systole images; right panels are diastole images. The bicuspid nature of the valves is apparent on all three forms of imaging.

The Aortic Valve  |  Chapter 1

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Figure 1-12.  Ascending aortic dilation and very mild coarctation of the aorta (“aortopathy”) associated with bicuspid aortic valvulopathy. Upper images: Transthoracic views obtained from the supersternal position. Color Doppler flow mapping (upper left) reveals flow convergence in the isthmus portion of the descending aorta. Spectral Doppler (upper right) demonstrates mild flow acceleration and also spectral broadening, consistent with a mild gradient. Middle images: Long-axis 2D transesophageal echocardiography images with color Doppler flow mapping reveal a near-field fold, or shelf, in the aorta with some flow convergence depicted as a result. Continuous wave Doppler sampling (middle left) at the site of flow convergence yields a similar-shaped spectral profile to that obtained by transthoracic echocardiography (middle right); due to less than optimal alignment, however, it has undersampled the true velocity. Lower images: Magnetic resonance imaging. Lower left: The contrast-enhanced aortic MR aortogram nicely depicts the shape and course aorta and its branches. Only a mild degree of coarctation is present. The fold in the proximal descending aorta is well depicted. Lower right: Steady-state free precession sequence reveals mild dilation of the ascending aorta and mild coarctation. This view, however, overdepicts the severity of the coarctation, because the plane of imaging is not through the center line of the aorta.

2

Aortic Stenosis

iven the prevalence of valvar aortic stenosis (AS), its huge clinical burden, and the impressive salvage rate with surgical valve replacement, and now with percutaneous valve replacement, identification and description of AS is a prime application of echocardiography. It is also one of the most elegant and relevant applications of Doppler physics in the evaluation of cardiac disease. Although the basic principles of gradient and area determination are simple, the disease of AS and its innumerable permutations are not, and neither are the subtleties of testing that are responsible for many instances of discordance between different modalities. Rigorous attention to scanning details is paramount, as is proficiency with both noninvasive and invasive aortic valve assessment of hemodynamics, and the ability to navigate discordance with catheterizationderived estimates of aortic stenosis.

G

GOALS OF ECHOCARDIOGRAPHY IN AORTIC STENOSIS r To r To

determine that aortic stenosis is present determine the level(s) of obstruction/stenosis (valvar versus other) r To determine the hemodynamic severity of the aortic stenosis r To assess the regional and overall left ventricular (LV) function carefully r To determine the stroke volume r To assess for bicuspid valve anomaly, its associations, and its complications

SCANNING ISSUES Required Parameters to Obtain from Scanning

Valve parameters r Morphology (bicuspid?)—use a zoom view, focus in systole r Mean gradient, V1, V2 r Severity of associated aortic insufficiency r Left ventricular outflow tract (LVOT) diameter 18

LV parameters r Stroke volume r Ejection fraction (EF) or “grade” of dysfunction r Wall motion abnormalities Aortic diameters r Sinotubular junction (STJ) level (more pressure recovery when STJ is 1.5 m/sec) is likely, record the pre-subvalvar flow velocity, the pre-valvar velocity (V1), and also the V2. The modified Bernouilli equation should not be used if V1 is ≥1.5 m/sec. r AVA calculations traditionally are made from integrals; peak velocities are a surrogate, although a reasonably accurate one. r If sinus rhythm: measure three spectral profiles. r If in atrial fibrillation: measure five spectral profiles. r If in the idea world: measure ten spectral profiles. r Annotate the site of sampling for future reference comparison. Confounders r Verify whether there is/is not concurrent intra­ cavitary flow acceleration (subaortic valve velocity ≥ 1.5 m/sec), as discussed in the following section. r A narrow aortic root (STJ ≤ 30 mm): a narrow aorta facilitates the “pressure recovery” phenomenon that detects a higher gradient than the recovered gradient measured by catheterization.

EQUATIONS r Continuity

equation:

AVA = (CSALVOT × VTILVOT ) / VTIAV r Velocity

ratio (VR) equation: VR = VLVOT / VAV

r Mean

r LV

gradient equation: ∑ ΔP = 4V2/N

stroke work loss (LVSWL) equation:

LVSWL = AVGmean × (AVGmean + SBP) × 100

where AVG = average gradient, CSA = cross-sectional area, SBP = systolic blood pressure, and VTI = ­velocity time integral.

PATHOPHYSIOLOGY AND FINDINGS OF AORTIC STENOSIS The fundamental pathophysiology of AS is the excess pressure imposed on the LV, known as pressure overload.

19

Secondarily, or indirectly, a lesser pressure load is imposed on the LA by diastolic failure of the LV. The LV response to pressure overload—concentric hypertrophy— is adaptive; it normalizes the wall stress on myocytes, but it is physiologically expensive. Essentially, the wall thickness increases in proportion to the pressure increase. Laplace’s law states that wall stress (i.e., myocyte stress) is proportional to intracavitary pressure and radius, and inversely proportional to wall thickness. Therefore, if the proportional increase in LV wall thickness is the same as the proportional increase in left ventricular pressure (due to imposition of the transvalvar gradient), then wall stress is normalized, and myocyte preservation is facilitated. The pattern of hypertrophy in AS is typical of pressure overload, therefore, and should be present in most cases of severe AS. In concentric hypertrophy, myocardial sarcomeres replicate in parallel; therefore the walls thicken and the cavity dimensions do not increase (in fact, they often decrease). Therefore, the pattern is thick walls and no increase in cavitary dimensions, unless complications arise, or the disease is in a terminal state. In severe AS, where the systolic pressure within the LV doubles, LV mass essentially doubles (increases to 178 g/m2 vs. normal of 86 g/m2),1 due to near ­doubling of the wall thickness to normalize wall stress that otherwise would be nearly doubled (Fig. 2-1). Given the increase in both myocardial mass and generated systolic pressure, myocardial O2 demand increases (mVO2 ∝ LV mass, developed systolic pressure, contractility, and heart rate). In AS, coronary flow (supply) is a problematic issue that compounds the potential problem of increased demand; about half of adult patients with AS have concurrent coronary artery disease (CAD). Severe AS may remain seemingly static and compensated for years, or may progress. The rate of progression depends on many factors, few of which are well understood. Progression rates between –0.01 cm2/ year and –0.1 cm2/year have been described. Calcification of the aortic valve is somewhat predictive of a faster rate of progression, but it is not known how to quantify calcification toward this purpose. Electron beam CT studies have not shown good correlation of calcification quantification by Agatston score with aortic valve area, especially for moderate and severe AS.2 Both increasing left ventricular systolic pressure and LV hypertrophy impair LV compliance; left atrial hypertrophy and augmented atrial systolic function occur to maintain left ventricular filling. In severe AS, the left atrium typically is mildly enlarged. In summary, the pathophysiology of severe AS generates expected findings: increased wall thickness, no increase in left ventricular cavitary size, and left atrial dilation. An increase in cavitary size requires additional explanation, such as concurrent volume overload from aortic insufficiency or mitral regurgitation, impaired systolic function from CAD or cardiomyopathy, or terminal decompensated AS.

20

Chapter 2  |  Aortic Stenosis

ROLE OF TRANSESOPHAGEAL ECHOCARDIOGRAPHY IN AORTIC STENOSIS There is no routine role for TEE in the assessment of AS. A minor role for TEE is in cross-sectional imaging of the aortic valve, in cases where the severity of the stenosis is unclear, to enable planimetry for valve area—but this assumes that the orifice is planar, which is a considerable assumption. TEE is a technically demanding and difficult means by which to sample aortic valve gradients. TEE Doppler sampling from the lower esophagus is never acceptably aligned; deep retroflexed transgastric five-chamber sampling is validated to detect the gradient accurately, but is prone to misalignment and under-sampling in unpracticed hands. TEE probably is the best test available to image subvalvar lesion morphology in detail. TEE assumes an important useful role intraoperatively to validate the preoperative diagnosis of severe AS; identify or exclude complications, associations, and confounders; and verify successful aortic valve replacement. TEE is a standard test prior to percutaneous aortic valve replacement (AVR) (see Chapter 26) and optimally is used to determine the size of the prosthesis and the morphology of the annuli, valve, and root.

REPORTING ISSUES Aortic valve gradient is a per-beat (volume) function. The gradient of aortic stenosis occurs through the systolic ejection period. The mean gradient is the most suitable expression of the average pressure load imposed on the LV through this period. The gradient reflects both the severity of the impedance to ejection (imparted by the aortic valve) and the function of the LV. The expression of LV function that is most germane to aortic stenosis is the stroke volume, not the EF or CO.

Gradient Issues

When reporting, the combination of mean gradient and stroke volume must be emphasized. For example: “The mean gradient is 65 mm Hg with a normal stroke volume of 75 mL.” Normal stroke volume index is 45 ± 13 mL/m2. It is not necessary to describe the peak instantaneous gradient; this just generates unjustifiable confusion with the (different) catheterizationderived peak-to-peak gradient, and is not the criterion for severity. Gradients, valve area, and LV function must be compared to previous determinations. If there is a difference in the gradient, ensure that the recording was obtained from a comparable sampling site. It is important to enter annotations (e.g., apical, right parasternal, suprasternal) on all spectral Doppler recordings, to make appropriate comparisons possible.

Gradients may be enhanced by numerous factors, only a few of which may be apparent when reading an echocardiogram. Factors that increase the aortic valve grad­ ient include the following: r Bradycardia in the context of normal LV function or contractile recruitment r Causes of larger stroke volume ± lower peripheral resistance • Anemia • Fever • Thyrotoxicosis • Pregnancy • Large dialysis fistulae • Inotropic stimulation • Peripheral vasodilation r Undersampling of the V2 spectral profile is a ­common clinical problem, as the spectral profile boundary may be vague. • If the sampling appears incomplete (i.e., not a full parabola), appropriate efforts must be made to try to obtain it. • Equally important is that the report does not convey that the real gradient was only as low as it was sampled to be, when the sampling was clearly incomplete. r Fewer than 5% of cases of AS will have inadequate spectral profiles; the percentage is very much determined by the time and effort made to acquire the spectral recording. r Adequate spectral profiles are complete and plausible parabolic profiles. r If the peak velocity is to be marked with cross-hairs, the cross-hairs should not be placed on the peak of a spectral profile, because that may falsely confer an impression of the true peak to the reviewer. The cross-hairs should be placed off to the side of the presumed peak to allow the reviewing or reporting physician to establish independently that the peak was true, as a useful internal check. r If the profile initially does not appear complete, persistence in attempting better ones is required, as there is a (albeit diminished) return. Techniques that should be used include the following: • Use of the “stand-off ” probe • Sampling from several parasternal, supraclavicular, and suprasternal sites • Variable positioning of the patient • Use of the most experienced sonographer r The published correlation of Doppler versus catheterization mean gradients averages 0.90,3,4 but importantly, 1 standard error of estimate (SEE) of Doppler gradient versus catheterization gradient is actually 10 mm Hg [SEE range, 6–12 mm Hg].5 r Rahimtoola5 emphasized consideration of the SEE by Doppler when describing AS severity (by gradient): • Highly likely severe: mean gradient >  70 mm Hg • Probably  severe:  mean  gradient  >  60  and 10 mm Hg in the gradient recording from a femoral sidearm. r Low-gradient AS should be reported as a possibility or probability, depending on how strongly it is believed to be present. r Valve resistance has been proposed as a means of establishing the severity of AS (>300 dynes/ sec/cm−5 = severe disease) that is independent of flow output, but it has not been proved to be better than valve area calculation,9 nor has it been popular. It appears less useful than LVSWL.6 r Determination of contractile reserve in low-gradient severe AS cases • Consideration of pharmacologic stress (dobutamine up to 20 μg/min/m2) • Determination of AVG and AVA in suspected cases of low-gradient AS (exercise or dobutamine) via echocardiography or catheterization to increase stroke volume by more than 20% and cardiac output (CO) to 4.5 L/min in non-­coronary cases is reasonable. The gradient changes can be interpreted in the context of the change of the stroke volume across the valve. • If stroke volume increases and the AVA increases outside the severe range, then the cause of the low gradient was low output (i.e., pseudostenosis), but the AS is not severe. • If the stroke volume increases but the AVA remains within the severe range, then the AS is severe (and pseudostenosis is not present). • However, AVR reduces mortality whether or not there is contractile reserve, and medical therapy is a poor option whether or not there is contractile reserve. Therefore, provocative testing should be done, although it has not been unequivocally proven to be helpful.9,13

Aortic Stenosis  |  Chapter 2

• Rahimtoola15 would caution that changes in stroke volume are labeled as an index of contractility and as the hemodynamic responses to dobutamine are complex. r In cases of suspected low-gradient severe AS, ­particular scrutiny should be afforded to the size of the aortic annulus/root. If the root is unusually small (e.g., 19–20 mm), then the size of prosthesis that would be implanted would confer a moderate gradient, which might be little different from the preoperative gradient.

DISCORDANCE OF CATHETERIZATION AND ECHOCARDIOGRAPHIC DETERMINATION OF THE SEVERITY OF AORTIC STENOSIS When catheterization and echocardiographic assessments of the hemodynamics of AS differ, either test may be in error, both may be correct, or both may be wrong. Whenever there is discordance, each test should be scrutinized for potential errors in recording, calculation, or interpretation.

Possible Reasons for Discordance of Catheterization and Echocardiographic Determination of the Severity of Aortic Stenosis r Recall

that nonsimultaneous (echocardiographic and catheterization) estimates of gradient and area are obviously likely to differ more as stroke volume (cardiac output) and peripheral load is variable over time. r Recall that the published SEE of Doppler gradients versus catheterization gradients averages 10 mm Hg. r Recall that the published SEE of Doppler AVA versus catheterization gradients is about 0.3 cm2. r Recall that the following invariably reduce the accuracy of echocardiographic estimates of AVG and AVA: • Measuring  1.5 m/sec • Must be analyzed in the context of the total forward stroke volume (normal stroke volume index = 45 ± 13 mL/m2) • Prone to undersampling • Pressure recovery within a small aortic root may yield a higher mean gradient than is appreciated by catheterization. • Less suited to low-flow states

• TEE short-axis planimetry to measure the orifice area offers the best echocardiographic means to establish AVA by flow- and Dopplerindependent means. Short-axis planimetry has been validated by generally small series that demonstrate high feasibility (93%), except when the orifice is “pin-hole.” Correlation with Gorlin determinations of AVA is excellent: r = 0.95; with 96% sensitivity and 88% specificity for AVA 60% r Compare all findings to previous studies. r As with the use of deceleration time (DT) or pressure half-time (PHT) to describe MS severity, their use to describe AI severity is easily confounded by anything that renders the LV compliance abnormal. r Describe the aorta in some anatomic detail. Echocardiography should detect signs of most root diseases relevant to AI. r AI peak velocity is quite variable and depends on blood pressure, the LV diastolic pressure, and the gradient between the two. r In the context of AI, do not report the total forward cardiac output (CO) as the net forward CO. r False-positives of abdominal aortic flow reversal are rare. r Avoid the term “trivial” for AI in general, because it is essentially a normal finding (if the valve is normal); and use of that term may generate confusion about whether or not the valve is pathologic. If the valve is morphologically abnormal, use of the term “mild” is consistent with the inference that the valve is functionally abnormal.

NOTES ON ECHOCARDIOGRAPHIC METHODS TO DESCRIBE SEVERITY OF AORTIC INSUFFICIENCY Retrograde Holodiastolic Flow in the Abdominal Aorta

Retrograde holodiastolic flow in the abdominal aorta is sensitive (100%) and specific (96%) for level 3+ or 4+ AI. Consequently, it is one of the best signs to determine whether AI is severe. The potential false-positives include

44

Chapter 3  |  Aortic Insufficiency

aortopulmonary shunts and patent ductus arteriosus2 and also, possibly, aortic root to left atrial, right ventricular, or right atrial fistulae, all of which should be evident from color Doppler scanning. Abdominal diastolic flow reversal is analogous to the time-honored peripheral pulse signs used in physical diagnosis.

Retrograde Flow Profiles in the Proximal Thoracic Descending Aorta

Although it is more feasible to sample retrograde flow in the proximal descending aorta, it is of less worth to determine the severity of AI. The amount of regurgitant flow in the descending thoracic aorta (sampled by PW just beneath the aortic isthmus) can be expressed by several echocardiographic means: the peak velocity of the diastolic regurgitant volume; the time velocity interval (TVI) of the regurgitant flow; the TVI of the regurgitant flow indexed to the systolic flow, or the TVI indexed to the diastolic filling period. As would be anticipated, given the multitude of parameters, it is, overall, less trustworthy as a sign. The peak velocity of the regurgitant (diastolic) flow correlates with the regurgitant fraction (r = 0.82) and the regurgitant grade by angiography (r = 0.81). AI of 3+ by angiography correlates with a TVI of 22 ± 6 cm/ sec SD, and 4+ by angiography with 34 ± 9 cm/sec).3 End-diastolic flow velocity of 40 cm/sec or greater predicts a regurgitant fraction of 40% or more with a sensitivity of 89% and a specificity of 96%.4 The integral of the spectral display of diastolic flow recorded from the proximal descending aorta (divided by the integral of the systolic flow) mapped in the proximal descending aorta correlates well with angiographic regurgitant fraction: r = 0.915 and r = 0.90; standard error of estimate (SEE) 9%.6 However, the sign is inaccurate in the presence of aortic stenosis,7 because the high-velocity systolic aortic stenosis jet continues around the arch in some cases. Neither the “cut-off ” for the diastolic flow nor that for the diastolic flow integral/systolic flow integral that it constitutes has been conclusively established for severe AI. Some centers use 15 cm as the threshold above which AI is defined as severe. Obvious pan-diastolic flow above the baseline correlates well with the presence of severe AI,6 as long as no aorticopulmonary shunt is present.

Color Flow Mapping of the Descending Aorta

Color flow mapping of the descending aorta adds little (if anything) to a standard assessment, and is only useful to set up spectral sampling.

Color Doppler Flow Mapping of the Left Ventricular Outflow Tract

Color Doppler flow mapping of the LVOT is useful to detect AI. Indexing improves correlation8 with angiography (r = 0.88) and can classify the majority of central AI jets with thoracic (83%) and abdominal (86%)9 aortic flow profiles. It is a poor technique to

assess eccentric AI jets, however, and overall tends to be inaccurate. Indexing is performed to the height or area of the LVOT, to the aortic valve area, or to body surface area, and correlates with severity (r = 0.87).10 Oblique jets are problematic, because they result in overestimation of severity. Jet length into the LV has been proved to be an inaccurate means of describing AI severity, because jets of severe AI can be shorter than jets of moderate AI. Perry8 proposed the categorizations shown in Table 3-1.

Vena Contracta Width and Area

The vena contracta imaged in the posterior long-axis view correlates well (P < 0.0001) with Doppler effective regurgitant orifice (ERO; r = 0.89) and RVolume (0.90), and 2D methods (r = 0.90, r = 0.90), as well as with angiographic grading (r = 0.82; P = 0.01).11,12 A vena contracta width of ≥6 mm is 95% sensitive and 90% specific for diagnosing severe AI (ERO ≥ 30 mm2),11 and vena contracta area ≥7.5 mm2 is 100% sensitive and specific for severe AI (RVolume > 50 mL).12 Vena contracta width appears to be afterload independent.12 Because small differences in vena contracta dimension measurement (1–2 mm) result in different grading, the technique is very demanding and image quality dependent, and its applicability can be disappointing. The advent of anti-aliasing software may improve the utility of this method.

Effective Regurgitant Oriface Method: Proximal Isovelocity Surface Area and Doppler

The proximal isovelocity surface area (PISA) ERO method correlates well with reference techniques (P < 0.0001) but exhibits a trend to underestimate ERO due to cases where the AI jet is obtuse.4 ­Doppler ERO correlates well with angiographic estimates of ERO (r = 0.97) when the aortic diameter is less than 4.8 cm.13 Aortic pressure changes may influence the ERO, depending on whether the defect causing the AI is central (dynamic ERO: 51 ± 33% change with pharmacologic hypertension) versus a perforation in a leaflet proper (minimally dynamic orifice (9 ± 7%).14 Aortic root area is strongly dependent on the aortic diastolic pressure and can vary widely with pharmacologic hypertension.14 r Regurgitant volume of AI (RVolume): Anterograde SVLVOT − SVmitral (if mild or less than mild mitral regurgitation) = 0.785 × DiamLVOT 2 × TVILVOT − 0.785 × Diammitral 2 × TVIannulus

where Diam = diameter, PA = pulmonary artery, and SV = stroke volume. Anterograde SVLVOT − SVPA (if mild or less than mild pulmonary insufficiency) = 0.785 × DiamLVOT 2 × TVILVOT − 0.785 × DiamPA × TVIPA 3

Aortic Insufficiency  |  Chapter 3 r Regurgitant

fraction of AI (RFraction):

Regurgitant fraction of AI (RFraction ) = RVolume / total anterograde SV

The regurgitant fraction of AI can be calculated by left ventricular outflow as the total forward systolic volume (RVolume + net forward SV) minus anterograde flow anywhere there is no regurgitant flow (mitral level or PA).3,15,16 RFraction by Doppler correlates well with RFraction by catheterization: r = 0.96.3 Using this technique, 3+ and 4+ AI by angiography are associated with 53% and 62% RFraction by Doppler.3 The technique is less accurate with depressed left ventricular ejection fraction, and, as would be anticipated, in the presence of mitral regurgitation.15 r Suggested grading for AI: MILD

MODERATE

SEVERE

RVolume

55 mm).† (Level of evidence: B) Class IIb 1. AVR may be considered in patients with moderate AR while undergoing surgery on the ascending aorta. (Level of evidence: C) 2. AVR may be considered in patients with moderate AR while undergoing CABG. (Level of evidence: C) 3. AVR may be considered for asymptomatic patients with severe AR and normal LV systolic function at rest (ejection fraction > 0.50) when the degree of LV dilatation exceeds an end-diastolic dimension of 70 mm or end-systolic dimension of 50 mm, when there is evidence of progressive LV dilatation, declining exercise tolerance, or abnormal hemodynamic responses to exercise.† (Level of evidence: C) Class III AVR is not indicated for asymptomatic patients with mild, moderate, or severe AR and normal LV systolic function at

rest (ejection fraction > 0.50) when degree of dilatation is not moderate or severe (end-diastolic dimension < 70 mm, end-systolic dimension < 50 mm).† (Level of ­evidence: B) Medical Therapy Class I Vasodilator therapy is indicated for chronic therapy in patients with severe AR who have symptoms or LV dysfunction when surgery is not recommended because of additional cardiac or noncardiac factors. (Level of evidence: B) Class IIa Vasodilator therapy is reasonable for short-term therapy to improve the hemodynamic profile of patients with severe heart failure symptoms and severe LV dysfunction before proceeding with AVR. (Level of evidence: C) Class IIb Vasodilator therapy may be considered for long-term ­therapy in asymptomatic patients with severe AR who have LV dilatation but normal systolic function. (Level of ­evidence: B) Class III 1. Vasodilator therapy is not indicated for long-term therapy in asymptomatic patients with mild to moderate AR and normal LV systolic function. (Level of evidence: B) 2. Vasodilator therapy is not indicated for long-term therapy in asymptomatic patients with LV systolic dysfunction who are otherwise candidates for aortic valve replacement. (Level of evidence: C) 3. Vasodilator therapy is not indicated for long-term therapy in symptomatic patients with either normal LV function or mild to moderate LV systolic dysfunction who are otherwise candidates for aortic valve ­replacement. (Level of evidence: C)   

AR, aortic regurgitation; CABG, coronary artery bypass grafting; LV, left ventricular. *AVR refers to both aortic valve replacement and repair. †Consider

lower threshold values for patients of small stature of either gender.

From ACC/AHA 2006 guidelines for the management of patients with valvular heart disease. J Am Coll Cardiol. 2006; 48(3):e1–e148.

BOX 3-2  Appropriateness Criteria and Indications for Cardiac Imaging Modalities and Cardiac Catheterization for the Assessment of Aortic Insufficiency TRANSTHORACIC ECHOCARDIOGRAPHY ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/ SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography 30 Native Valvular Regurgitation with TTE n Routine surveillance of trace valvular regurgitation Appropriateness criteria: I; median score: 1 n Routine surveillance (12 mm Hg at rest, and an area of  1 cm2 (1.2–1.3 cm2). r “Critical” = mean gradient > 12 mm Hg at rest, and an area of 2+. r There is substantial risk of arterial embolism if there is clot within the body of the left atrium, because valvuloplasty wires invariably are in the body of the atrium. There is a smaller risk of embolism if clot is within the LAA, because the wires that must traverse the LA body may avoid the LAA. TEE is clearly superior to evaluate for the presence of LA and LAA clot.

SURGICAL ISSUES r Establish

the degree of submitral (annular) calcification. There is a greater risk of periprosthesis (paravalvar) MR when submitral (annular) calcification is severe. r Determine the degree of AI: in severe MR, IABP should not be used if there is concurrent AI ≥2+.

Mitral Stenosis  |  Chapter 5 r Describe

the RV in detail (RVH/systolic dysfunction/size), as well as the RVSP. r RA size is a reasonable descriptor of RV diastolic function, if neither TR nor atrial fibrillation is present.

PROVOCATIVE TESTING TO ENHANCE TRANSMITRAL GRADIENTS AND RIGHT VENTRICULAR SYSTOLIC PRESSURE Simple bedside maneuvers (e.g., a few sit-ups) or more sophisticated ones (e.g., supine bicycle, upright treadmill testing, or dobutamine) may be used to increase the heart rate and cardiac output, and thereby enhance the mitral gradient and RVSP. The role of such testing is unclear: in mitral stenosis the gradient would be expected to increase, and generally it does, about twofold, when patients are subjected to a Bruce or modified Bruce protocol: from 9 ± 7 mm Hg at rest to 17 ± 8 mm Hg, as does the RVSP, from 41 ±1 9 mm Hg to 70 ± 32 mm Hg.11 The optimal interpretation of the provoked hemodynamics is unclear. Advocates suggest that it better describes the basis of exertional symptoms and may be contributory when the resting hemodynamics are less striking than the (exertional) symptoms and findings. Dobutamine stress echo (a gradient cut-off of 18 mm Hg) has been shown to predict clinical events (90% sensitivity, 87% specificity, and 90% accuracy) over a 5-year period, and increases the detection of medium- and higher-risk cases.12 Dobutamine stress echocardiography may assist with the evaluation of patients whose symptoms are out of proportion to the calculated valve area, and who may benefit from “medical or invasive intervention.”13

NOTES ON MITRAL STENOSIS Etiologies of Mitral Stenosis

Congenital r Congenital valvular MS is rare. r Cor triatriatum sinister also is rare. It is a baffle-like ridge across the mid-LA that obstructs flow across the atrium, not at the mitral valve level. Acquired r Rheumatic origin is by far the most common cause of MS (>99% of all cases). r Severe mitral annular calcification may cause mild/moderate MS but very rarely causes severe MS. r LA myxoma/thrombus is an uncommon cause of MS ( 60 mm Hg with exercise) in the absence of left atrial thrombus or moderate to severe MR. (Level of evidence: C) Class IIa n Percutaneous mitral balloon valvotomy is reasonable for patients with moderate or severe MS who have a nonpliable calcified valve, are in NYHA functional class III–IV, and are either not candidates for surgery or are at high risk for surgery. (Level of evidence: C) Class IIb n Percutaneous mitral balloon valvotomy may be considered for asymptomatic patients with moderate or severe MS and valve morphology favorable for

percutaneous mitral balloon valvotomy who have new onset of atrial fibrillation in the absence of left atrial thrombus or moderate to severe MR. (Level of evidence: C) n Percutaneous mitral balloon valvotomy may be considered for symptomatic patients (NYHA functional class II, III, or IV) with mitral valve area >1.5 cm2 if there is evidence of hemodynamically significant MS based on pulmonary artery systolic pressure >60 mm Hg, pulmonary artery wedge pressure ≥25 mm Hg, or mean MV gradient >15 mm Hg during exercise. (Level of evidence: C) n Percutaneous mitral balloon valvotomy may be considered as an alternative to surgery for patients with moderate or severe MS who have a nonpliable calcified valve and are in NYHA class III–IV. (Level of evidence: C) Class III n Percutaneous mitral balloon valvotomy is not indicated for patients with mild MS. (Level of evidence: C) n Percutaneous mitral balloon valvotomy should not be performed in patients with moderate to severe MR or left atrial thrombus. (Level of evidence: C)

  

From ACC/AHA 2006 guidelines for the management of patients with valvular heart disease. J Am Coll Cardiol. 2006;48(3):e1–e148.

76

Chapter 5  |  Mitral Stenosis

BOX 5-2  Indications for Surgery for Mitral Stenosis: ACC/AHA 2006 Recommendations Class I n Mitral valve (MV) surgery (repair, if possible) is indicated in patients with symptomatic (NYHA functional class III–IV) moderate or severe MS when • Percutaneous mitral balloon valvotomy is unavailable. • Percutaneous mitral balloon valvotomy is contraindicated because of left atrial thrombus, despite anticoagulation or because concomitant moderate to severe MR is present. • The valve morphology is not favorable for ­percutaneous mitral balloon valvotomy in a patient with acceptable operative risk. (Level of evidence: B) n Symptomatic patients with moderate to severe MS who also have moderate to severe MR should receive MV replacement, unless valve repair is possible at the time of surgery. (Level of evidence: C)

Class IIa n MV replacement is reasonable for patients with severe MS and severe pulmonary hypertension (i.e., pulmonary artery systolic pressure >60 mm Hg) with NYHA functional class I–II symptoms who are not considered candidates for percutaneous mitral balloon valvotomy or surgical MV repair. (Level of evidence: C) Class IIb n MV repair may be considered for asymptomatic patients with moderate or severe MS who have had recurrent embolic events while receiving adequate anticoagulation and who have valve morphology favorable for repair. (Level of evidence: C) Class III n MV repair for MS is not indicated for patients with mild MS. (Level of evidence: C) n Closed commissurotomy should not be performed in patients undergoing MV repair; open commissurotomy    is the preferred approach. (Level of evidence: C)

From ACC/AHA 2006 guidelines for the management of patients with valvular heart disease. J Am Coll Cardiol. 2006;48(3):e1–e148.

BOX 5-3  Valvular Disease: Focused Update on Endocarditis: ACC/AHA 2008 Guidelines Class IIa indication: Antibiotic prophylaxis is no longer indicated in patients with mitral stenosis for prevention of infective endocarditis.    From ACC/AHA 2008 guideline update on valvular heart disease: focused update on infective endocarditis. J Am Coll Cardiol. 2008; 52:676–685.

Mitral Stenosis  |  Chapter 5

77

BOX 5-4  Appropriateness Criteria and Indications for Cardiac Imaging Modalities and Cardiac Catheterization for the Assessment of Mitral Stenosis TRANSTHORACIC ECHOCARDIOGRAPHY ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/ SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography 25 Native Valvular Stenosis with TTE n Routine surveillance ( 8

52

NA

NA

28% at 5 yr

Score ≤ 8

211

48 ± 14

98% at 4 yr

98% at 4 yr

Score > 8

116

64 ± 11

72% at 4 yr

39% at 4 yr

Death, MVR, NYHA FC III–IV symptoms NA

Score < 8

272

49 ± 13

95% at 4 yr

NA

Death

Score 8–12 Score > 12

306 24

58 ± 15 58 ± 15

83% at 4 yr 24% at 4 yr

NA NA

NA NA

Com Ca

120

NA

NA

86% at 3 yr

29

NA

NA

40% at 3 yr

Death, MVR, repeat PMBV NA

Com Ca+

NO. OF PATIENTS

EVENTS Death, MVR, repeat PMBV NA

Com Ca, commissural calcification; echo, echocardiographic; FC, functional class; MVR, mitral valve replacement; NA, not available; NYHA, New York Heart Association; PMBV, percutaneous mitral balloon valvotomy. From ACC/AHA/ASE 2003 guideline update for the clinical application of echocardiography: summary article. Circulation. 2003;108(9): 1146–1162.

80 TABLE 5-3  Utility of Different Imaging Modalities and Cardiac Catheterization in the Assessment of Mitral Stenosis MODALITY

PROS

CONS/CAVEATS

Transthoracic Echocardiography

2D echocardiography • Short-axis planimetry of the MVA is a valuable and accurate means of directly determining MVA. • “Scoring” of the valve is predictive of success of balloon valvuloplasty, and is better performed by TTE than by TEE. • Commissural calcification predicts risk of balloon valvuloplasty.

• Accurate planimetry is technically demanding. • More severe stenosis may exist at the subvalvar level, which is difficult to recognize by short-axis imaging.

Color Doppler echocardiography • PISA determination of MVA, if feasible, is accurate. • Color Doppler is able to recognize associated MI. Spectral Doppler echocardiography • CW Doppler determinations of mitral valve gradients are nearly equivalent to those determined by LA (trans-septal) to LV catheterization. • CW Doppler determinations of MVA by the PHT method are accurate within the range of 1–1.5 cm2, in the absence of variables that influence LV and LA compliance. The PHT relation is not confounded by the all-too-common presence of mitral insufficiency. The method is validated between 1 and 1.5 cm2. Transesophageal Echocardiography

• Offers the best means to identify LA and LA appendage thrombi that are relevant to balloon valvuloplasty procedures • Can guide catheter balloon valvuloplasty procedures (confirms safety of trans-septal punctures, and identifies significant increments in MI with successive balloon inflations) • MS hemodynamics by TEE are similar to those of TTE, as long as Doppler alignment remains favorable. • MS determination of PISA estimates of orifice area are generally better than those of TTE because PISAs are better depicted by TEE.

Cardiac CT

Cardiac CT is able to provide some measure, by planimetry, of the mitral valve orifice.

• Many non–mitral valve factors influence the transmitral gradient. (E.g., tachycardia, fever, anemia, pregnancy, and large dialysis fistula increase the gradient, and bradycardia and severe pulmonary hypertension reduce the gradient.) • Many factors reduce the accuracy of the PHT method: e.g., valvuloplasty within three months, LVH, AS, AI, and prior MI.

• Irregular heart rhythms (atrial fibrillation, common in mitral valve disease) are a significant technical problem for cardiac CT. • Valvular (and annular) calcification confer the problem of spatial “blooming.”

Cardiac MRI

SSFP sequences: Grossly, the mitral orifice can be planimetered.

• Irregular heart rhythms (atrial fibrillation) and valvular calcification conspire to limit the accuracy of CMR in assessing MS hemodynamics.

LGE sequences: NA

• Afford little to the assessment of MS

VEPC sequences: Are able to approximate the gradient across, but only roughly

• VEPC sequences are often unruly. • Irregular heart rhythms (atrial fibrillation) decrease the accuracy. • CMR currently tends to underestimate the severity of MS when compared to echocardiography and catheterization estimates.36,37

Nuclear

NA

• Afford little to the assessment of MS

Chest Radiography

Useful to depict pulmonary vasculature and the presence of left-sided heart failure, and other findings such as pulmonary hemorrhage and pulmonary hemosiderosis.

Cardiac Catheterization

• The traditional test to assess gradient and area, and the traditional reference standard to which other tests to compare their determinations of transmitral gradient and of valve area • The most reliable means by which to determine the pulmonary artery pressures, and the only means by which to determine the pulmonary vascular resistence • The platform from which to provide catheter balloon valvuloplasty

NA • LV to pulmonary capillary wedge gradients are less accurate (tend to overestimate) than are LV to LA gradient determinations or TTE Doppler determinations of mean gradient.

2D, two-dimensional; AI, aortic insufficiency; AS, aortic stenosis; CMR, cardiac magnetic resonance; CW, continuous wave; LA, left atrium; LGE, late gadolinium enhancement; LV, left ventricle; LVH, left ventricular hypertrophy; MI, mitrial insufficiency; MS, mitral stenosis; MVA, mitral valve area; NA, not applicable; PHT, pressure half time; PISA, proximal isovelocity surface area; SSFP, steady-state free precession; TEE, transesophageal echocardiography; TTE, transthoracic echocardiography; VEPC, velocity-enhanced phase contrast.

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PISA

  180° Mitral leaflet

  120°

Mitral leaflet

  ?°

Mitral leaflet

Figure 5-1.  Angle correction. Upper image: The top proximal isovelocity surface area (PISA) is a full hemisphere, because the orifice is planar; no angle correction is necessary. Middle image: The PISA is less than a full hemisphere, because the orifice is not planar. Angle correction is advised. Lower image: The PISA is not a full hemisphere, because the orifice is not clearly planar; it is not clear how to determine the optimal angle for correction. Surgery

Balloon valvuloplasty 70

25 20

*

*

*

*

15

*

†

10 5

Pulmonary artery systolic pressure (mm Hg)

Pulmonary artery wedge pressure (mm Hg)

30

‡

*

50 40

* * * *

30 20 10 0

0 Baseline

1 week 6 months 3 years

Baseline

25

3.0

20

2.5

15 10

* *

*

*

* *

5 0

Mitral valve area (cm2)

Mitral valve gradient (mm Hg)

60

1 week 6 months 3 years

* *

2.0

*

§

*

*

1.5 1.0 0.5 0.0

Baseline

1 week 6 months 3 years

Baseline

1 week 6 months 3 years

Figure 5-2.  Hemodynamic variables at baseline, 1 week, 6 months, and 3 years after balloon mitral valvuloplasty or open surgical commissuortomy. The bars indicate the standard errors. *All panels: P < 0.001 for the comparison with the baseline value. †Upper left panel: P < 0.001 for the comparison with the values at baseline, one week, and 6 months. ‡Upper right panel: P = 0.002 for the comparison with the balloon valvuloplasty group and P = 0.16 (not significant) for the comparison with the baseline value. §Lower right panel: P < 0.001 for the comparison with the surgery group. (From Reyes VP, Raju BS, Wynne J, et al. Percutaneous balloon valvuloplasty compared with open surgical commissurotomy for mitral stenosis. N Engl J Med. 1994;331[15]:961–967.)

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Figure 5-3.  Pliable cases of rheumatic mitral stenosis with thin leaflets, doming, no calcification, and no subvalvar disease. The ventricles are small, consistent with severity of the mitral stenosis, and the lack of aortic insufficiency or mitral regurgitation.

Figure 5-4.  Left: A standard posterior long-axis view that demonstrates the leaflet features of the mitral stenosis well. Right: This image is slightly off-axis (note the oblique view of the aortic valve) and reveals the subvalvar disease well. Accurate determination of subvalvar disease generally requires additional views.

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Figure 5-5.  Left: Normal mitral valve orifice in early diastole (4–6 cm2). Right: Rheumatic mitral stenosis:mitral valve area 0.6 cm2. The left commissure is prominently thickened and may be calcified, features that render balloon valvuloplasty more likely to split into the leaflet.

Figure 5-6.  Planimetry of the mitral orifice in MS. Left: A well-formed and well-imaged central and elliptical orifice lending itself to planimetry. Right: A complex orifice with such severe adjacent calcification that the margins of the orifice are susceptible to blooming artifact, which, in this image, is compounded by the overly high gain setting.

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Figure 5-7.  Left: Zoom apical view to demonstrate severe subvalvar disease. The subvalvar apparatus is so thickened and shortened that the demarcation of the papillary muscles, the rheumatically thickened chordae, and the leaflets is impossible. Right: Posterior short-axis view at the level of the mitral valve orifice. The orifice is central but asymmetric and teardrop shaped, not elliptical. The left commissure is not only thickened, but also calcified, which is apparent by the shadowing artifact.

Figure 5-8.  Transthoracic views of the left atrium in mitral stenosis often are revealing. Left: This image demonstrates how the dilation of the left atrium may enable visualization of the appendage, which does not appear to contain thrombus in this view. Middle: Off-axis posterior long-axis view demonstrating a thrombus along the left margin of the body of the left atrium. Right: The thrombus is seen extending out of the left atrial appendage.

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Figure 5-9.  Doppler assessment of mitral stenosis (MS). Unless the mitral leaflets are severely calcified, apical views generally yield good quality proximal isovelocity surface areas. The zoom view should always be used. Left: Mild MS in atrial fibrillation. The deceleration slope is well-formed and linear and amenable to pressure half-time assessment. Planimetry of the profile yields the mean gradient (7 mm Hg). Right: Severe MS in sinus rhythm. The deceleration slope is notably less, and there is presystolic acceleration consistent with atrial contraction. The mean gradient is 15 mm Hg.

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Figure 5-10.  An unusual case of severe mitral annular calcification resulting in severe mitral stenosis in a patient with decades of renal failure. Upper left: The mitral valve is extensively involved with calcification, so that recognition of the valve components is difficult. The leaflets per se do not seem to be as calcified as the annulus. Upper right: The calcification at the annular level is well seen. The proximal isovelocity surface area is still imaged, though. Lower left: Subvalvar disease. Lower right: Posterior short-axis view at the level of the orifice, with commissural calcification also seen. Mean gradient 17 mm Hg, mitral valve area 0.5 cm2. The patient underwent mitral valve replacement, with reconstruction of the annulus to enable insertion of a prosthetic valve.

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Figure 5-11.  Transesophageal echocardiography during a mitral catheter balloon valvuloplasty. Upper left: “Tenting” of the interatrial septum by the Brockenbrough needle jut before puncture. Upper right: Flushing the needle with saline after puncture of the interatrial septum: bubbles injected into the left atrium. Middle left: The wire is seen in the mid–left atrium, not yet into the valve orifice. Middle right: The wire has now crossed the valve orifice. Lower left: The first balloon inflation. The balloon still has a prominent “waist,” indicating that the orifice is incompletely opened. Lower right: Repeat inflation. There is now little waist to the balloon: the orifice has opened. Mean gradient: pre-, 11 mm Hg; post-, 5 mm Hg.

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Figure 5-12.  Submitral calcification and resultant mild mitral stenosis. The upper images depict the calcific accumulation within the mitral valve annulus lateral to the posterior leaflet, and, as well, the flow acceleration and turbulence at the mitral valve level. Pulsed wave Doppler recording from the tips of the mitral leaflets (lower left) and continuous wave Doppler sampling across the mitral orifice (lower right) demonstrate A-wave dominance with prolongation of the deceleration time. The difference in the contours is due to the difference in sampling—that of pulsed wave Doppler at the leaflet tips, where there is no restriction to flow, and that of continuous wave Doppler along the incident axis, which captures the highest velocities.

6

Mitral Insufficiency

GOALS OF ECHOCARDIOGRAPHY IN MITRAL INSUFFICIENCY r To r To r To

establish that mitral insufficiency is present establish the severity of mitral insufficiency determine the hemodynamic consequences of mitral regurgitation (MR), pulmonary venous flow, cardiac index (CI), and right ventricular systolic pressure r To establish the underlying cause(s), when possible • “Organic” causes: myxomatous causes (prolapse, flail), rheumatic, infective, papillary rupture • “Functional” causes: ischemic, cardiomyopathy r To determine the reparability of the valve lesion r To verify adequacy of repair (intraoperative transesophageal echocardiography [TEE]) r To identify complications of MR (e.g., pulmonary hypertension, left ventricle [LV] dysfunction) r To identify concurrent cardiac disturbances (e.g., other valve lesions, coronary artery disease)

SCANNING ISSUES Required Parameters to Obtain from Scanning r Valve

apparatus details to explain the cause of the MR • Leaflets, chords, annulus • Papillary muscle bodies and heads • LV geometry and size, wall motion abnormality r MR severity—quantified if more than moderate MR (i.e., not if mild) • RVolume, RFraction • Effective regurgitant orifice (ERO) • Pulmonary venous systolic flow pattern r LV size and systolic function r Stroke volume (SV; net forward, not total) and CI r Indirect volume/pressure overload descriptors • Left atrium (LA) size, right ventricular systolic pressure • Right ventricle (RV) size, systolic function, tricuspid regurgitation etiology if present and suitability of repair r The height and weight for body surface area normalization r Blood pressure, if ≥2+ MR 90

Valid Methods to Determine Severity of Mitral Regurgitation r Proximal

isovelocity surface area (PISA):ERO, RVolume r Volumetric: RVolume, RFraction r Pulmonary venous flow reversal

Scanning Notes

r If sinus rhythm: measure three spectral profiles r If atrial fibrillation: measure five spectral profiles r Spectral profiles should be two-thirds the height of

the display and wide enough to show two to three per display.

Use Zoom Views Liberally r For PISA depiction r For mitral leaflet detail r For papillary muscle detail r For mitral annular diameter Volumetric r The volumetric method (using the left ventricular outflow tract [LVOT] as a standard) is unsuitable if there is ≥mild aortic insufficiency (AI). For Proximal Isovelocity Surface Area r Shift the color baseline down for MR (if transthoracic echocardiography [TTE]). r Measure at mid-systole to correspond to peak MR velocity. PISA is measured at mid-systole by convention, although this may be less accurate when the regurgitant orifice is dynamic and mid-systole does not characterize its mean size. r Record the aliasing velocity. r VAliasing to 35-45-52 cm/sec to optimize depiction of PISA hemisphere r The PISA method is unsuitable if there is frankly poor depiction of PISA.

Methods where

RVolume = ERO × TVIMR ERO = 2πr2 × VAlias / VPeak

RVolume = mitral anterograde SV − LVOT SV (if ≤ mild AI) = 0.785 × Diam2Annulus × TVIAnnulus − 0.785 × Diam2LVOT × TVILVOT

RF = RVolume / (Total) anterograde SV

Mitral Insufficiency  |  Chapter 6

where RF = regurgitant fraction and TVI = time velocity interval. Total anterograde SV is determined from diastolic transmitral anterograde flow using Simpson’s method of the LV (in the absence of AI).

Grading of Mitral Regurgitation1

The most important distinction is to differentiate severe from moderate MR.

REPORTING ISSUES r Describe the cause of the MR. r Describe the severity of the MR. r If ≥2+, describe the hemodynamic effect of

the MR: • Pulmonary venous flow pattern • Q  uantification of ERO, if >2+ MR r Describe the LV • Systolic function (overall and regional) • End-systolic dimension r Use of color Doppler flow mapping • Establishes presence/absence of MR • Does not alone establish the presence of severe MR Severe r  Large ERO, RVolume, RFraction r Severe hemodynamic effect (pulmonary venous flow reversal) Severe MR r ERO > 0.4 cm2 r PISA ≥ 1 cm at VAlias –40 cm/sec r RVolume > 60 mL r RF > 60% r Pulmonary venous systolic flow reversal (for TTE) • 60% sensitive • 92% specific r Describe the LV in detail: size, end-systolic diameter, end-systolic volume, ejection fraction, wall motion abnormality. • Compare to previous studies r Describe the RV in some anatomic detail, beyond the right ventricular systolic pressure r Do not make assumptions about peak mitral ­velocity as it is quite variable. r Pay attention to the aortic root if severe mitral valve prolapse (MVP), because Marfan syndrome may underlie both. r Avoid the use of the term “trivial” in general and whenever the mitral valve is abnormal. • “Trivial” MR is within normal finding and therefore does not need to be recorded.

ROLE OF TRANSESOPHAGEAL ECHOCARDIOGRAPHY IN MITRAL REGURGITATION r To

define pathologies responsible for MR that are not evident on some TTE examinations—such as infective endocarditis, flail chordae

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r To

determine severity when TTE and clinical or angiographic assessment are discordant r To determine suitability of MV to surgical repair, if TTE is unclear

WHEN THE GRADE OF MITRAL REGURGITATION IS DIFFERENT ON SERIAL ECHOCARDIOGRAPHIC STUDIES r If the change is >1 grade, it probably is a true change. r None/mild/moderate/severe is the most logical

grading system. The greater the number of grades, the greater the intraobserver, interobserver, and interstudy reclassification rates. Therefore, using fewer categories yields more consistent grading. r When serial studies suggest difference in grade, a careful review of the basis of grading of each study should be entertained. If the studies have different components (e.g., one without pulmonary venous flow) then true comparison is not possible. r When apparent changes have occurred, it is important to evaluate the likelihood of improvement. Some pathologies responsible for MR are unlikely to change: for example, a flail leaflet nearly always results in severe MR, and the associated degree of MR is unlikely to be altered by medical therapy. Conversely, peri-infarction MR often is evanescent, and “functional MR” associated with chronic ischemic cardiomyopathy and with dilated cardiomyopathy, may be significantly improved with load alteration on the LV via medical therapy or blood pressure changes. r TEE is able to record pulmonary venous flow patterns in all cases; TTE under-detects abnormalities of pulmonary venous flow because of less successful interrogation of the pulmonary veins. Since pulmonary venous systolic flow reversal is a criterion to establish severe MR, TEE will more often establish that MR is severe than will TTE. r TEE is more sensitive than TTE to record MR flow mapping, and, therefore, for any given MR jet, the MR generally looks worse by TEE.

ECHOCARDIOGRAPHY– CATHETERIZATION DISCORDANCE OF THE ASSESSMENT OF MITRAL REGURGITATION SEVERITY When Echocardiographic Assessment of Mitral Regurgitation Differs from the Contrast Ventriculographic Assessment of Mitral Regurgitation r Contrast

ventriculography may underrepresent the severity of MR. • The most common error in angiographic assessment of MR is underestimation of the severity of MR due to poor opacification (usually because of increased LV and LA volumes, and because not enough contrast dye was used).

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• C  ine-angiographic “panning” must show the left atrium adequately to allow assessment of opacification. Sometimes, it does not. r Contrast ventriculography may overrepresent the severity of MR: • Premature ventricular contractions may cause MR. • Catheter entrapment of chordal or leaflet elements may cause MR. r Inter- and intraobserver agreement of the “middle” grades of MR are not consistent. Differentiation of 2+ from 3+ MR may influence management, as 3+ MR may be operated upon at some centers. r Echocardiographers who rely on color Doppler flow mapping, and who subscribe to 1985-derived color Doppler metrics of MR severity, will systematically describe the extent of MR as worse than it really is. r TEE is more likely to agree with contrast ventriculographic assessment, because it is less likely to misclassify severe MR. TEE remains superior to TTE in sampling pulmonary venous flow.

V-Waves on the Pulmonary Capillary Wedge Pressure Tracing and Mitral Regurgitation Grading

The erroneous notion that large V-waves are sensitive and specific for severe MR is widespread. V-waves are neither sensitive nor specific for severe MR. r V-waves may be produced by pathologies other than severe MR: • Ventriculoseptal defect • Mitral stenosis • Left ventricular failure • Stiff LA r Errors in catheterization technique can confuse the issue as well: • Excessive tubing length, small catheter bore, and overdamping can obscure large V-waves. • Underdamping can exaggerate a V-wave. • Dye dilution techniques are less accurate when the CO is 45% (see later discussion) predicts failure to annuloplasty repair of ischemic MR (Fig. 6-1).3

NOTES ON SPECIFIC CAUSES OF MITRAL REGURGITATION A clear attempt to identify the specific cause of MR should be made in each case. MR is often grouped into “functional” (e.g., in nonmitral chords, leaflets and papillary muscles; the suspension of the chords, leaflets, and papillary muscles is the problem—i.e., the LV is the problem) and “organic” (i.e., diseased chords, leaflets, and papillary muscles). In general, functional MR is less likely to be severe, and often goes hand-inhand with impaired LV systolic function and geometry and, therefore, is of higher surgical risk. Axiomatically, the chance of having a good LV is greater with organic MR, because in that case the LV is not the cause of the MR. r Altered LV geometry (regional or global cavitary dilation) causing mitral apparatus distortion often is referred to as “functional MR” (as the mitral apparatus components are not diseased themselves) and is the most common cause of MR in patients with coronary artery disease and dilated cardiomyopathy. Lateral and apical displacement of the papillary muscles exerts radial and longitudinal traction on the mitral leaflet tips, reducing and then resulting in loss of coaptation. The mitral apparatus appears “tented” in systole as the leaflet tips are apically displaced; the leaflets appear as structurally normal. The extent of tenting (which can be described as the area in the triangle formed by the mitral leaflets and a line across the mitral annulus) roughly correlates (r = 0.74; P < 0.0001) with the ERO.4 The same study established that there was a wide range of ERO, and that ERO was not related to EF% (P = 0.32). Papillary muscle tethering length has been shown in at least one study to be an independent cause of severe MR.5 r Severe wall motion abnormality (e.g., infarction, stunning) • Some MR is present in 20% of infarction cases, and establishes a higher mortality. • Apical (r = 0.75; P < 0.0001) and lateral (r = 0.70; P < 0.0001) LV geometric alterations (displacement of papillary muscles), especially, are associated with increased ERO size.4 • LV dysfunction without alteration of geometry is unlikely to produce significant MR,6 underscoring that the attachments (papillary muscle position and annulus) of the mitral apparatus are of paramount importance in the development of functional MR.6 r Papillary muscle rupture (PMR)* • PMR is seen in 95%), as the sensitivity by TTE is only about 60%.16,23–26 The direction of the jet, the RV, and the LA pressure all influence as well the pulmonary venous systolic flow pattern.27 Therefore, systolic flow reversal is a highly specific marker of severe MR, whereas blunted flow is less reliable in grading MR severity.24 Proximal Isovelocity Surface Area Method to Calculate Effective Regurgitant Orifice and Volume The PISA method has gained considerable acceptance as being accurate and useful. It is, however, the most time-consuming method, and has the longest learning curve. The principle is based on the concept of flow through an infinitely small and flat (planar) orifice, across which nonviscous fluid is passing, resulting in acceleration of flow through a series of isovelocity “shells” or hemispheres, with the velocity being faster the closer it gets to the orifice. There are two caveats: (1) the innermost shell is partially flattened, which leads to underestimation of flow (the best hemispheric shells are >1 orifice dimension radius out) and (2) the level of the orifice may be difficult to detect, and if taken to be too proximal there again is underestimation of flow. Fortuitously, color Doppler flow mapping describes isovelocity radii (determined by the set of the aliasing velocity) at distances from the orifice that are related to the size of the orifice and the volume of

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flow across it. The volume of flow across one radius is the same as across the next, as per the conservation of mass principle. The flow rate is related to the shell area (2πr2) at that radius and the flow velocity (V) at that radius: Flow rate = 2πr2 × VAlias

This is well validated as long as VAlias45 mm has a 75% specificity for severe MR, a positive predictive value of 100%, and a negative predictive value of 60%.38 LV dimensions have lower sensitivities. In the presence of acute MR, atrial fibrillation, LV dysfunction, or associated valve lesions, chamber dimensions are not helpful to determine severity of MR.38 Pulmonary Artery Pressure Generally in the context of mitral valve disease, the larger the LA, the better the capacitor and the lower the pulmonary artery (PA) pressures. In general, only one of the two becomes severely abnormal, or both become moderately abnormal. It still remains difficult to understand exactly who will develop severe

Mitral Insufficiency  |  Chapter 6

pulmonary hypertension—for any given elevation of LA and pulmonary capillary pressure, the likelihood of developing a pulmonary arteriolar vasoconstriction is hard to predict. Color Doppler Flow Mapping Color Doppler flow mapping, using current equipment but older color Doppler criteria, is overly sensitive to MR jet depiction, and exhibits a strong tendency to classify MR as more severe than it is. It is also dependent on machine setting, chamber, and jet direction.39,40 Eccentric jets are less well depicted— those that impact a wall are underrepresented, and those that run close to and parallel to a wall are drawn toward it (Coanda effect). Orifice shape also influences jet area and volume—a square orifice produces a larger jet than a round orifice. Vena Contracta Width Although validated41 (generally against the modestly accurate methods of color flow mapping and angiography),42 color Doppler flow mapping to measure the vena contracta width as a measure of MR severity can be difficult to apply, especially by TTE. Measurement of the vena contracta (distal to an orifice) is best attempted with zoom views, and given that ultrasound axial resolution is better than lateral resolution, parasternal views would be expected to yield better depictions than apical views. Biplane vena contracta widths correlate well with RF (r = 0.85; SEE 20 mL) and RVolume (r = 0.86; SEE = 0.15 cm2), and biplane vena contracta width ≥6.5 cm predicts severe MR (RF and RVolume)42 with a positive predictive value of 88% and negative predictive value of 96%.43 Vena contracta width does not appear to be load independent.43 Proximal Jet Width Proximal jet width correlates with echocardiographic MR fraction and volume (r = 0.86–0.95; SEE = 7.7– 9.0 mL, 6–7.3%) and angiographic MR (r = 0.85– 0.91; SEE = 4–5%). Although the technique can be applied with TTE, multiplane TEE offers better data,44 because of better imaging in most cases (unless the LA is huge). TEE jet width of ≥6 mm identifies angiographically severe MR with a sensitivity of 95% and a specificity of 98% and echocardiographically severe MR (RVolume >80 mL) with a sensitivity of 86% and a specificity of 95%.44 Occasionally Helpful, but “Minor” Signs of Mitral Regurgitation r Systolic bulging of the LA r Wall hugging jet extending along the LA roof r Rightward bulging of the interatrial septum r V-wave “cut-off ” of a tricuspid regurgitation jet r Peak mitral E wave velocity > 1.2 m/sec45 r MR jet area over LA area Because echocardiography is able to offer the largest number of parameters that characterize MR, it

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is probably the single best test to describe MR severity. Uncertainty of grade of severity by echocardiography is a very reasonable indication for contrast ventriculography.

SELLERS GRADE (CONTRAST VENTRICULOGRAPHY) 1+: contrast in LA < contrast in LV and clears from the LA in a single beat 2+: contrast in LA > contrast in LV and clears from the LA in 3 to 5 beats 3+: contrast in LA = contrast in LV 4+: contrast in LA > contrast in LV ±opacification of the pulmonary veins ±opacification of the left atrial appendage Pros r Widely known r A “work-horse” of clinical medicine that clinicians are comfortable with r Enables recording of LV diastolic pressures Cons r Subjective, nonquantitative r Interpretation rendered difficult by irregular rhythms, too little dye for the size of the LV or LA, poor “panning” r Catheter end in the mitral apparatus can artifactually induce MR r Reclassification of intermediate grades r Invasiveness

NOTES ON TIMING OF SURGICAL INTERVENTION IN MITRAL REGURGITATION Possible indications for mitral repair or replacement include combinations of the following, so they should be noted and described if present: r Severe MR+ r Reparable valve r Left ventricular end-systolic dimension >45 mm r LV EF 20% r Pulmonary hypertension

SUMMARY r Echocardiography

is useful to identify mitral insufficiency, and to establish the cause and severity of mitral regurgitation, as well as the reparability of the valve. r Some cases still elude determination of the mechanism by echocardiography. r Multiple diagnostic criteria should be used, with emphasis on the more robust ones. r In addition to identifying the severity of mitral insufficiency, echocardiography can garner some indices of surgical timing.

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REFERENCES 1. Monin JL, Dehant P, Roiron C, et al. Functional assessment of mitral regurgitation by transthoracic echocardiography using standardized imaging planes diagnostic accuracy and outcome implications. J Am Coll Cardiol. 2005;46(2):302–309. 2. Hillis LD, Firth BG, Winniford MD. Analysis of factors affecting the variability of Fick versus indicator dilution measurements of cardiac output. Am J Cardiol. 1985; 56(12):764–768. 3. Magne J, Pibarot P, Dagenais F, et  al. Preoperative posterior leaflet angle accurately predicts outcome after restrictive mitral valve annuloplasty for ischemic mitral regurgitation. Circulation. 2007;115(6):782–791. 4. Yiu SF, Enriquez-Sarano M, Tribouilloy C, et al. Determinants of the degree of functional mitral regurgitation in patients with systolic left ventricular dysfunction: A quantitative clinical study. Circulation. 2000;102(12): 1400–1406. 5. Otsuji Y, Kumanohoso T, Yoshifuku S, et  al. Isolated annular dilation does not usually cause important functional mitral regurgitation: comparison between patients with lone atrial fibrillation and those with idiopathic or ischemic cardiomyopathy. J Am Coll Cardiol. 2002;39(10): 1651–1656. 6. Otsuji Y, Handschumacher MD, Schwammenthal E, et al. Insights from three-dimensional echocardiography into the mechanism of functional mitral regurgitation: direct in vivo demonstration of altered leaflet tethering geometry. Circulation. 1997;96(6):1999–2008. 7. Nishimura RA, McGoon MD, Shub C, et al. Echocardiographically documented mitral-valve prolapse. Longterm follow-up of 237 patients. N Engl J Med. 1985; 313(21):1305–1309. 8. Duren DR, Becker AE, Dunning AJ. Long-term followup of idiopathic mitral valve prolapse in 300 patients: a prospective study. J Am Coll Cardiol. 1988;11(1):42–47. 9. Ling LH, Enriquez-Sarano M, Seward JB, et al. Clinical outcome of mitral regurgitation due to flail leaflet. N Engl J Med. 1996;335(19):1417–1423. 10. Grigioni F, Enriquez-Sarano M, Ling LH, et al. Sudden death in mitral regurgitation due to flail leaflet. J Am Coll Cardiol. 1999;34(7):2078–2085. 11. Grigioni F, Avierinos JF, Ling LH, et al. Atrial fibrillation complicating the course of degenerative mitral regurgitation: determinants and long-term outcome. J Am Coll Cardiol. 2002;40(1):84–92. 12. Freed LA, Levy D, Levine RA, et  al. Prevalence and clinical outcome of mitral-valve prolapse. N Engl J Med. 1999;341(1):1–7. 13. Gilon D, Buonanno FS, Joffe MM, et al. Lack of evidence of an association between mitral-valve prolapse and stroke in young patients. N Engl J Med. 1999;341(1):8–13. 14. Nishimura RA, McGoon MD. Perspectives on mitralvalve prolapse. N Engl J Med. 1999;341(1):48–50. 15. Enriquez-Sarano M, Sinak LJ, Tajik AJ, et al. Changes in effective regurgitant orifice throughout systole in patients with mitral valve prolapse. A clinical study using the proximal isovelocity surface area method. Circulation. 1995;92(10):2951–2958. 16. Enriquez-Sarano M, Basmadjian AJ, Rossi A, et  al. Progression of mitral regurgitation: a prospective Doppler echocardiographic study. J Am Coll Cardiol. 1999; 34(4):1137–1144.

17. Imamura T, McDermott PJ, Kent RL, et  al. Acute changes in myosin heavy chain synthesis rate in pressure versus volume overload. Circ Res. 1994;75(3):418–425. 18. Rozich JD, Carabello BA, Usher BW, et al. Mitral valve replacement with and without chordal preservation in patients with chronic mitral regurgitation. Mechanisms for differences in postoperative ejection performance. Circulation. 1992;86(6):1718–1726. 19. Otto CM. Timing of surgery in mitral regurgitation. Heart. 2003;89(1):100–105. 20. Castello R, Lenzen P, Aguirre F, Labovitz A. Variability in the quantitation of mitral regurgitation by Doppler color flow mapping: comparison of transthoracic and transesophageal studies. J Am Coll Cardiol. 1992;20(2): 433–438. 21. Yoshida K, Yoshikawa J, Yamaura Y, et al. Assessment of mitral regurgitation by biplane transesophageal color Doppler flow mapping. Circulation. 1990;82(4):1121–1126. 22. Castello R, Fagan Jr L, Lenzen P, et al. Comparison of transthoracic and transesophageal echocardiography for assessment of left-sided valvular regurgitation. Am J Cardiol. 1991;68(17):1677–1680. 23. Enriquez-Sarano M, Miller FA Jr, Seward JB. Pulmonary venous flow pattern in mitral regurgitation: pathophysiologic considerations and clinical implications. Circulation. 1995;92(8):I-720–I-720. 24. Pu M, Vandervoort P, Griffin BP, et  al. Quantitative assessment of accuracy and pitfalls of Doppler pulmonary venous flow in assessment of mitral regurgitant severity. Circulation. 1995;92(8):I-720. 25. Klein AL, Obarski TP, Stewart WJ, et al. Transesophageal Doppler echocardiography of pulmonary venous flow: a new marker of mitral regurgitation severity. J Am Coll Cardiol. 1991;18(2):518–526. 26. Castello R, Pearson AC, Lenzen P, Labovitz AJ. Effect of mitral regurgitation on pulmonary venous velocities derived from transesophageal echocardiography colorguided pulsed Doppler imaging. J Am Coll Cardiol. 1991; 17(7):1499–1506. 27. Passafini A, Shiota T, Depp M, et al. Factors influencing pulmonary venous flow velocity patterns in mitral regurgitation: an in vitro study. J Am Coll Cardiol. 1995; 26(5):1333–1339. 28. Rodriguez L, Anconina J, Flachskampf FA, et  al. Impact of finite orifice size on proximal flow convergence. Implications for Doppler quantification of valvular regurgitation. Circ Res. 1992;70(5):923–930. 29. Vandervoort PM, Rivera JM, Mele D, et al. Application of color Doppler flow mapping to calculate effective regurgitant orifice area. An in  vitro study and initial clinical observations. Circulation. 1993;88(3):1150–1156. 30. Enriquez-Sarano M, Miller Jr FA, Hayes SN, et  al. Effective mitral regurgitant orifice area: clinical use and pitfalls of the proximal isovelocity surface area method. J Am Coll Cardiol. 1995;25(3):703–709. 31. Dujardin KS, Enriquez-Sarano M, Bailey KR, et  al. Grading of mitral regurgitation by quantitative Doppler echocardiography: calibration by left ventricular angiography in routine clinical practice. Circulation. 1997; 96(10):3409–3415. 32. Shiota T, Jones M, Teien DE, et al. Dynamic change in mitral regurgitant orifice area: comparison of color Doppler echocardiographic and electromagnetic flowmeter-based methods in a chronic animal model. J Am Coll Cardiol. 1995;26(2):528–536.

Mitral Insufficiency  |  Chapter 6 33. Pu M, Vandervoort PM, Greenberg NL, et al. Impact of wall constraint on velocity distribution in proximal flow convergence zone. Implications for color Doppler quantification of mitral regurgitation. J Am Coll Cardiol. 1996;27(3):706–713. 34. Hung J, Otsuji Y, Handschumacher MD, et al. Mechanism of dynamic regurgitant orifice area variation in functional mitral regurgitation: physiologic insights from the proximal flow convergence technique. J Am Coll Cardiol. 1999;33(2):538–545. 35. Blumlein S, Bouchard A, Schiller NB, et al. Quantitation of mitral regurgitation by Doppler echocardiography. Circulation. 1986;74(2):306–314. 36. Ascah KJ, Stewart WJ, Jiang L, et al. A Doppler-twodimensional echocardiographic method for quantitation of mitral regurgitation. Circulation. 1985;72(2):377–383. 37. Kleaveland JP, Kussmaul WG, Vinciguerra T, et  al. Volume overload hypertrophy in a closed-chest model of mitral regurgitation. Am J Physiol. 1988;254(6 Pt 2): H1034–H1041. 38. Burwash IG, Blackmore GL, Koilpillai CJ. Usefulness of left atrial and left ventricular chamber sizes as predictors of the severity of mitral regurgitation. Am J Cardiol. 1992;70(7):774–779. 39. Chen CG, Thomas JD, Anconina J, et  al. Impact of impinging wall jet on color Doppler quantification of mitral regurgitation. Circulation. 1991;84(2):712–720. 40. Sahn DJ. Instrumentation and physical factors related to visualization of stenotic and regurgitant jets by Doppler color flow mapping. J Am Coll Cardiol. 1988;12(5): 1354–1365. 41. Hall SA, Brickner ME, Willett DL, et al. Assessment of mitral regurgitation severity by Doppler color flow mapping of the vena contracta. Circulation. 1997;95(3): 636–642. 42. Fehske W, Omran H, Manz M, et al. Color-coded Doppler imaging of the vena contracta as a basis for quantification of pure mitral regurgitation. Am J Cardiol. 1994;73(4):268–274. 43. Kizilbash AM, Willett DL, Brickner ME, et al. Effects of afterload reduction on vena contracta width in mitral regurgitation. J Am Coll Cardiol. 1998;32(2):427–431. 44. Grayburn PA, Fehske W, Omran H, et al. Multiplane transesophageal echocardiographic assessment of mitral regurgitation by Doppler color flow mapping of the vena contracta. Am J Cardiol. 1994;74(9):912–917. 45. Thomas L, Foster E, Schiller NB. Peak mitral inflow velocity predicts mitral regurgitation severity. J Am Coll Cardiol. 1998;31(1):174–179. 46. ACC/AHA 2006 guidelines for the management of patients with valvular heart disease. J Am Coll Cardiol. 2006;48:e1–e148. 47. Douglas PS, Garcia MJ, Haines DE, et al. ACCF/ASE/ AHA/ASNC/HFSA/HRS/SCAI/SCCM/SCCT/ SCMR 2011 appropriate use criteria for echocardiography. J Am Coll Cardiol. 2011;57(9):1126–1166. 48. Cheitlin MD, Armstrong WF, Aurigemma GP, et  al. ACC/AHA/ASE 2003 guideline update for the clinical application of echocardiography: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASE Committee to Update the 1997 Guidelines for the Clinical Application of Echocardiography). Circulation. 2003;108(9):1146–1162.

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49. Cheitlin MD, Chair JS, Alpert JS, et  al. ACC/AHA guidelines for the clinical application of echocardiography: a report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines (Committee on Clinical Application of Echocardiography). Circulation. 1997;95:1686–1744. 50. Bonow RO, Blase AC, Chatterjee K, et al. ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2006;114: e84–e231. 51. Douglas PS, Khandheria BK, Stainback RF, Weissman NJ. ACCF/ASE/ACEP/AHA/ASNC/SCAI/SCCT/ SCMR 2008 appropriateness criteria for stress echocardiography. Circulation. 2008;117(11):1478–1497. 52. Bonow RO, Blase AC, Chatterjee K, et al. ACC/AHA 2006 guidelines for the management of patients with valvular heart disease. Circulation. 2006;114:e84–e231. 53. Taylor AJ, Cerqueira M, Hodgson JM, et  al. ACCF/ SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/ SCMR 2010 appropriate use criteria for cardiac ­computed tomography. J Am Coll Cardiol. 2010;56(22): 1864–1894. 54. Hendel RC, Manesh PR, Kramer CM, Poon M. ACCF/ACR/SCCT/SCMR/ASNC/NASCI/SCAI/ SIR appropriateness criteria for cardiac computed tomography and cardiac magnetic resonance imaging. J Am Coll Cardiol. 2006;48(7):1475–1497. 55. Pennell DJ, Sechtem UP, Higgins CB, et  al. Clinical indications for cardiovascular magnetic resonance (CMR): Consensus Panel report. J Cardiovasc Magn Reson. 2004; 6(4):727–765. 56. Hendel RC, Berman DS, Di Carli MF, et  al. ACCF/ ASNC/ACR/AHA/ASE/SCCT/SCMR/SNM 2009 appropriate use criteria for cardiac radionuclide imaging. J Am Coll Cardiol. 2009;53(23):2201–2229. 57. Klocke FJ, Baird MG, Bateman TM, et al. ACC/AHA/ ASNC guidelines for the clinical use of cardiac radionuclide imaging: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASNC Committee to revise the 1995 Guidelines for the Clinical Use of Cardiac Radionuclide Imaging). Circulation. 2003;108(11): 1404–1418. 58. Nishimura RA, Carabello BA, Faxon DP, et al. ACC/ AHA 2008 guideline update on valvular heart disease: focused update on infective endocarditis. J Am Coll Cardiol. 2008;52(8):676–685. 59. Sondergaard L, Lindvig K, Hildebrandt P, et  al. Quantification of aortic regurgitation by magnetic resonance velocity mapping. Am Heart J. 1993;125(4): 1081–1090. 60. Honda N, Machida K, Hashimoto M, et  al. Aortic regurgitation: quantitation with MR imaging velocity mapping. Radiology. 1993;186(1):189–194. 61. Zuppiroli A, Mori F, Favilli S, et  al. Arrhythmias in mitral valve prolapse: relation to anterior mitral leaflet thickening, clinical variables, and color Doppler echocardiographic parameters. Am Heart J. 1994;128: 919–927. 62. Babuty D, Cosany P, Breuillac JC, et  al. Ventricular arrhythmia factors in mitral valve prolapse. Pacing Clin Electrophysiol. 1994;17:1090–1099.

100 Chapter 6  |  Mitral Insufficiency 63. Takamoto T, Nitta M, Tsujibayashi T, et al. The prevalence and clinical features of pathologically abnormal mitral valve leaflets (myxomatous mitral valve) in the mitral valve prolapse syndrome: an echocadiographic and pathological comparative study. J Cardiol Suppl. 1991;25:75–86. 64. Marks AR, Choong CY, Sanfilippo AJ, et  al. Identifi­ cation of high-risk and low-risk subgroups of patients with mitral-valve prolapse. N Engl J Med. 1989;320: 1031–1036.

65. Chandraratna PA, Nimalasuriya A, Kawanishi D, et al. Identification of the increased frequency of cardiovascular abnormalities associated with mitral valve prolapse by two-dimensional echocardiography. Am J Cardiol. 1984;54:1283–1285.

BOX 6-1  Indications for Mitral Valve Operation: ACC/AHA 2006 Recommendations Class I 1. Mitral valve (MV) surgery is recommended for the symptomatic patient with acute severe mitral ­regurgitation (MR). (Level of evidence: B) 2. MV surgery is beneficial for patients with chronic severe MR and New York Heart Association (NYHA) functional class II, III, or IV symptoms in the absence of severe left ventricular (LV) dysfunction (severe LV dysfunction is defined as ejection fraction 55 mm. (Level of evidence: B) 3. MV surgery is beneficial for asymptomatic patients with chronic severe MR and mild to moderate LV dysfunction, ejection fraction 0.30 to 0.60, and/or end-systolic dimension ≥ 40 mm. (Level of evidence: B) 4. MV repair is recommended over MV replacement in the majority of patients with severe chronic MR who require surgery, and patients should be referred to surgical centers experienced in MV repair. (Level of evidence: C) Class IIa 1. MV repair is reasonable in experienced surgical centers for asymptomatic patients with chronic severe MR with preserved LV function (ejection fraction > 0.60 and end-systolic dimension < 40 mm) in whom the likelihood of successful repair without residual MR is > 90%. (Level of evidence: B) 2. MV surgery is reasonable for asymptomatic patients with chronic severe MR, preserved LV function, and new onset of atrial fibrillation. (Level of evidence: C)

3. MV surgery is reasonable for asymptomatic patients with chronic severe MR, preserved LV function, and pulmonary hypertension (pulmonary artery systolic pressure > 50 mm Hg at rest or > 60 mm Hg with exercise). (Level of evidence: C) 4. MV surgery is reasonable for patients with chronic severe MR due to a primary abnormality of the mitral apparatus and NYHA functional class III–IV symptoms and severe LV dysfunction (ejection fraction < 0.30 and/­or end-systolic dimension > 55 mm) in whom MV repair is highly likely. (Level of evidence: C) Class IIb 1. MV repair may be considered for patients with chronic severe secondary MR due to severe LV dysfunction (ejection fraction < 0.30) who have persistent NYHA functional class III–IV symptoms despite optimal therapy for heart failure, including biventricular pacing. (Level of evidence: C) Class III 1. MV surgery is not indicated for asymptomatic patients with MR and preserved LV function (ejection fraction > 0.60 and end-systolic dimension < 40 mm) in whom significant doubt about the feasibility of repair exists. (Level of evidence: C) 2. Isolated MV surgery is not indicated for patients with mild or moderate MR. (Level of evidence: C)   

From ACC/AHA 2006 guidelines for the management of patients with valvular heart disease. Circulation. 2006;114:e84–e231.

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BOX 6-2  Appropriateness Criteria and Indications for Cardiac Imaging Modalities and Cardiac Catheterization for the Assessment of Mitral Insufficiency TRANSTHORACIC ECHOCARDIOGRAPHY ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/ SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography 47 Native Valvular Regurgitation with TTE n Routine surveillance of trace valvular regurgitation Appropriateness criteria: I; median score: 1 n Routine surveillance (14 mm6 If present, note systolic expansion of the abscess, or check for flow into and out of it—these findings indicate contiguity with a vascular channel. Valve ring abscesses may lead to paravalvular leak and dehiscence, occasionally to a VSD and/or other fistulous communication, such as aortic root to right ventricle or right atrial fistula. TTE lacks sensitivity for the detection of infective abscesses (about 15%). “Early” prosthetic valve IE is the term usually applied to infection occurring within the first 60 days postoperatively. Staphylococci are the most common organisms (47.5%), and S. epidermidis is the most common subset (27% overall). The incidence of “early” prosthetic valve IE peaks at 15 days following the operation. The fatality rate is very high (about 75%). “Late” prosthetic valve IE is the term usually applied to infection occurring later than the first 60 days postoperatively. The usual native valve organisms are seen (streptococci predominate, at about 42%). The case fatality rate is considerably less; about 10%.

RIGHT-HEART INFECTIVE ENDOCARDITIS Right-sided IE accounts for 5% to 10% of cases of most IE series, and is of rising incidence in many North American cities. The tricuspid valve is involved more often than is the pulmonic valve, at a ratio of 10 to 20 to 1. But both right-sided valves may be ­simultaneously

infected. Frequently, pulmonic valve IE is associated with underlying congenital heart disease. Right-sided IE may feature as part of a more complex disease process, for example, VSD with left-to-right flow, infected septal leaflet of the tricuspid valve (impact site of the VSD jet). Extracardiac manifestations predominate: 60% to 100% have either a “pulmonary emboli”-like or “pneumonia-­like” picture, with little systemic arterial disease activity. Most are of “acute” clinical course. S. aureus accounts for half of cases; Streptococcus pneumoniae, Neisseria gonorrhoeae, Streptococcus fecalis, S. viridans, and mixed flora account for most of the remainder. Predisposing factors include skin infections, respiratory infections (S. pneumoniae), dental sepsis, septic abortion, pelvic infection, IV drug abuse, ethanol abuse, and immune compromise. Pulmonary complications include pulmonary infarctions, septic pulmonary arteritis, pneumonia, cavitation, pleural infarction/effusion The typical clinical course of right-sided IE is that of recurrent “pneumonia,” followed by hepatomegaly, jaundice, and, finally, renal failure in persistently febrile patients. How the course evolves depends largely on the virulence of the embolized organism: viridans rarely causes septic complications. Blood cultures often are negative initially and become positive after established pulmonary sepsis occurs. Pulmonary artery blood cultures may help. Right-sided IE caused by Pseudomonas species, fungi, or gram-­negative bacteria may have a better prognosis with partial or complete (usually) tricuspid valve excision. If the pulmonary artery pressures are normal, the hemodynamic tolerance of tricuspid valve excision is fair.

NOTES ON VEGETATIONS Vegetations may be bacterial, fungal, noninfective (marantic), or rheumatic in origin. The differential diagnosis of a vegetation includes the following: r Tumor, especially papillary fibroelastoma r Wear-and-tear lesions (e.g., Lambl’s excrescences) r Valve strands r F lail valve elements r Artifact r Paravalvular structures r Myxomatous changes r Noninfective calcific degeneration Vegetations generally take multiple weeks to form. S. aureus may produce large vegetations. Fungal vegetations often are the largest and may present as obstructive embolus to a large artery. Some cases of endocarditis occur without well-defined vegetations, the so-called “nonvegetant” endocarditis.

Marantic Vegetations

Noninfective (marantic) vegetations usually are not very large, and may be seen on both sides of leaflets. They may be seen in a number of scenarios, including systemic lupus erythematosus, anti-cardiolipin antibodies,

Infective Endocarditis  |  Chapter 9

and malignancy (especially pancreatic adenocarcinoma and lymphoma).

Localization of Vegetations

Vegetations characteristically occur on the low pressure side of valves (original model described by Rodbard in 1964)7 or at the impact site of a regurgitant jet. In aortic insufficiency, jets may appear in a number of locations: r The underside of aortic valve leaflets r The anterior mitral leaflet, ventricular side r The anterior mitral leaflet chordae In MR, they appear in the following locations: r The atrial side of mitral valve leaflets r The left atrial wall Characteristic imaging features of vegetation are as follows: r Mobility r Occurrence on valve leaflets or sites of jet impact r Reflectiveness r Association with insufficiency r Usually have shaggy borders

Serial Assessment of Vegetations

Vegetations have been observed to shrink, remain the same size, or to increase in size with both appropriate and inappropriate antimicrobial therapy. Vegetations can persist after the IE illness. Typically, in appropriately treated infections, bacterial vegetations become smaller and more echoreflective over months after the illness.8

Significance of Vegetations and Their Size

Valve destruction, insufficiency, the risk of embolization, and the requirement for surgery are greater in patients in whom vegetations have been documented,4,9,10 suggesting that there was significantly more systemic embolization with vegetations >10 mm (especially so for mitral valve vegetations). However, severity of CHF is the most important prognosticator, vegetation size did not correlate well with degree of insufficiency, and large vegetations were not more common in patients with Class 4 CHF or death.

Limitations on Identifying Vegetations

Small vegetations (1–2 mm in diameter) are beneath the resolution of TTE, and 10% to 15% of patients have technically limited transthoracic examinations. TTE is approximately 50% sensitive for vegetations; TEE is >90% sensitive.11 Although the validation is older, there has been little in the way of development of TEE probes in the last decade.

INFECTIVE ENDOCARDITIS AND THE ROLE OF TRANSESOPHAGEAL ECHOCARDIOGRAPHY TTE and TEE are complementary in the evaluation of IE. TTE should be the initial investigation. Before TEE is performed, the TTE should be carefully

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scrutinized, so that the TEE is directed toward elaborating remaining questions. TTE is superior to TEE for the functional assessment and ongoing evaluation of aortic valve disease, mitral insufficiency, and left ventricular dysfunction. TEE is superior to TTE in the following situations: r Identifying small vegetations, and vegetations on the pulmonic valve10 r Identifying valve perforation without vegetation12 r In obtaining images in critically ill patients who have technically poor TTE studies r In identifying some complications of endovascular infection such as root, annular, and myocardial abscesses, as well as fistulae.13 For the diagnosis of IE, TEE has occasional false negatives and imperfect negative predictive value. Although often quoted as 100%, the negative predictive value may be less. Among a series of 84 cases of suspected IE and initially negative TEEs, one developed definite IE and eight developed “possible IE,” yielding a negative predictive value of 98.6% for definite IE and 88% for “possible IE.”14 In another series of 105 consecutive cases of suspected IE, of 65 cases with initially negative TEEs, five cases were subsequently proven by either repeat TEE study (n = 3), pathologic findings (n = 1), or diagnostic clinical courses (n = 1) to have IE. Grampositive bacteremia in the presence of a prosthetic aortic valve tended to be more common among the group subsequently proven to have IE, leading the authors to conclude that although an initially negative TEE exam reduces the likelihood of IE, repeat TEE examination should be considered in high risk cases.15 The ACC/AHA 2006 guidelines for the management of patients with valvular disease and recommendations for surgery are presented in Boxes 9-3 and 9-4. The ACC/AHA 2008 guideline focused update on IE is presented in Table 9-1.

SUMMARY r Echocardiography is the most useful test to evaluate

suspected cases of endocarditis. vegetations are more accurately detected by TEE, as are abscesses r Prosthetic valves are challenging to assess, even by TEE in some cases. r Small

REFERENCES 1. Durack DT, Lukes AS, Bright DK. New criteria for diagnosis of infective endocarditis: utilization of specific echocardiographic findings. Duke Endocarditis Service. Am J Med. 1994;96(3):200–209. 2. Task Force ACC/AHA 2006 guidelines for the management of patients with valvular heart disease. J Am Coll Cardiol. 2006;48(3):e1–e148.

160 Chapter 9  |  Infective Endocarditis 3. Thuny F, Di SG, Belliard O, et al. Risk of embolism and death in infective endocarditis: prognostic value of echocardiography: a prospective multicenter study. ­Circulation. 2005;112(1):69–75. 4. Jaffe WM, Morgan DE, Pearlman AS, Otto CM. Infective endocarditis, 1983–1988: echocardiographic findings and factors influencing morbidity and mortality. J Am Coll Cardiol. 1990;15(6):1227–1233. 5. Middlemost S, Wisenbaugh T, Meyerowitz C, et  al. A case for early surgery in native left-sided endocarditis complicated by heart failure: results in 203 patients. J Am Coll Cardiol. 1991;18(3):663–667. 6. Ellis SG, Goldstein J, Popp RL. Detection of endocarditis-­associated perivalvular abscesses by twodimensional echocardiography. J Am Coll Cardiol. 1985; 5(3):647–653. 7. Rodbard S. Hemodynamic considerations in endocarditis. Med Sci. 1964;15:43–49. 8. Stafford A, Wann LS, Dillon JC, et al. Serial echocardiographic appearance of healing bacterial vegetations. Am J Cardiol. 1979;44(4):754–760. 9. Stewart JA, Silimperi D, Harris P, et  al. Echocardiographic documentation of vegetative lesions in infective endocarditis: clinical implications. Circulation. 1980; 61(2):374–380. 10. Mugge A, Daniel WG, Frank G, Lichtlen PR. Echocardiography in infective endocarditis: reassessment of prognostic implications of vegetation size determined by the transthoracic and the transesophageal approach. J Am Coll Cardiol. 1989;14(3):631–638. 11. Erbel R, Rohmann S, Drexler M, et  al. Improved ­diagnostic value of echocardiography in patients with infective endocarditis by transoesophageal approach. A prospective study. Eur Heart J. 1988;9(1):43–53. 12. Roudaut R, Gosse P, Dallocchio M. Assessing prosthetic heart valve function. Value of Doppler echocardiography and patient/prosthetic valve identity and follow-up card. Echocardiography. 1992;9(6):597–603. 13. Daniel WG, Mugge A, Martin RP, et al. Improvement in the diagnosis of abscesses associated with endocarditis by transesophageal echocardiography. N Engl J Med. 1991;324(12):795–800. 14. Law A, Honos G, Huynh T. Negative predictive value of multiplane transesophageal echocardiography in the diagnosis of infective endocarditis. Eur J Echocardiogr. 2004;5(6):416–421.

15. Sochowski RA, Chan KL. Implication of negative results on a monoplane transesophageal echocardiographic study in patients with suspected infective endocarditis. J Am Coll Cardiol. 1993;21(1):216–221. 16. Douglas PS, Garcia MJ, Haines DE, et al. ACCF/ASE/ AHA/ASNC/HFSA/HRS/SCAI/SCCM/SCCT/ SCMR 2011 appropriate use criteria for echocardiography. J Am Coll Cardiol. 2011;57(9):1126–1166. 17. Bonow RO, Carabello BA, Chatterjee K, et al. ACC/AHA 2006 guidelines for the management of patients with valvular heart disease. J Am Coll Cardiol. 2006;48(3):e1–e148. 18. Cheitlin MD, Armstrong WF, Aurigemma GP, et  al. ACC/AHA/ASE 2003 guideline update for the clinical application of echocardiography—summary article. J Am Coll Cardiol. 2003;42(5):954–970. 19. Cheitlin MD, Chair JS, Alpert JS, et  al. ACC/AHA guidelines for the clinical application of echocardiography: a report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines (Committee on Clinical Application of Echocardiography). Circulation. 1997;95:1686–1744. 20. Bonow RO, Carabello AC, Chatterjee K, et  al. ACC/ AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2006;114:e84–e231. 21. Taylor AJ, Cerqueira M, Hodgson JM, et  al. ACCF/ SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/ SCMR 2010 appropriate use criteria for cardiac computed tomography. J Am Coll Cardiol. 2010;56(22):1864–1894. 22. Hendel RC, Manesh PR, Kramer CM, Poon M. ACCF/ ACR/SCCT/SCMR/ASNC/NASCI/SCAI/SIR appropriateness criteria for cardiac computed tomography and cardiac magnetic resonance imaging. J Am Coll Cardiol. 2006;48(7):1475–1497. 23. Pennell DJ, Sechtem UP, Higgins CB, et al. Clinical indications for cardiovascular magnetic resonance (CMR): Consensus Panel report. J Cardiovasc Magn Reson. 2004; 6(4):727–765. 24. Hendel RC, Berman DS, Di Carli MF, et  al. ACCF/ ASNC/ACR/AHA/ASE/SCCT/SCMR/SNM 2009 appropriate use criteria for cardiac radionuclide imaging. J Am Coll Cardiol. 2009;53(23):2201–2229.

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BOX 9-1  Definition of Terms Used in the Proposed Modified Duke Criteria for the Diagnosis of Infective Endocarditis*

BOX 9-2  Definition of Infective Endocarditis According to the Proposed Modified Duke Criteria*

Major Criteria Blood culture positive for infective endocarditis (IE) n Typical microorganisms consistent with IE from two separate blood cultures • Streptococcus viridans, Streptococcus bovis, HACEK group (Haemophilus spp., Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae), ­Staphylococcus aureus • Community-acquired enterococci in the absence of a primary focus n Microorganisms consistent with IE from persistently positive blood cultures, defined as follows: • At least two positive cultures of blood samples drawn more than 12 hours apart or • All of 3 or a majority of >4 separate cultures of blood (with first and last sample drawn at least 1 hour apart) n Single positive blood culture for Coxiella burnetti or anti–phase 1 IgG antibody titer >1:800 Evidence of endocardial involvement n Echocardiogram positive for IE (transesophageal echocardiography recommended in patients with prosthetic valves, rated at least “possible IE” by clinical criteria, or complicated IE [paravalvular abscess]; transthoracic echocardiography as first test in other patients), defined as follows: • Oscillating intracardiac mass on valve or supporting structures, in the path of regurgitant jets, or on implanted material in the absence of an alternative anatomic explanation or • Abscess or • New partial dehiscence of prosthetic valve New valvular regurgitation (worsening or changing of pre-existing murmur insufficient for diagnosis)

Definite Infective Endocarditis n Pathologic criteria • Microorganisms demonstrated by culture or histologic examination of a vegetation, a vegetation that has embolized, or an intracardiac abscess specimen or • Pathologic lesions; vegetation, or intracardiac abscess confirmed by histologic examination showing active endocarditis n Clinical criteria • Two major criteria or • One major criterion and three minor criteria or • Five minor criteria

Minor Criteria n Predisposition, predisposing heart condition, or injection drug use n Fever, temperature >38°C n Vascular phenomena, major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, and ­Janeway’s lesions n Immunologic phenomena; glomerulonephritis, Osler’s nodes, Roth’s spots, and rheumatoid factor n Microbiologic evidence: positive blood culture but does not meet a major criterion,† or serologic evidence of active infection with organism consistent with IE n Echocardiographic minor criteria eliminated    *Modifications to the original criteria are shown in bold type. †Excludes

single positive cultures for coagulase-negative staphylococci and organisms that do not cause endocarditis.

Reprinted with permission from Li JS, Sexton DJ, Mick N, et al. Proposed modifications to the Duke criteria for the diagnosis of infective endocarditis. Clin Infect Dis. 2000;30:633–638.

Possible Infective Endocarditis n One major criterion and one minor criterion or n Three minor criteria Rejected n Firm alternate diagnosis explaining evidence of infective endocarditis (IE) or n Resolution of IE syndrome with antibiotic therapy for 10 mm) vegetations are generally well depicted by TTE.

NA

Transesophageal Echocardiography

• TEE adds incrementally to the evaluation of IE, given its superior detection of • Intermediate-sized (5–10 mm) vegetations • Small (2 SD above the mean value for the test and method employed. r For an echocardiographer, LVH usually is >225 g, but gender-specific definitions are appropriate, because LV mass is very clearly influenced by gender. r LV mass correlates with many clinical factors (height, body surface area, body mass index, lean weight, skin thickness, and blood pressure). Therefore, some attempt to “index” or “normalize” LV mass for common clinical parameters should be undertaken. Generally, LV mass is indexed to either body surface area or height. r In small ventricles, volume normalization of LV mass (LV mass/LVEDV [left ventricular end-­ diastolic volume]) is reasonable to describe LVH. • Normal is 0.80 ± 15 mL/g; LVH is 134 g/m2 • LVH in women: >110 g/m2 Using these paramenters, though, results in a 3% incidence of LVH in normotensive individuals.3 Changing the definition to >140 g/m2 in men reduces the incidence to 1.3%.3 As left ventricular mass index is a linear variable, a prominent effect is imparted by establishing a cut-off to dichotomize the variable as “LVH” or “no LVH.” r Left ventricular mass index grading (g/m2) • Male: normal, 225 g)

92

43

73

2D, two-dimensional; ECG, electrocardiogram; LVH, left ventricular hypertrophy; PPV, positve predictive value. Data from Woythaler JN, Singer SL, Kwan OL, et al. Accuracy of echocardiography versus electrocardiography in detecting left ventricular hypertrophy: comparison with postmortem mass measurements. J Am Coll Cardiol. 1983;2(2):305–311. Used with permission.

TABLE 10-4  Normal Cardiac Volume by Right Anterior Oblique Cineangiography LV end-diastolic volume (mL)

132 ± 36

LV end-systolic volume (mL)

39 ± 15

LV stroke volume (mL)

93

LV ejection fraction (%)

71 ± 7

LV, left ventricular. Data from Wynne J, Green LH, Mann T, et al. Estimation of left ventricular volumes in man from biplane cineangiograms filmed in oblique projections. Am J Cardiol. 1978;41(4):726–732. Used with permission.

TABLE 10-5  Accuracy and Variability of Simpson’s Volumetric Method versus Angiographic Assessment of Left Ventricular Ejection Fraction R

1 SEE

VARIABILITY

95% CI

EF%

0.80–0.90

7–10%

± 7%

10%

ESV (mL)

0.88–0.94

20–30%

± 15%

17%

EDV (mL)

0.80–0.90

25–35%

± 11%

17%

CI, confidence interval; EDV, end-diastolic volume; EF%, ejection fraction; ESV, end-systolic volume; SEE, standard error of the estimate. Data from references 40–42.

Echocardiographic Assessment of the Left Ventricle  |  Chapter 10

185

TABLE 10-6 Left Ventricular Ejection Fraction (Biplane Simpson’s) MEAN ± SD (%) Males

70 ± 7

Females

65 ± 10

Data from Schiller NB, Shah PM, Crawford M, et al: Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-Dimensional Echocardiograms. J Am Soc Echocardiogr. 1989;2(5):358–367. Used with permission.

TABLE 10-7 Sample Size Required to Detect the Same Change by Echocardiography and Cardiac Magnetic Resonance with a Power of 90% and P < 0.05 CLINICAL CHANGE

ECHO

CMR N

EDV, 10 mL

23.8

121

7.4

12

90

ESV, 10 mL

15.8

53

6.5

10

81

6.6

102

2.5

15

85

36.4

273

6.4

9

97

EF, 3% Mass, 10 g

SD

N

PERCENT REDUCTION IN SAMPLE SIZE

SD

CMR, cardiac magnetic resonance; EDV, end-diastolic volume; EF, ejection fraction; ESV, end-systolic volume; N, number of patients; SD, standard deviation. Data from Bellenger NG, Davies LC, Francis JM, et  al: Reduction in sample size for studies of remodeling in heart failure by the use of cardiovascular magnetic resonance. J Cardiovasc Magn Reson. 2000;2(4):271–278. Used with permission.

TABLE 10-8  Cardiac Magnetic Resonance Determination of Left Ventricular Volume DIFFERENCE BETWEEN SINGLE BREATH-HOLD AND MULTIPLE BREATH-HOLDS

CORRELATION

LV EDV

9 ± 15 mL

0.97

LV ESD

6 ± 12 mL

0.98

LV ejection fraction

2 ± 5%

0.95

EDV, end-diastolic volume; ESD, end-systolic diameter; LV, left ventricular. Data from Hendel RC, Mancsh PR, Kramer CM, Poon M. ACCF/ACR/ SCCT/SCMR/ASNC/NASCI/SCAI/SIR appropriateness criteria for cardiac computed tomography and cardiac magnetic resonance imaging. J Am Coll Cardiol. 2006;48(7):1475–1497. Used with permission.

186 Chapter 10  |  Echocardiographic Assessment of the Left Ventricle TABLE 10-9  Interobserver and Intraobserver Variability of LV EDV, ESV, and EF from Repeated Measurement by CMR, CT, and RT3DE VARIABILITY, BIAS, CONFIDENCE

CCT

CMR

RT3DE

Six 30-degree planes around long axis, 16-slice/0.5-mm slice thickness, retrospective gating, diastole: 90% RR/ systole: 0% RR

Six 30-degree planes around long axis, 1.5T, spin echo, 10-sec breath-hold

Six 30-degree planes around long axis, Philips SONOS 7500, X4 matrix array transducer, harmonic mode

LV EDV

Interobserver variability Intraobserver variability Bias 95% confidence limit vs. CMR

2.6 ± 2.0 2.0 ± 1.3 26 mL (sig) 42 mL (sig)

6.3 ± 5.7 2.4 ± 2.3

11.2 ± 8.6 3.9 ± 2.0 –5 mL (ns) 52 mL

LV ESV

Interobserver variability Intraobserver variability Bias 95% confidence limit vs. CMR

5.7 ± 5.2 2.2 ± 3.1 19 mL (sig) 50 mL (sig)

7.7 ± 6.6 6.3 ± 4.6

14.2 ± 11.8 5.6 ± 3.9 –6 mL (ns) 52 mL

LV EF

Interobserver variability Intraobserver variability Bias 95% confidence limit vs. CMR

6.5 ± 4.9 2.1 ± 3.4 –2.8% (ns) 13%

8.5 ± 9.7 6.2 ± 6.2

10.5 ± 8.3 5.6 ± 3.4 0.3% (ns) 8%

CCT, cardiac computed tomography; CMR, cardiac magnetic resonance; EDV, end-diastolic volume; EF, ejection fraction; ESV, end-diastolic volume; LV, left ventricle; ns, nonsignificant; RT3DE, real-time three-dimensional echocardiography; sig, significant. Data are mean ± standard deviation. Data from Sugeng L, Mor-Avi V, Weinert L, et al. Quantitative assesment of left ventricular size and function side-by-side comparison of realtime three-dimensional echocardiography and computed tomography with magnetic resonance reference. Circulation. 2006;114(7):654–661. Used with permission.

TABLE 10-10  Reference Limits and Partition Values of Left Ventricular Size LV DIMENSION

UNITS

NORMAL

MILDLY ABNORMAL

MODERATELY ABNORMAL

SEVERELY ABNORMAL

LV diastolic diameter

Males Females

cm cm

4.2–5.9 3.9–5.3

6.0–6.3 5.4–5.7

6.4–6.8 5.8–6.1

≥6.9 ≥6.2

LV diastolic diameter (BSA)

Males Females

cm/m2 cm/m2

2.2–3.1 2.4–3.2

3.2–3.4 3.3–3.4

3.5–3.6 3.5–3.7

≥3.7 ≥3.8

LV diastolic diameter (height)

Males Females

cm/m cm/m

2.4–3.3 2.5–3.2

3.4–3.5 3.3–3.4

3.6–3.7 3.5–3.6

≥3.8 ≥3.7

BSA, body surface area; LV, left ventricle. Data from Lang RM, Bierig M, Devereux RB, et  al. Recommendations for chamber quantification: a report from the American Society of Echocardiography’s Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. J Am Soc Echocardiogr. 2005;18(12):1440–1463. Used with permission.

Echocardiographic Assessment of the Left Ventricle  |  Chapter 10

187

TABLE 10-11 Echocardiographic Reference Limits and Partition Values of Left Ventricular Mass and Geometry

LV EDV LV EDVI (BSA)* LV ESV LV ESVI (BSA)* LV EF

UNITS

NORMAL

MILDLY ABNORMAL

MODERATELY ABNORMAL

SEVERELY ABNORMAL

Males

mL

67–155

156–178

179–201

≥201

Females

mL

56–104

105–117

118–130

≥131

Males

mL/m2

35–75

76–86

87–96

≥97

Females

mL/m2

35–75

76–86

87–96

≥97

Males

mL

22–58

59–70

71–82

≥83

Females

mL

19–49

50–59

60–69

≥70

Males

mL/m2

12–30

31–36

37–42

≥43

Females

mL/m2

12–30

31–36

37–42

≥43

Males

%

≥55

45–54

30–44

65%) of inhospital mortality from acute MI. It may occur with a first, and massive, infarction, or with a second or third infarction. Severe WMAs in extensive territories are expected in cardiogenic shock due to pump failure.

CAD: Ischemia, Infarction, and Complications  |  Chapter 11

The LV may or may not be dilated. Massive acute first MI is unlikely to have prominent dilation. It is the com­ bination of abrupt fall in ejection fraction and lack of dilation that is responsible for the low stroke volume, and resultant low output, despite tachycardia. Right Ventricular Infarction RV infarction is a common cause of hypotension and the principal cause of shock in inferior infarction. The RV is under-assessed on most echocardiograms; there­ fore, a diligent effort to assess it regionally and globally is required. The size of RV infarction relates, in general, to how proximally the right coronary artery is occluded. A posterior RV infarction is common in the context of most inferior infarctions. An anterior RV infarction is common in the context of anterior LV infarction, as an apical RV infarction is common in the setting of an LV apical infarction. The right ventricular outflow tract (seen on the posterior long-axis view) usually is spared in RV infarction. The hemodynamically significant, important RV infarction involves the lateral RV (seen on the apical four-chamber view and the posterior short-axis view) and the posterior RV (seen on the pos­ terior short-axis view and the subcostal view). Rarely, complications other than hemodynamic compromise— such as RV thrombi, RV papillary muscle rupture, and RV rupture—will arise from RV infarction. The most severe RV infarctions also involve the right atrium, which is difficult to assess by echocardiography.

Mechanical Complications of Infarction

Free Wall Rupture Free wall rupture accounts for approximately 10% of postinfarction sudden deaths. Rupture typically occurs through the lateral (but it may be through any) wall of the left ventricle. The right ventricle is one-seventh as likely to rupture as the LV. Rupture occurs only follow­ ing a transmural infarction. The time is typically 3 to 5 days following MI, but may be earlier, especially if the patient received fibrinolytics. A subset of patients with free wall rupture will not experience immediate sudden death: this group is said to have “subacute rupture”7 with echocardiographic signs of tampon­ ade, pericardial effusion >5 mm, and echo­densities in the pericardial space that represent coagulated blood. Suspected clot in the pericardial space, which appears as an echo-dense mass in the pericardial space, may be a sign of free wall rupture8 and renders the likelihood of evacuation through a pericardiocentesis needle unlikely. Urgent surgical repair will salvage some cases. Bedside echocardiography is the most suitable test to identify free wall rupture. Ultimately, there is no per­ fect echocardiographic sign to distinguish severe early postinfarction tamponade from rupture. Identification of clot in the pericardial space is useful, however. Left Ventricular (or Other) False Aneurysm Ventricular false or “pseudo” aneurysms contain no myocardial layer; a free wall rupture is contained by

203

adherence of overlying pericardium or by a thin layer of epicardium beneath pericardium. A false aneurysm develops because a tear into a portion of recently trans­ murally infarcted myocardium extended up to the epicar­ dium or even through it, and complete rupture of the LV into the pericardial cavity was avoided because pericar­ dial adhesions (the result of prior pericarditis) contained the rupture. Thus, a false aneurysm is to be considered an intermediate form of rupture, and reparative surgery is urgently indicated. The contained rupture typically extends away from the neck to appear as an echo-free space with the shape of a mushroom cap. The neck usu­ ally is less than half the width of the body of the false aneurysm. This is in contradistinction to the wide neck of a (true) aneurysm, which usually is as wide as the body of the aneurysm itself (the dimension of the neck/the dimension of the body is 0.9 to 1.0).9 It is the width of the neck, more than any other detail, that renders the out­ pouching of the LV a false aneurysm rather than a true aneurysm. In systole, the false aneurysm typically bulges out as it receives part of the LV stroke volume. The flow in and out (or “to-and-fro”) is evident by color and spec­ tral Doppler.10 Two-­dimensional echocardiography is the procedure of choice to establish the presence of a pseu­ doaneurysm. Cineangiography and MRI also are excel­ lent means to image false aneurysms. Confusion occurs about aneurysms of the base of the LV between the body of the posteromedial papillary muscle and the mitral annulus. Often the traction of the papillary muscle keeps the neck narrow, replicating the sign of a false aneurysm. Thus the “neck” sign is best applied away from the trouble spot on the posterolateral wall, where both aneu­ rysms and false aneurysms occur, but where they cannot be easily distinguished by neck morphology alone. The diagnosis can be made by TTE in most cases. TEE offers confirmation in some cases that the neck is narrow, and the wall disrupted. TEE is probably better able to image posterior wall false aneurysms and may increase the detection rate of small posterior false aneurysms. Septal Rupture Ventricular septal ruptures are less common than free wall ruptures (about 1–3% of MI). They are almost invariably associated with a septal dilation (aneurysm) with thinning. Septal ruptures may occur in anterior/ apical locations, or basal–posterior locations. r Anterior/apical septal ruptures • Twice as common as posterior–basal ruptures • May have a single, well-defined hole • LAD-infarct related • Association of a substantial-sized aneurysm is usual • Less RV infarction associated • Easier to access surgically r Posterior–basal septal ruptures • Less common • Seldom have a single, well-defined hole—most are complex or serpiginous • PDA infarct–related

204 Chapter 11  |  CAD: Ischemia, Infarction, and Complications Associated RV MI is common, which indicates a poor prognosis.11 Two-dimensional echocardiography identi­ fies the defect in more than half of cases, but color Doppler will find nearly 100% of defects.12–14 Agitated saline contrast studies are not needed. Urgent surgical repair is indicated. Patients with large concurrent RV infarctions do very poorly with or without surgery. TTE is able to make the diagnosis in almost all cases, and detects and localizes the septal rupture by color flow mapping. TEE will give more detail of the anatomic disruption, which may be necessary for the surgeon. Intraoperative TEE is required to determine adequacy of the repair (ablation of the shunt) and to assist with elucidating the all too common hemody­ namic problems coming off pump. Papillary Muscle Rupture Papillary muscle rupture causes severe disruption of the mitral apparatus and leads to severe mitral insuf­ ficiency and marked reduction in forward cardiac output. Clinically, papillary muscle rupture is a severe event, progressive, and usually fatal if not successfully operated upon (80% mortality within 1 week). In the setting of inferior infarction, the posteromedial papil­ lary muscle usually is the affected one. In the setting of anterolateral infarction, the anterolateral papillary muscle usually is the affected one. Overall, the pos­ teromedial papillary muscle, which usually is supplied by the posterior descending artery alone, is 5 to 10 times more likely to rupture than the anterolateral one, which usually is supplied by both the posterior descending artery and the left circumflex coronary artery.15 In a short-axis view, the anterolateral papil­ lary muscle is seen at 3 o’clock, and the posteromedial papillary muscle is seen at 7  o’clock. Of note, even tricuspid papillary muscles can rupture in the case of RV MI. Rupture may be complete or partial. Partial rupture results in severe MR, not cardiogenic shock. In a posterior long-axis view, the posteromedial papil­ lary muscle or muscles are seen. On an A4CV, the anterolateral papillary muscle is seen. On TEE trans­ gastric short-axis views, as with transthoracic shortaxis views, both papillary muscle sets are seen. On a TEE long-axis view, both papillary muscles can be seen, although often with slight angulations to opti­ mize the imaging of each. Imaging of papillary mus­ cles requires specific views to assess their integrity. Zoom views are helpful. The echocardiographic signs of papillary muscle rupture depend on whether the rupture is complete or partial. r Complete papillary muscle rupture • Flailing mass attached to the mitral leaflets, mov­ ing back and forth between the left atrium and the LV • If the papillary muscle head becomes “wrappedup” in its chordae, the appearance of the mass is less obviously that of a ruptured papillary muscle trunk.

• Severe MR. The absence of a large jet does not exclude the diagnosis of severe MR. The size of the jet depends on the transmitral gradient, which may be low if there is systemic hypotension and the left atrial pressure is high. • WMA r Partial papillary muscle rupture • “Wobbling” of the body of the papillary muscle • Stretching of the body of the papillary muscle • Usually, there is severe MR due to prolapse of the mitral valve. Conspicuously, the mitral valve leaflet thickness is normal, suggesting that myxo­ matous disease is not responsible for the prolapse and that another cause should be sought. r A WMA may not be apparent. There typically are two posteromedial papillary muscle bodies or heads; seeing one of them does not establish that the entire apparatus is intact. The left atrium, even if not enlarged, may show systolic bulg­ ing secondary to the large volume load of severe MR. The maximal velocity is reached in early systole, with a rapid systolic decline, indicating rapid equilibration of the left ventricular and left atrial pressures. Although TTE, carefully performed (i.e., with zoom views of each of the papillary muscles) is able to estab­ lish the diagnosis in most cases, TEE can be confirma­ tory when uncertainty persists or diagnostic when images are poor by TTE or when the echocardiogra­ pher is unsure of the diagnosis.

Left Ventricular Aneurysm

An LV aneurysm is a localized dilation of the LV, with the wall intact but usually thinned. To clinicians, aneu­ rysms are recognized by the following: r Their diastolic dilation r The wide neck Two-dimensional echocardiography is the procedure of choice to establish the presence and size of ventricu­ lar aneurysms (sensitivity 93%, specificity 94%).16 Aneu­ rysms may occur anywhere, but most commonly occur over the anterior or apical regions. Typically, a recently formed aneurysm is dyskinetic. Chronically, as they scar and often calcify, they become less dyskinetic. Early for­ mation of aneurysm (0.4 or area ratios >0.3 have significantly more congestive heart failure and mortality.18,22 The location of the aneurysm and the systolic function of the remainder of the LV are considered when surgical aneurysmectomy is entertained. Surgical aneurysmec­ tomy is not a primary indication for surgery, but may

CAD: Ischemia, Infarction, and Complications  |  Chapter 11

be entertained when coronary bypass or valve surgery is the primary indication. If the aneurysm involves the papillary muscles, then surgical results are less good, as the mitral apparatus will be affected by the surgery. Similarly, if the condition of the nonaneurysmal LV (what will be left after the surgery) is poor, then the outcome will be poor.19,20 Inferior/posterior aneurysms often lead to MR, and hence to mitral valve replacement with aneurysmectomy. Ventricular aneurysms frequently contain thrombus. The role OF TEE in assessing aneurysms is very small, unless TTE views are very poor. Because most aneurysms are apical, TEE is less well suited to depict most aneurysms, because of the longer distance to the apex using an inherently higher frequency transducer, and the invariably foreshortened view of the apex from the lower esophageal four-chamber view.

Other Complications

Intracavitary Thrombus Intracavitary thrombus may occur in almost any loca­ tion of the heart where regional aneurysm or dyskine­ sis (or possibly akinesis) has occurred. Thrombus typically is seen at the apex, which is prone to the most stagnant flow following infarction. The second most common site is over the anterior wall. Thrombi may be laminated and flat, round and pedunculated, single or multiple, obvious or difficult to distinguish from trabeculations. Thrombi are a sign of low flow within that region of the heart, and potentially of overall low cardiac output. When they form very early postinfarc­ tion, they are associated with high mortality. The echocardiographic signs of thrombi are as follows: r Thrombus to blood pool interface r Specular echoes within the thrombus r Endocardial to thrombus interface underneath False-positives include prominent trabeculations, false tendons, and near-field artifacts. False tendons are linear and have blood pool on both sides. Near-field artifacts typically cross tissue borders. False-negatives occur because of insufficient time taken to scan an enlarged apex (where a small thrombus resides), an overlying near-field artifact, or poor image quality. Intravenous echo contrast may help to recognize some thrombi not seen on poor quality TTE, as may TEE. The thrombi most likely to embolize are those that are mobile and located at the margin of an infarct that is subject to violent rocking motion. Dynamic Left Ventricular Outflow Tract Obstruction Dynamic left ventricular outflow tract obstruction can occur post–apical infarction or stunning. The predis­ posing factor is a small-cavity dynamic LV. With apical infarction or stunning, the basal (noninfarct) portion becomes hyperdynamic and develops a dynamic obstruction at the base of the left ventricular outflow

205

tract. The condition has a favorable prognosis, unlike most postinfarction causes of hypotension or shock, but is load and inotrope sensitive. “Functional” Mitral Regurgiation By objective testing, at least 20% of MI cases develop “functional” MR, which may be transient or persis­ tent. Any peri-infarction MR portends higher risk. The term “functional” MR denotes that the mitral components are intact (using zoom views, it is neces­ sary to exclude papillary muscle rupture). The basis of “functional” mitral insufficiency post-MI is distortion of the LV and tethering/malalignment of the chordae and leaflets. Apical or lateral displacement of the pap­ illary muscles exerts traction on the mitral leaflets that results in loss of coaptation. The greater the regional or overall remodeling of the LV, the greater the likeli­ hood of development of MR. Hence, functional MR postinfarction is an indirect descriptor of LV function, geometry, or remodeling.

REFERENCES 1. Wilkins GT, Southern JF, Choong CY, et al. Correlation between echocardiographic endocardial surface map­ ping of abnormal wall motion and pathologic infarct size in autopsied hearts. Circulation. 1988;77:978–987. 2. Parisi AF. The case for echocardiography in acute ­myocardial infarction. J Am Soc Echocardiogr. 1988;1: 173–178. 3. Force T, Kemper A, Perkins L, et al. Overestimation of infarct size by quantitative two-dimensional echocar­ diography: the role of tethering and of analytic proce­ dures. Circulation. 1986;73:1360–1368. 4. Jaarsma W, Visser CA, Eenige van MJ, et al. Predictive value of two-dimensional echocardiographic and hemo­ dynamic measurements on admission with acute myocar­ dial infarction. J Am Soc Echocardiogr. 1988;1:187–193. 5. Jaarsma W, Visser CA, Eenige van MJ, et al. Prognostic implications of regional hyperkinesia and remote asyn­ ergy of noninfarcted myocardium. Am J Cardiol. 1986; 58:394–398. 6. Isaacsohn JL, Earle MG, Kemper AJ, et al. Postmyocar­ dial infarction pain and infarct extension in the coro­ nary care unit: role of two-dimensional echocardiography. J Am Coll Cardiol. 1988;1988(11):246–251. 7. Lopez-Sendon J, Gonzalez A, Lopez DS, et al. Diagno­ sis of subacute ventricular wall rupture after acute myocardial infarction: sensitivity and specificity of clini­ cal, hemodynamic and echocardiographic criteria. J Am Coll Cardiol. 1992;19:1145–1153. 8. Knopf WD, Talley JD, Murphy DA. An echo-dense mass in the pericardial space as a sign of left ventricular free wall rupture during acute myocardial infarction. Am J Cardiol. 1987;59:1202. 9. Gatewood Jr RP, Nanda NC. Differentiation of left ventricular pseudoaneurysm from true aneurysm with two dimensional echocardiography. Am J Cardiol. 1980; 46:869–878. 10. Roelandt JR, Sutherland GR, Yoshida K, et  al. Improved diagnosis and characterization of left ven­

206 Chapter 11  |  CAD: Ischemia, Infarction, and Complications tricular pseudoaneurysm by Doppler color flow imag­ ing. J Am Coll Cardiol. 1988;12:807–811. 11. Moore CA, Nygaard TW, Kaiser DL, et al. Postinfarc­ tion ventricular septal rupture: the importance of loca­ tion of infarction and right ventricular function in determining survival. Circulation. 1986;74:45–55. 12. Maurer G, Czer LS, Shah PK, et  al. Assessment by Doppler color flow mapping of ventricular septal defect after acute myocardial infarction. Am J Cardiol. 1989; 64:668–671. 13. Harrison MR, MacPhail B, Gurley JC, et al. Usefulness of color Doppler flow imaging to distinguish ventricular septal defect from acute mitral regurgitation complicat­ ing acute myocardial infarction. Am J Cardiol. 1989;64: 697–701. 14. Helmcke F, Mahan III EF, Nanda NC, et  al. Twodimensional echocardiography and Doppler color flow mapping in the diagnosis and prognosis of ventricular septal rupture. Circulation. 1990;81:1775–1783. 15. Barbour DJ, Roberts WC. Rupture of a left ventricular papillary muscle during acute myocardial infarction: analysis of 22 necropsy patients. J Am Coll Cardiol. 1986; 8:558–565. 16. Visser CA, Kan G, David GK, et  al. Echocardio­ graphic-cineangiographic correlation in detecting left ventricular aneurysm: a prospective study of 422 patients. Am J Cardiol. 1982;50:337–341. 17. Visser CA, Kan G, Meltzer RS, et al. Incidence, timing and prognostic value of left ventricular aneurysm for­ mation after myocardial infarction: a prospective, serial echocardiographic study of 158 patients. Am J Cardiol. 1986;57:729–732. 18. Visser CA, Kan G, Meltzer RS, et al. Assessment of left ventricular aneurysm resectability by two-dimensional echocardiography. Am J Cardiol. 1985;1985(56):857–860. 19. Edwards BS, Edwards WD, Edwards JE. Ventricular septal rupture complicating acute myocardial infarction:

identification of simple and complex types in 53 autop­ sied hearts. Am J Cardiol. 1984;54:1201–1205. 20. Mann JM, Roberts WC. Rupture of the left ventricular free wall during acute myocardial infarction: analysis of 138 necropsy patients and comparison with 50 necropsy patients with acute myocardial infarction without rup­ ture. Am J Cardiol. 1988;62:847–859. 21. Cabin HS, Roberts WC. True left ventricular aneurysm and healed myocardial infarction. Clinical and necropsy observations including quantification of degrees of coro­ nary arterial narrowing. Am J Cardiol. 1980;46:754–763. 22. Matsumoto M, Watanabe F, Goto A, et  al. Left ven­ tricular aneurysm and the prediction of left ventricular enlargement studied by two-dimensional echocardiog­ raphy: quantitative assessment of aneurysm size in rela­ tion to clinical course. Circulation. 1985;72:280–286. 23. Douglas PS, Garcia MJ, Haines DE, et  al. ACCF/ ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/ SCCT/SCMR 2011 appropriate use criteria for echo­ cardiography. J Am Coll Cardiol. 2011;57(9):1126–1166. 24. Cheitlin MD, Armstrong WF, Aurigemma GP, et  al. ACC/AHA/ASE 2003 guideline update for the clinical application of echocardiography—summary article. J Am Coll Cardiol. 2003;42(5):954–970. 25. Taylor AJ, Cerqueira M, Hodgson JM, et  al. ACCF/ SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/ SCMR 2010 appropriate use criteria for cardiac computed tomography. J Am Coll Cardiol. 2010;56(22):1864–1894. 26. Hendel RC, Patel MR, Kramer CM, et al. ACCF/ACR/ SCCT/SCMR/ASNC/NASCI/SCAI/SIR 2006 appro­ priateness criteria for cardiac computed tomography and cardiac magnetic resonance imaging. J Am Coll Cardiol. 2006;48(7):1475–1497. 27. Hendel RC, Berman DS, Di Carli MF, et  al. ACCF/ ASNC/ACR/AHA/ASE/SCCT/SCMR/SNM 2009 appropriate use criteria for cardiac radionuclide imag­ ing. J Am Coll Cardiol. 2009;53(23):2201–2229.

CAD: Ischemia, Infarction, and Complications  |  Chapter 11

207

BOX 11-1  Appropriateness Criteria and Indications for Cardiac Imaging Modalities for the Assessment of Coronary Artery Disease TRANSTHORACIC ECHOCARDIOGRAPHY ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/ SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography 23 Hypotension or Hemodynamic Instability with TTE n Hypotension or hemodynamic instability of uncertain or suspected cardiac etiology Appropriateness criteria: A; median score: 9 n Assessment of volume status in a critically ill patient Appropriateness criteria: U; median score: 5 Myocardial Ischemia/Infarction with TTE n Acute chest pain with suspected MI and nondiagnostic ECG when a resting ECG can be performed during pain Appropriateness criteria: A; median score: 9 n Evaluation of a patient without chest pain but with other features of an ischemic equivalent or laboratory markers indicative of ongoing MI Appropriateness criteria: A; median score: 8 n Suspected complication of MI, including, but not limited to, acute mitral regurgitation, ventricular septal defect, free-wall rupture/tamponade, shock, RV involvement, HF, or thrombus Appropriateness criteria: A; median score: 9 Evaluation of Ventricular Function after ACS with TTE n Initial evaluation of ventricular function following ACS Appropriateness criteria: A; median score: 9 n Re-evaluation of ventricular function following ACS during recovery phase when results will guide therapy Appropriateness criteria: A; median score: 9 Respiratory Failure with TTE n Respiratory failure or hypoxemia of uncertain etiology Appropriateness criteria: A; median score: 8 n Respiratory failure or hypoxemia when a noncardiac etiology of respiratory failure has been established Appropriateness criteria: U; median score: 5 ACC/AHA/ASE 2003 Guideline Update for the Clinical Application of Echocardiography 24 Recommendations for Echocardiography in the Diagnosis of Acute MI Syndromes n Class I • Diagnosis of suspected acute ischemia or infarction not evident by standard means TRANSESOPHAGEAL ECHOCARDIOGRAPHY ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/ SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography 23 TEE as Initial or Supplemental Test—General Uses n Use of TEE when there is a high likelihood of a nondiagnostic TTE due to patient characteristics or inadequate visualization of relevant structures Appropriateness criteria: A; median score: 8 n Routine use of TEE when a diagnostic TTE is reasonably anticipated to resolve all diagnostic and management concerns Appropriateness criteria: I; median score: 1

• Measurement of baseline LV function • Evaluation of patients with inferior myocardial infarction and bedside clinical evidence suggesting possible RV infarction • Assessment of mechanical complications and mural thrombus* n Class IIa • Identification of location/severity of disease in patients with ongoing ischemia n Class III • Diagnosis of acute MI already evident by standard means Recommendations for Echocardiography in Risk Assessment, Prognosis, and Assessment of Therapy in Acute MI Syndromes n Class I • Assessment of infarct size and/or extent of jeop­ar­ dized myocardium • In-hospital assessment of ventricular function when the results are used to guide therapy • In-hospital or early postdischarge assessment of the presence/extent of inducible ischemia whenever baseline abnormalities are expected to compromise electrocardiographic interpretation† • Assessment of myocardial viability when required to define potential efficacy of revascularization‡ n Class IIa • In-hospital or early postdischarge assessment of the presence/extent of inducible ischemia in the absence of baseline abnormalities expected to compromise ECG interpretation† • Assessment of myocardial viability when required to define potential efficacy of revascularization‡ • Re-evaluation of ventricular function during recovery when results are used to guide therapy • Assessment of ventricular function after revascularization n Class IIb • Assessment of long-term late prognosis (≥2 years after acute MI) n Class III • Routine re-evaluation in the absence of any change in clinical status

ACC/AHA/ASE 2003 Guideline Update for the Clinical Application of Echocardiography 24 Recommendations for Echocardiography in the Diagnosis of Acute Myocardial Ischemic Syndromes n Class I • Assessment of mechanical complications and mural thrombus*

   Continued

208 Chapter 11  |  CAD: Ischemia, Infarction, and Complications BOX 11-1  Appropriateness Criteria and Indications for Cardiac Imaging Modalities for the Assessment of Coronary Artery Disease—cont’d CARDIAC COMPUTED TOMOGRAPHY ACCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/SCMR 2010 Appropriate Use Criteria for Cardiac CT 25 Evaluation of Ventricular Morphology and Systolic Function n Initial evaluation of LV function Following acute MI or in HF patients Appropriateness criteria: I; median score: 2 n Evaluation of LV function Following acute MI or in HF patients Inadequate images from other noninvasive methods Appropriateness criteria: A; median score: 7

Elevated Troponin of Uncertain Clinical Significance n Elevated troponin without additional evidence of ACS or symptoms suggestive of CAD Appropriateness criteria: U; median score: 6

CARDIAC MAGNETIC RESONANCE ACCF/ACR/SCCT/SCMR/ASNC/NASCI/SCAI/SIR 2006 Appropriateness Criteria for Cardiac Computed Tomography and Cardiac Magnetic Resonance Imaging 26 Evaluation of Ventricular and Valvular Function n Procedures may include LV/RV mass and volumes, MR angiography, quantification of valvular disease, and delayed contrast enhancement Appropriateness criteria: A; median score: 9 n Evaluation of LV function following MI or in heart failure patients Appropriateness criteria: U; median score: 6

n Evaluation of LV function following MI or in heart failure patients Patients with technically limited images from echocardiogram Appropriateness criteria: A; median score: 8 n Quantification of LV function Discordant information that is clinically significant from prior tests Appropriateness criteria: A; median score: 8

NUCLEAR ACCF/ASNC/AHA/ASE/SCCT/SCMR/SNM 2009 Appropriate Use Criteria for Cardiac Radionuclide Imaging 27 Ischemic Cardiomyopathy/Assessment of Viability n Known severe LV dysfunction Patient eligible for revascularization Appropriateness criteria: A; median score: 9

Evaluation of LV Function n Assessment of LV function with radionuclide angiography (ERNA or FP RNA) In absence of recent reliable diagnostic information regarding ventricular function obtained with another imaging modality Appropriateness criteria: A; median score: 8 n Routine† use of rest/stress ECG-gating with SPECT or PET MPI     Appropriateness criteria: A; median score: 9

Appropriateness criteria: A, appropriate; I, inappropriate; U, uncertain. ACS, acute coronary syndrome; CAD, coronary artery disease; ECG, electrocardiogram; HF, heart failure; LV, left ventricle; MI, myocardial infarction/ischemia; MPI, myocardial perfusion imaging; PET, positron emission tomography; RV, right ventricle; SPECT, single-photon emission computed tomography; TEE, transesophageal echocardiography; TTE, transthoracic echocardiography. *TEE is indicated when TTE studies are not diagnostic. †Exercise

or pharmacologic stress echocardiogram.

‡Dobutamine

stress echocardiogram.

TABLE 11-1 Cardiac Events According to the Presence or Absence of Left Ventricular Systolic Dysfunction*

Cardiac events† within 24 hours Cardiac

events†

from 48 hours to 2 years

LVSD

NO LVSD

P

24%

6%

2 segments) developing at low dose of dobutamine (≤10 mg/kg/min) or at a low heart rate (150 msec. The primary aim of a pre-CRT echocardiogram for intraventricular dyssynchrony is to identify those individuals who do not have significant mechanical dyssynchrony and therefore may be less likely to respond to CRT. Furthermore, echocardiography may identify a subset of individuals with QRS

duration 65 msec is defined as intraventricular dyssynchrony.15 The corresponding cut-off for intraventricular dyssynchrony using the Yu index is a standard deviation of 12 segments >33 msec.21 Technique10 ECG to have relatively noise-free optimal QRS waveform. r Optimal standard 2D images are obtained in the apical two-chamber, long-axis, and four-chamber views. r Frame rate, depth, and time-gain settings are optimized. Optimal frame rate is >90 frames/sec. The depth setting should include the mitral annulus. r Align the LV cavity in the center of the sector and align the LV to allow for optimal Doppler angle of incidence to interrogate longitudinal velocity r Adjust

301

r Activate

color TD and optimize sector width to achieve frame rate >90 frames/sec. r Suspend patient breathing to allow image capture of 3 to 5 beats. This is often optimal at end-expiration but can be done at the time when optimal images are obtained. Increase the number of beats sampled if premature atrial or ventricular beats are present. r Record the same acquisition sequence in three standard apical imaging planes: apical four-chamber, three-chamber, and two chamber. r Determine the LV ejection interval using pulsedwave Doppler in the LV outflow tract in the apical five-chamber view. Color Doppler Tissue Analysis Determine the timing of LV ejection by marking the beginning and end of Doppler flow in the LV outflow tract as described earlier. The timing reference is usually the ECG signal for most software platforms. The timing of aortic valve opening and aortic valve closure are then superimposed as points on the time–velocity curves to assist with analysis. Regions of interest measuring a minimum of 5 × 10 mm to 7 × 15 mm are placed in the basal and ­mid-regions of opposing LV walls (4 regions per view; 12 regions in total). These sampling volumes are used to generate time–velocity plots. Identify components of the time–velocity curve to ensure physiologic signal quality. These components include the isovolumic contraction velocity (150 msec, the cutoff SD value of 33 msec has a sensitivity of 83% and a specificity of 86%.21 In the multicenter PROSPECT study, TVI did not perform as well in predicting CRT clinical and reverse remodeling outcomes. For the Bax method, 66.8% of echocardiograms were evaluable.13 The predictive values for clinical composite score improvement and for improvement in LVESV were poor, with an AUC of 0.50 and 0.61, respectively.13 The Yu method was difficult to reproduce in a multicenter setting, with only 50% of echocardiograms evaluable.13 AUC for improvement in clinical composite score was 0.60; for improvement in LVESV it was 0.55.13 Thus, it appears that performance of these methods in single centers where the technique has been practiced and refined is much superior to a multicenter setting in terms of prediction of CRT outcomes. Tissue synchronization imaging (TSI) uses colorcoded time-to-peak-velocity data and superimposes this information on the standard 2D apical LV images. In this way, a visual rendering of the latest activated myocardial region is displayed. It is important to focus on peak tissue velocity during the early ejection period and to exclude early isovolumic contraction and late post-systolic shortening. Gorscan et  al.22 used color TSI to guide placement of regions of interest and assess an anteroseptal-to-posterior wall delay ≥65 msec. This technique was able to predict an acute improvement in stroke volume post-CRT. Yu et al. also used TSI in 56 patients and found the SD of 12-segment tissue velocities had a receiver operating curve of 0.90 to predict CRT response.23 However, as shown in the PROSPECT study, such techniques may not perform as well in a multicenter setting. Tissue displacement (tissue tracking) is displayed as a color overlay on 2D images and has been used to predict response to CRT. However, this technique is also limited by the Doppler angle of incidence. At present, cut-off values for predicting CRT response have not been established. Strain and Strain Rate Imaging Strain is defined as the change in myocardial length in relation to baseline length and is derived from tissue velocity imaging data. Strain curves are shown as percent change in length over time. For each region of

interest in the standard apical LV views, peak negative strain is determined. Some investigators believe that strain imaging is a more precise technique to measure dyssynchrony because measurement of strain is not affected by tethering of adjacent myocardial segments, a consideration that may be especially important in ischemic heart disease. However, as with TVI, strain and strain rate imaging depend on the Doppler angle of interrogation. For this reason, it may be difficult to determine strain and strain rate in the more spherical shaped LV cavities that are common in the HF population. Evidence. Sogaard et al.24 showed that basal segment measurement of delayed longitudinal contraction measured by myocardial strain predicted improvement in LVEF after CRT. However, Yu et al.21 compared TVI data and strain rate imaging and showed that strain rate imaging failed to predict improvement in LVESV post-CRT. Furthermore, in the PROSPECT study, strain imaging data performed poorly in a multicenter setting, with 81.4% of echocardiograms evaluable and an AUC of only 0.51 for predicting both clinical improvement and improvement in LVESV post-CRT.13 Currently, tissue strain and strain rate imaging are limited by a poor signal-to-noise ratio and, therefore, are not the preferred methods for determination of intraventricular dyssynchrony. Radial Strain Tissue Doppler radial strain imaging was first described in 2005 by Dohi et al.25 They studied 38 patients who underwent CRT and measured radial dyssynchrony derived from TVI data. Their technique was limited by poor signal-to-noise ratio associated with poor image quality and by the Doppler angle of incidence. In 2006, Suffoletto et al.16 described a new technique of radial strain imaging that tracked the motion of “speckles” derived from the raw radiofrequency tissue signal from the LV mid–short-axis image. The motion of grayscale speckles is tracked in the radial plane. This tracking allows for the quantification of tissue velocity and, therefore, strain in the radial plane. This technique has the major advantage of not being limited by the Doppler angle of interrogation. Also, unlike M-mode measurements, radial strain imaging is able to distinguish between passive movement related to tethering and active myocardial movement. Radial strain is measured using a mid-LV short-axis image at the papillary muscle level. Time to peak percent thickening of the septal and posterior wall segments is determined. Technique. In radial speckle tracking, 2D images are obtained in the parasternal short axis at the level of the papillary muscle. Frame rate is optimized to >100 fps. Radial speckle tracking software is run that allows selection of epicardial and endocardial borders. Then the software color-codes each segment. Analysis

Echocardiography and Its Role in Cardiac Resynchronization Therapy  |  Chapter 17

of radial strain is performed in the septal and posterior walls to quantify intraventricular dyssynchrony (Fig. 17-6). A difference in radial strain of >130 msec between the septal and posterior walls defines radial intraventricular dyssynchrony.16 Evidence. In the original description of radial strain measurement using speckle tracking, Suffolleto et al.16 studied 64 patients who were to undergo CRT. A baseline measurement of septal-to-posterior delay measured as radial strain >130 msec predicted an improvement in LVEF with a sensitivity of 89% and a specificity of 83% in 50 subjects who were followed up for 8 ± 5 months post-CRT. Another study of 176 subjects combined measurement of longitudinal dyssynchrony using TVI and radial dyssynchrony using radial strain speckle tracking.15 This study found that there was an additive predictive value to measurement of both longitudinal and radial dyssynchrony for prediction of post-CRT improvement in LVEF. Also, subjects who had no dyssynchrony detectable by either method showed a very low incidence of LVEF improvement post-CRT, while those subjects with a variable pattern of dyssynchrony had an intermediate improvement in LVEF.

Other Techniques to Quantify Intraventricular Dyssynchrony

Two other techniques have been used to quantify intraventricular dyssynchrony. Breithardt et  al.26 described a semi-automatic method of endocardial border detection using the apical four-chamber LV view. This method used mathematical Fourier transformation to detect septal-to-lateral wall dyssynchrony. Another method used a technique called vector velocity imaging, which measures LV myocardial velocities in reference to a reference point in the center of the LV cavity.27 This method showed modest success in predicting LVEF improvement post-CRT in 23 patients.

Real-Time Three-Dimensional Echocardiography to Analyze Dyssynchrony

Real-time 3D echocardiography (RT3DE) has been demonstrated to be an effective and feasible tool to analyze intraventricular dyssynchrony.17 The advantages of RT3DE include its integration of longitudinal, transverse, and radial dyssynchrony into a single measure, the systolic dyssynchrony index (SDI).17 The SDI is described as a percentage in relation to components of the 16-segment LV model. Time to minimal volume is measured and integrated over the 16 segments to generate the SDI. The SDI has been shown to inversely correlate with LV ejection independent of QRS duration.17 Furthermore, measurement of the SDI using RT3DE has been shown to predict response to CRT. CRT candidates who have a higher SDI are more likely to show improvement in NYHA class and LVESV.17

303

The following description of RT3DE technique is derived from Kapetanakis et al.17 RT3DE uses the X4 matrix array to obtain a pyramidal volume in real time. There are 3000 active elements sending and receiving simultaneously. The initially acquired volumes have a relatively narrow sector width (30 degrees × 50 degrees). To visualize the entire LV, full volume acquisition (FVA) is used. For acquisition of a fullvolume data set, four smaller real-time sets, acquired from alternate cardiac cycles, are combined to provide a larger pyramidal volume (up to 90 degrees × 90 degrees). FVA is performed during breathhold and requires a relatively stable R-R interval to minimize translation artifacts among the four acquired subvolumes. Apical FVA is acquired and used to measure time to minimal volume over the cardiac cycle. To optimize the frame rate of acquisition, depth is minimized and includes only the mitral and aortic valves. In patients with a significantly dilated LV, the scan line density is reduced to provide a larger pyramidal volume of acquisition. Quantitative analysis involves defining a number of 2D slices through the voxelbased 3D data set. In each of the slices, the endo­ cardial border is traced using a semi-automated detection program to create a “cast” of the LV cavity. This cast serves as a mathematical model and provides time–volume data for the entire cardiac cycle. By dividing this volume into pyramidal sub­ volumes based around a nonfixed central point, it is possible to gain an estimation of time–volume data corresponding to each of  the 16 standard myocardial segments, as defined by  the American Society of Echocardiography (Fig. 17-7).

DYSSYNCHRONY INDEX USING REAL-TIME THREE-DIMENSIONAL ECHOCARDIOGRAPHY Kapetanakis et  al.17 devised a dyssynchrony index using RT3DE. The index was derived by calculating the time taken to reach minimum regional volume for each segment as a percentage of the cardiac cycle. The SDI was defined as the standard deviation of these timings. Higher SDI signifies increasing intraventricular dyssynchrony. To allow comparisons between subjects with different heart rates, SDI is expressed as a percentage of the duration of the cardiac cycle rather than in milliseconds. The evidence for the use of RT3DE to analyze dyssynchrony and to predict CRT outcomes is limited. Kapetanakis et  al.17 studied 26 subjects who received CRT after dyssynchrony analysis using RT3DE. At 10 months follow-up, CRT responders, defined by improvement in NYHA functional class (mean improvement = 1.2), demonstrated LV reverse remodeling and improvement in their SDI from baseline. Furthermore, responders had a greater degree of baseline dyssychrony as measured by SDI when compared to nonresponders.

304 Chapter 17  |  Echocardiography and Its Role in Cardiac Resynchronization Therapy

PACING LEAD PLACEMENT: ROLE OF ECHOCARDIOGRAPHY TVI Doppler techniques have been used to guide LV lead placement for CRT by identifying the site of latest myocardial activation. Ansalone et  al.28 demonstrated that LV lead placement at the site of latest activation demonstrated by TVI echocardiography was associated with a more favorable response to CRT. In this study, the inferior or posterolateral wall was identified as the site of latest myocardial activation in 75% of cases. Murphy et al.29 also identified the site of latest mechanical activation pre-CRT to guide lead placement. These investigators showed a gradient of response to CRT. Those subjects with lead placements near or at the site of latest activation had the most significant improvement in LV remodeling parameters, symptoms, and immediate hemodynamic response. In subjects with lead placement more than one segment away from the site of latest activation, there was no significant improvement in LV remodeling parameters at 6 months post-CRT. Suffoletto et al.16 evaluated the site of latest myocardial activation using 2D speckle tracking to quantify LV radial strain. In 22 patients who had LV leads placed in the region of latest activation, there was a modest improvement in LVEF (10 ± 5%) compared to the 24 patients who had leads positioned in other sites (6 ± 5%; P < 0.05). It is not yet clear what the role of echocardiography will be in guiding LV lead placement.

OPTIMIZING CARDIAC RESYNCHRONIZATION THERAPY: ATRIOVENTRICULAR AND BIVENTRICULAR OPTIMIZATION Biventricular pacing allows the clinician choices in terms of CRT device settings. Echocardiography may provide guidance through the use of real-time hemodynamic and imaging data that may be used to optimize device settings. There are two types of CRT optimization. Atrioventricular (AV) optimization adjusts the timing relationship of atrial and ventricular events (either sensed or paced intervals) to maximize LV filling at the time of LV contraction. Ventricular–ventricular, or biventricular (V-V), optimization adjusts the timing between the pacing of the right and left ventricles to both optimize ventricular filling and promote optimal synchrony of biventricular contraction. Thus far, the literature has not shown a clear, long-term patient outcome benefit for either AV or V-V optimization, but studies are ongoing using novel techniques.

Techniques for Determining Atrioventricular Optimization

Electrocardiogram-Derived Algorithm An ECG-based algorithm for AV optimization has been described. One algorithm uses both the PR and QRS interval to determine the programmed AV delay.

In this algorithm, the optimal AV delay is defined as [PR (msec) × 0.50] if QRS >150 msec or [PR (msec) × 0.70] if QRS 40% r Tissue Doppler imaging to exclude myopathic disease (e.g., restrictive cardiomyopathy) r Hepatic venous flow pattern • Increased diastolic flow reversal in the hepatic veins, a Kussmaul-like phenomenon, is specific for constriction (100%), although with limited sensitiv­ ity (60%). r Tricuspid regurgitation • For right ventricular systolic pressure (RVSP). RVSP > 60 mm Hg is typical of restrictive cardiomyopathy and unusual for constrictive pericarditis. • For RVSP variation with the respiratory cycle: RVSP increases with inspirations, a Kussmaul-like phenomenon, may be detected in constriction. r Exclusion of significant primary valve dysfunction or ventricular systolic dysfunction r M-mode of the septum • For the “early diastolic dip” • For the “late systolic dip” • For ventricular interdependence r M-mode of the posterior wall • Flattened mid-diastole motion due to limited filling imparted by the constrictive pericardium r Dilated IVC r Stroke volume and cardiac output/index Use of a phonocardiograph as well is commendable, and affords teaching opportunities. About 50% of cases of constriction have a discernable “knock.” The older approach to evaluating pericardial constriction employed observations seen per cardiac cycle. The contemporary approach is to view observations over the respiratory cycle; hence the need for respirometry physiologic tracing. Unfortunately, digital echocardiographic recording is inclined to single R-R interval acquisition, and acquisition of multiple cycles to establish a respiratory cycle requires the intention to do so from the outset. To conclusively associate respiratory phenomena and cardiac phenomena, use of the respirometer is critical.

Echocardiographic Signs of Constriction

Although the traditional presentation of echocardiographic signs was to group them by modality, it is more useful to group them by relevant pathophysiology and

similarity to catheterization findings, because such an approach encourages physiologic insight and a means to scrutinize catheterization findings in cases of suspected constriction. Signs of Ventricular Interdependence Inspiratory Septal Shift. The inspiratory septal shift is the volume corollary of the catheterization pressure sign of ventricular interdependence. In constriction, with inspiration, the RV diastolic and systolic pressures increase, and the LV diastolic and systolic pressures decrease. This is evident on 2D imaging by the transient movement of the septum according to the fluctuations of the pressure gradient between the ventricles. Ventricular interdependence is evident on 2D imaging when the RV and RA (over) fill and the interventricular and interatrial septa shift over to the left during the first cardiac cycles of inspiration. The posterior short-axis and apical fourchamber 2D views are the most helpful. M-mode from the posterior long or short axis is useful to display the RV overfilling/LV underfilling associated with inspiration. Inspiratory Fall in Left Ventricular Early Diastolic Inflow Velocities. Increased phasic variation of mitral and tricuspid inflow occurs in constriction, but is not specific for it. In fact, respiratory diseases are a more common cause. The effect of constriction is greater on right heart loading; typically, flow variations of over 40% occur, but respiratory diseases (increased respiratory effort) also increase right heart filling variations. Nonetheless, increased flow variation, especially across the tricuspid valve, should be seen in conjunction with 2D signs of interdependence. The Doppler sign is, therefore, of variation (>25%) in mitral inflow velocity from is 88% predictive of constriction.1,2 If typical variation of transmitral flow is not apparent with the patient supine, have him or her sit up.2 Some have advocated interrogation of the superior vena cava flow as well. In constriction, there is little variation (i.e., difference between inspiration and expiration) in the systolic and diastolic velocities, whereas with chronic obstructive pulmonary disease (COPD) the systolic difference averages 45% and the diastolic difference averages 35%.3 Although statistically significant, they are not clinically significant differences in variation. Early Diastolic Pressure Dips. In some cases of constriction, the early diastolic pressure dip of the LV exceeds that of the RV. Typically, the difference is augmented in inspiration. The higher RV and LV diastolic pressure can transiently deflect the interventricular septum to the left side in early diastole. Best seen from a parasternal (long- or short-axis) view, this amounts to a brief dip into the LV of the septum in early diastole. It is most conclusively seen on M-mode tracing.

Pericardial Diseases  |  Chapter 22

Reduced Right Ventricular (Extrinsic) Compliance Early Diastolic Pressure Plateau r Flattened LV posterior wall in mid-diastole r Limitation of LV filling by the constrictive pericardium after the early diastolic dip renders the LV cavity of fixed volume through the rest of diastole • On M-mode tracing, this is apparent as a lack of mid-diastolic expansion of the LV cavity. Kussmaul Phenomena r Increased end-expiratory flow reversal–hepatic veins • The IVC and its branches typically are very distended unless the patient is volume contracted by high-dose diuretics. This generally facilitates pulsed-wave Doppler recording from the superior hepatic vein. • Expiratory diastolic flow reversal in the hepatic veins is 68% sensitive, 100% specific4 for constriction. r Inspiratory increase in RVSP • An elegant sign of constriction is the surrogate of the catheterization observation that with constriction in inspiration, the RV systolic pressures increase and the LV systolic pressures decrease. • Although maintaining alignment throughout the respiratory cycle is a challenge, the inspiratory increase in RV systolic pressure (TR velocity) is recorded with the use of a respirometer. • Phasic inspiratory increases in RVSP associated with inspiration are present and describe the right heart pressure aspect of interdependence— that RV pressure increases while LV pressure decreases. • Inspiratory increase in RVSP with constriction (13 ± 6%) versus fall in RVSP with restriction (–8 ± 7%).5 Pericardial Thickening r Transthoracic echocardiography is notoriously poor for the detection of pericardial thickening, although TEE is validated to evaluate pericardial thickness and has very good correlation (r = 0.97, P < 0.001).6 r TEE is able to evaluate pericardium only over the RV free-wall.7 • Detection of pericardial thickening on TEE requires experience, more than most echocardiographic signs, and has considerable interphysician variation. r Studies validating CT are very dated (sensitivity 78%, specificity 100%),8 because they were generated in lower temporal resolution nongated scanners. r Later studies using cine-CT appeared better, studying small series of normal versus restrictive cardiomyopathy versus constriction.9 The advent of 32-, 40- and 64-detector scanners with cardiac gating has revolutionized pericardial imaging. r The pericardium is most apparent over the RV free wall, as there is more pericardial fat to delineate it.

391

r CT

is the best imaging test to identify pericardial calcification. Most cases of pericardial constriction are no longer calcified, unless they are tuberculous in origin. r Gated MRI was considered, for a time, the definitive modality for detection of pericardial thickening (88% sensitivity, 100% specificity),10 using an extraordinarily improbable cut-off value of >4 mm to identify pericardial thickening. In contradistinction to CT, MRI is essentially insensitive to the presence of pericardial calcification. r Gated cardiac CT is not proven to be more accurate at depicting pericardial thickness than is MRI, but it is far better able to depict calcification. Tissue Doppler

r Normal tissue Doppler velocities. Tissue Dop­

pler imaging plays an important role in excluding restrictive cardiomyopathy, where E′ is lower than normal. In (pure) pericardial constriction, with the caveat that the underlying heart is normal, myocardial relaxation is normal. Unfortunately, a few confusing cases, notably postradiotherapy cases, will have concurrent restrictive cardiomyopathy and constrictive pericarditis. Many postoperative heart surgery cases, especially post–valve replacement cases, have neither a normal left heart nor a normal tissue Doppler finding. r Peak tissue Doppler >8 cm/sec is 89% sensitive and 100% specific for constriction versus restriction,11 but does not distinguish between constriction and normal without either constriction or restriction.12 r Another useful tissue finding in support of constriction is that the medial/septal tissue Doppler velocities are higher than are those of the lateral mitral annulus. Elevated Cardiovascular Central Venous ­Pressure IVC dilation and lack of variation indicate elevated cardiovascular pressure. Elevated Right Ventricular Diastolic Pressure r Late diastolic septal dip • In constriction, the late diastolic A-wave pressure increase in the RV may exceed that in the LV, transiently deflecting the interventricular septum toward the LV in late diastole. • The sign is best appreciated on M-mode tracing. Given variable PR intervals, the sign may be difficult to differentiate from the common presence of an early diastolic septal dip, but it is an elegant corollary of the elevated RV diastolic pressure catheterization sign of constriction. r The emphasis of Doppler in constrictive pericarditis should stay focused on the following: • Tissue Doppler to exclude restrictive cardiomyopathy • Hepatic venous flow • Mitral flow variations

392 Chapter 22  |  Pericardial Diseases The great confounder of 2D and Doppler signs of ventricular interdependence is atrial fibrillation, where R-R cycle variation produces effects that contaminate and may dominate those of respiration. Other confounders include severe underlying structural heart disease (e.g., valve disease, systolic dysfunction), which would confer abnormal hemodynamics that would mask those of constriction, and concurrence of restrictive cardiomyopathy and constrictive pericarditis.

Valid Means to Make the Diagnosis of Constriction

r No alternate pathology evident r Ventricular interdependence on 2D and Doppler r A septal diastolic dip r Normal myocardial tissue Doppler imaging at

annulus

r Expiratory

increase in hepatic diastolic flow reversal Suspected or possible constriction cases should be reviewed case by case and examined by the echocardiography attending before they leave the laboratory. Not all cases have “classic” physical findings13: r Prominent Y descent: 94% r Jugular venous distention: 93% r Edema: 76% r Ascites: 37% r Kussmaul phenomena: 21% r Pulsus paradoxicus: 19% r Knock: 47%

Surgical Risk and Outcomes r RA

pressure predicts surgical mortality: • 15 mm Hg: 5% mortality • 20 mm Hg: 10% mortality • 30 mm Hg: 30% mortality14 r Radiation-induced constriction is a major problem. There is a high incidence of concurrent myocardial fibrosis (restriction), and the postoperative outcomes are dismal—88% mortality or New York Heart Association Class III–IV congestive heart failure at 4 years.13

PERICARDIAL CYST Most pericardial cysts lie at the cardiophrenic angle. Only the ones that lie against the chest wall can be directly imaged by transthoracic echocardiography. Some can be imaged through a heart cavity as a structure beyond the heart into the chest. The ratio of right versus left cardiophrenic angle location is 3:1. If the cyst contacts the chest wall, it may be detected by transthoracic imaging as a large lucent cavity without flow in it. Full delineation of the cyst is not possible by either transthoracic or TEE echocardiography. Cardiac magnetic resonance is better suited to depict the typical thin-walled, fluid-filled cavity of a cyst than is CT. TEE may image a pericardial cyst that does not abut the chest wall via a posterior view.

REFERENCES 1. Hatle LK, Appleton CP, Popp RL. Differentiation of constrictive pericarditis and restrictive cardiomyopathy by Doppler echocardiography. Circulation. 1989;79:357– 370. 2. Oh JK, Tajik AJ, Appleton CP, et al. Preload reduction to unmask the characteristic Doppler features of constrictive pericarditis. A new observation. Circulation. 1997; 95:796–799. 3. Boonyaratavej S, Oh JK, Tajik AJ, et al. Comparison of mitral inflow and superior vena cava Doppler velocities in chronic obstructive pulmonary disease and constrictive pericarditis. J Am Coll Cardiol. 1998;32:2043–2048. 4. von Bibra H, Schober K, Jenni R, et  al. Diagnosis of constrictive pericarditis by pulsed Doppler echocardiography of the hepatic vein. Am J Cardiol. 1989;63:483–488. 5. Klodas E, Nishimura RA, Appleton CP, et al. Doppler evaluation of patients with constrictive pericarditis: use of tricuspid regurgitation velocity curves to determine enhanced ventricular interaction. J Am Coll Cardiol. 1996;28:652–657. 6. Ling LH, Oh JK, Tei C, et al. Pericardial thickness measured with transesophageal echocardiography: feasibility and potential clinical usefulness. J Am Coll Cardiol. 1997;29:1317–1323. 7. Hutchison SJ, Thaker KB, Chandraratna PA. Effects of intraaortic balloon counterpulsation on flow velocity in stenotic left main coronary arteries from transesophageal echocardiography. Am J Cardiol. 1994;74:1063–1065. 8. Killian DM, Furiasse JG, Scanlon PJ, et al. Constrictive pericarditis after cardiac surgery. Am Heart J. 1989;118: 563–568. 9. Oren RM, Grover-McKay M, Stanford W, Weiss RM. Accurate preoperative diagnosis of pericardial constriction using cine computed tomography. J Am Coll Cardiol. 1993;22:832–838. 10. Masui T, Finck S, Higgins CB. Constrictive pericarditis and restrictive cardiomyopathy: evaluation with MR imaging. Radiology. 1992;182:369–373. 11. Rajagopalan N, Garcia MJ, Rodriguez L, et  al. Comparison of new Doppler echocardiographic methods to differentiate constrictive pericardial heart disease and restrictive cardiomyopathy. Am J Cardiol. 2001;87:86–94. 12. Garcia MJ, Rodriguez L, Ares M, et al. Differentiation of constrictive pericarditis from restrictive cardiomyopathy: assessment of left ventricular diastolic velocities in longitudinal axis by Doppler tissue imaging. J Am Coll Cardiol. 1996;27:108–114. 13. Ling LH, Oh JK, Schaff HV, et  al. Constrictive pericarditis in the modern era: evolving clinical spectrum and impact on outcome after pericardiectomy. Circulation. 1999;100:1380–1386. 14. Seifert FC, Miller DC, Oesterle SN, et al. Surgical treatment of constrictive pericarditis: analysis of outcome and diagnostic error. Circulation. 1985;72:II264–II273:(3 Pt 2). 15. Douglas PS, Garcia MJ, Haines DE, et  al. ACCF/ ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/ SCCT/SCMR 2011 appropriate use criteria for echocardiography. J Am Coll Cardiol. 2011;57(9):1126–1166. 16. Cheitlin MD, Armstrong WF, Aurigemma GP, et  al. ACC/AHA/ASE 2003 guideline update for the clinical application of echocardiography: summary article: a report of the American College of Cardiology/

Pericardial Diseases  |  Chapter 22 ­ merican Heart Association Task Force on Practice A Guidelines (ACC/AHA/ASE Committee to Update the 1997 Guidelines for the Clinical Application of Echocardiography). Circulation. 2003;108:1146–1162. 17. Cheitlin MD, Chair JS, Alpert JS, et  al. ACC/AHA guidelines for the clinical application of echocardiography: a report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines (Committee on Clinical Application of Echocardiography). Circulation. 1997;95:1686–1744. 18. Taylor AJ, Cerqueira M, Hodgson JM, et  al. ACCF/ SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/ SCMR 2010 appropriate use criteria for cardiac computed tomography. J Am Coll Cardiol. 2010;56(22): 1864–1894. 19. Hendel RC, Manesh PR, Kramer CM, Poon M. ACCF/ACR/SCCT/SCMR/ASNC/NASCI/SCAI/ SIR appropriateness criteria for cardiac computed tomography and cardiac magnetic resonance imaging. J Am Coll Cardiol. 2006;48:1475–1497. 20. Pennell DJ, Sechtem UP, Higgins CB, et  al. Clinical indications for cardiovascular magnetic resonance (CMR): Consensus Panel report. J Cardiovasc Magn Reson. 2004;6:727–765. 21. Hendel RC, Berman DS, Di Carli MF, et  al. ACCF/ ASNC/ACR/AHA/ASE/SCCT/SCMR/SNM 2009

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appropriate use criteria for cardiac radionuclide imaging. J Am Coll Cardiol. 2009;53(23):2201–2229. 22. Nishimura RA, Carabello BA, Faxon DP, et al. ACC/ AHA 2008 guideline update on valvular heart disease: focused update on infective endocarditis. J Am Coll Cardiol. 2008;52(8):676–685. 23. Klocke FJ, Baird MG, Bateman TM, et al. ACC/AHA/ ASNC guidelines for the clinical use of cardiac radionuclide imaging: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASNC Committee to revise the 1995 Guidelines for the Clinical Use of Cardiac Radionuclide Imaging). Circulation. 2003;108:1404–1418. 24. Douglas PS, Khandheria BK, Stainback RF, Weissman NJ. ACCF/ASE/ACEP/ASNC/SCAI/SCCT/SCMR 2007 appropriateness criteria for transthoracic and transesophageal echocardiography: a report of the American College of Cardiology Foundation Quality Strategic Directions Committee Appropriateness Working Group, American Society of Echocardiography, American College of Emergency Physicians, American Society of Nuclear Cardiology, Society for Cardiovascular Angiography and Interventions, Society of Cardiovascular Computed Tomography and the Society for Cardiovascular Magnetic Resonance. J Am Soc Echocardiogr. 2007; 20:787–805.

394 Chapter 22  |  Pericardial Diseases BOX 22-1  Appropriateness Criteria and Indications for Cardiac Imaging Modalities for the Assessment of Pericardial Effusions TRANSTHORACIC ECHOCARDIOGRAPHY ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/ SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography 15 TTE for Evaluation of Intracardiac and Extracardiac Structures and Chambers Indication n Suspected pericardial conditions Appropriateness criteria: A; median score: 9 n Routine surveillance of known small pericardial effusion with no change in clinical status Appropriateness criteria: I; median score: 2 n Re-evaluation of known pericardial effusion to guide management or therapy Appropriateness criteria: A; median score: 8 2003 ACC/AHA Update of the Guidelines for the Clinical Application of Echocardiography16 No specific entries 1997 ACC/AHA Guidelines for the Clinical Application of Echocardiography 17 n For patients with suspected pericardial disease, including effusion, constriction, or effusive–constrictive process • Class I

n For patients with suspected bleeding in the pericardial space, e.g., trauma, perforation • Class I n Follow-up study to evaluate recurrence of effusion or to diagnose early constriction. Repeat studies may be goal-directed to answer a specific clinical question • Class I n For a pericardial friction rub developing in acute myocardial infarction accompanied by symptoms such as persistent pain, hypotension, and nausea • Class I n For follow-up studies to detect early signs of tamponade in the presence of large or rapidly accumulating effusions. A goal-directed study may be appropriate. • Class IIa n For routine follow-up of small pericardial effusion in clinically stable patients • Class III n For follow-up studies in patients with cancer or other terminal illness for whom management would not be influenced by echocardiographic findings • Class III

TRANSESOPHAGEAL ECHOCARDIOGRAPHY ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/ SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography 15 No specific entries CARDIAC COMPUTED TOMOGRAPHY ACCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/SCMR 2010 Appropriate Use Criteria for Cardiac CT 18 n Evaluation of pericardial anatomy Appropriateness criteria: A; median score: 8 CARDIAC MAGNETIC RESONANCE ACCF/ACR/SCCT/SCMR/ASNC/NASCI/SCAI/SIR 2006 Appropriateness Criteria for Cardiac Magnetic Resonance Imaging19 n For the evaluation of pericardial conditions (pericardial mass, constrictive pericarditis) Appropriateness criteria: A; median score: 8

SCMR Consensus Indication for Cardiac Magnetic Resonance Imaging 20 n For pericardial effusion • Class III

NUCLEAR ACCF/ASNC/AHA/ASE/SCCT/SCMR/SNM 2009 Appropriate Use Criteria for Cardiac Radionuclide Imaging 21 No specific entries Appropriateness criteria: A, appropriate; I, inappropriate; U, uncertain. TEE, transesophageal echocardiography; TTE, transthoracic echocardiography.

Pericardial Diseases  |  Chapter 22

395

BOX 22-2  Appropriateness Criteria and Indications for Cardiac Imaging Modalities for the Assessment of Pericardial Tamponade TRANSTHORACIC ECHOCARDIOGRAPHY ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/ SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography 15 TTE for Evaluation of Intracardiac and Extracardiac Structures and Chambers Indication n Suspected pericardial conditions Appropriateness criteria: A; median score: 9 n Routine surveillance of known small pericardial effusion with no change in clinical status Appropriateness criteria: I; median score: 2 n Re-evaluation of known pericardial effusion to guide management or therapy Appropriateness criteria: A; median score: 8

n For pericardial friction rub developing in acute myocardial infarction accompanied by symptoms such as persistent pain, hypotension, and nausea • Class I n For follow-up studies to detect early signs of tamponade in the presence of large or rapidly accumulating effusions. A goal-directed study may be appropriate. • Class IIa n For echocardiographic guidance and monitoring of pericardiocentesis • Class IIa n For follow-up studies in patients with cancer or other terminal illness for whom management would not be influenced by echocardiographic findings • Class III

1997 ACC/AHA Guidelines for the Clinical Application of Echocardiography 17 n For patients with suspected pericardial disease, including effusion, constriction, or effusive–constrictive process • Class I TRANSESOPHAGEAL ECHOCARDIOGRAPHY ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/ SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography 15 No specific entries CARDIAC COMPUTED TOMOGRAPHY ACCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/SCMR 2010 Appropriate Use Criteria for Cardiac CT 18 n Evaluation of pericardial anatomy Appropriateness criteria: A; median score: 8 CARDIAC MAGNETIC RESONANCE ACCF/ACR/SCCT/SCMR/ASNC/NASCI/SCAI/SIR 2006 Appropriateness Criteria for Cardiac Magnetic Resonance Imaging 19 n For the evaluation of pericardial conditions (pericardial mass, constrictive pericarditis) Appropriateness criteria: A; median score: 8

SCMR Consensus Indication for Cardiac Magnetic Resonance Imaging 21 No specific entries

NUCLEAR ACC/AHA/ASNC 2003 Guidelines for the Clinical Use of Radionuclide Imaging 23 No    specific entries Appropriateness criteria: A, appropriate; I, inappropriate; U, uncertain. TEE, transesophageal echocardiography; TTE, transthoracic echocardiography.

396 Chapter 22  |  Pericardial Diseases BOX 22-3  Appropriateness Criteria and Indications for Cardiac Imaging Modalities for the Assessment of Suspected Intrapericardial Blood Clot TRANSTHORACIC ECHOCARDIOGRAPHY ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/ SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography 15 TTE for Evaluation of Intracardiac and Extracardiac Structures and Chambers Indication n Suspected pericardial conditions Appropriateness criteria: A; median score: 9 n Routine surveillance of known small pericardial effusion with no change in clinical status Appropriateness criteria: I; median score: 2 n Re-evaluation of known pericardial effusion to guide management or therapy Appropriateness criteria: A; median score: 8

Hypotension for Hemodynamic Instability n Hypotension or hemodynamic instability of uncertain or suspected cardiac etiology Appropriateness criteria: A; median score: 9 1997 ACC/AHA Guidelines for the Clinical Application of Echocardiography 17 n For patients with suspected bleeding in the pericardial space, e.g., trauma, perforation • Class I

TRANSESOPHAGEAL ECHOCARDIOGRAPHY ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/ SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography 15 No specific entries CARDIAC COMPUTED TOMOGRAPHY ACCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/SCMR 2010 Appropriate Use Criteria for Cardiac CT 18 n Evaluation of pericardial anatomy Appropriateness criteria: A; median score: 8 CARDIAC MAGNETIC RESONANCE ACCF/ACR/SCCT/SCMR/ASNC/NASCI/SCAI/SIR 2006 Appropriateness Criteria for Cardiac Magnetic Resonance Imaging 19 n For the evaluation of pericardial conditions (pericardial mass, constrictive pericarditis) Appropriateness criteria: A; median score: 8 NUCLEAR ACC/AHA/ASNC 2003 Guidelines for the Clinical Use of Radionuclide Imaging 23 No specific entries

SCMR Consensus Indication for Cardiac Magnetic Resonance Imaging 20 No specific entries

  

Appropriateness criteria: A, appropriate; I, inappropriate; U, uncertain. TEE, transesophageal echocardiography; TTE, transthoracic echocardiography.

Pericardial Diseases  |  Chapter 22

397

BOX 22-4  Appropriateness Criteria and Indications for Cardiac Imaging Modalities for the Assessment of Constrictive Pericarditis TRANSTHORACIC ECHOCARDIOGRAPHY ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/ SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography 15 TTE for Evaluation of Intracardiac and Extracardiac Structures and Chambers Indication n Suspected cardiovascular source of embolus Appropriateness criteria: A; median score: 9 n Suspected pericardial conditions Appropriateness criteria: A; median score: 9

n For follow-up study to evaluate recurrence of effusion or to diagnose early constriction. Repeat studies may be goal directed to answer a specific clinical question • Class I n For postsurgical pericardial disease, including postpericardiotomy syndrome, with potential for hemodynamic impairment • Class IIb n Assessment of pericardial thickness in patients without clinical evidence of constrictive pericarditis • Class III

ACC/AHA 1997 ACC/AHA Guidelines for the Clinical Application of Echocardiography 17 n For patients with suspected pericardial disease, including effusion, constriction, or effusive–constrictive process • Class I TRANSESOPHAGEAL ECHOCARDIOGRAPHY ACCF/ASE/ACEP/ASNC/SCAI/SCCT/SCMR 2007 Appropriateness Criteria for Transesophageal Echocardiography 24 No specific entries

ACC/AHA 1997 ACC/AHA Guidelines for the Clinical Application of Echocardiography 17 n In the presence of a strong clinical suspicion and nondiagnostic TTE, TEE assessment of pericardial thickness to support a diagnosis of constrictive pericarditis • Class IIb

CARDIAC COMPUTED TOMOGRAPHY ACCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/SCMR 2010 Appropriate Use Criteria for Cardiac CT 18 n Evaluation of pericardial anatomy Appropriateness criteria: A; median score: 8 CARDIAC MAGNETIC RESONANCE ACCF/ACR/SCCT/SCMR/ASNC/NASCI/SCAI/SIR 2006 Appropriateness Criteria for Cardiac Magnetic Resonance Imaging 19 n For the evaluation of pericardial conditions (pericardial mass, constrictive pericarditis) Appropriateness criteria: A; median score: 8 NUCLEAR ACC/AHA/ASNC 2003 Guidelines for the Clinical Use of Radionuclide Imaging 23 No specific entries

SCMR Consensus Indication for Cardiac Magnetic Resonance Imaging 20 n For pericardial constriction • Class II

  

Appropriateness criteria: A, appropriate; I, inappropriate; U, uncertain. TEE, transesophageal echocardiography; TTE, transthoracic echocardiography.

398 Chapter 22  |  Pericardial Diseases BOX 22-5  Appropriateness Criteria and Indications for Cardiac Imaging Modalities for the Assessment of Suspected Pericardial Cysts TRANSTHORACIC ECHOCARDIOGRAPHY ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/ SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography 15 TTE for Evaluation of Intracardiac and Extracardiac Structures and Chambers Indication n Suspected cardiac mass Appropriateness criteria: A; median score: 9 n Suspected pericardial conditions Appropriateness criteria: A; median score: 9

1997 ACC/AHA Guidelines for the Clinical Application of Echocardiography 17 n For patients with suspected pericardial disease, including effusion, constriction, or effusive–constrictive process • Class I

TRANSESOPHAGEAL ECHOCARDIOGRAPHY ACCF/ASE/ACEP/ASNC/SCAI/SCCT/SCMR 2007 Appropriateness Criteria for Transesophageal Echocardiography 24 No specific entries CARDIAC COMPUTED TOMOGRAPHY ACCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/SCMR 2010 Appropriate Use Criteria for Cardiac CT 18 n Evaluation of pericardial anatomy Appropriateness criteria: A; median score: 8 CARDIAC MAGNETIC RESONANCE ACCF/ACR/SCCT/SCMR/ASNC/NASCI/SCAI/SIR 2006 Appropriateness Criteria for Cardiac Magnetic Resonance Imaging 19 n For the evaluation of pericardial conditions (pericardial mass, constrictive pericarditis) Appropriateness criteria: A; median score: 8 NUCLEAR ACC/AHA/ASNC 2003 Guidelines for the Clinical Use of Radionuclide Imaging 23 No specific entries

SCMR Consensus Indication for Cardiac Magnetic Resonance Imaging 20 No specific entries n For detection and characterization of cardiac and pericardiac tumors • Class I

  

Appropriateness criteria: A, appropriate; I, inappropriate; U, uncertain. TEE, transesophageal echocardiography; TTE, transthoracic echocardiography.

TABLE 22-1 Cardiac Catheterization Signs of Pericardial Constriction CRITERIA

SENSITIVITY (%)

SPECIFICITY (%)

PPV (%)

LVEDP – RVEDP < 5 mm Hg

60

38

4

7

RVEDP/RVSyst > 1/3

93

38

2

9

PASyst < 55 mm Hg

93

24

7

5

LV RFW > 7 mm Hg

93

57

1

2

PCWP/LV respiratory gradient > 5 mm Hg

93

81

8

4

100

95

94

100

LV:RV interdependence

NPV (%)

EDP, end-diastolic pressure; LV, left ventricular; NPV, negative predictive value; PPV, positive predictive value; PCWP, pulmonary capillary wedge pressure; RFW, rapid filling wave; RV, right ventricular; Syst, systolic. Data from Hurrell DG, Nishimura RA, Higano ST, et al. Value of dynamic respiratory changes in left and right ventricular pressures for the diagnosis of constrictive pericarditis. Circulation. 1996;93:2007–2013. Used with permission.

Pericardial Diseases  |  Chapter 22

399

TABLE 22-2 Utility of Different Imaging Modalities and Cardiac Catheterization in the Assessment of Pericardial Effusions MODALITY

PROS

CONS/CAVEATS

Transthoracic Echocardiography

2D echocardiography • An excellent, versatile, and portable test to identify both the presence of pericardial fluid and its physiologic consequence • Can be used to guide percutaneous drainage • Can identify some causes of pericardial effusion (aortic dissection, myocardial infarction)

• Other echolucent materials that may be mistaken for pericardial fluid include • Epicardial fat • Intrapericardial thrombus • Purulent material • Edematous (“aqueous”) pericardium

Doppler echocardiography: A useful, but overstated, method to determine the physiologic consequence of pericardial fluid

• Concurrent pulmonary and pleural diseases, which are common in the context of pericardial effusions, and mechanical ventilation may confound assessment of inflow variation.

Transesophageal Echocardiography

• Able to identify effusions well • May be better able to differentiate pericardial fluid from clot than TTE

• Has little to offer the average case

Cardiac CT

• (Chest CT): Can identify pericardial fluid and approximate its “size” • (Chest CT): Probably the best test to evaluate the thoracic and abdominal cavities for the presence of relevant disease • Cardiac CT more accurately represents the size of pericardial effusions than does chest CT.

• Chest CT is a relatively poor test in determining the size of pericardial effusions because the effusion often seems bigger by CT scanning than it does by TTE. • Without ECG gating, almost useless in establishing the physiologic sequelae of pericardial effusion

Cardiac MRI

SSFP sequences: SSFP sequencing detects effusions, although distinction from fat requires attention. (Chemical shift artifact indirectly reveals the presence of fluid, as do fat suppression sequences.)

NA

Nuclear

No role

Chest Radiography

• Enlargement of the CPS in a globular fashion is consistent with the development of a moderate or large pericardial effusion. • The ability to depict pleural effusions, lung masses, and aortic enlargement is diagnostically useful.

NA

Cardiac Catheterization

The gold standard of recording intracavitary pressures, including intrapericardial pressure, and confirming or refuting cardiac compression

• Seldom required in the routine evaluation of pericardial effusions • Respiratory effort engenders wide swings of intrathoracic pressure.

2D, two-dimensional; CPS, cardiopericardial silhouette; ECG, electrocardiographic; NA, not applicable; SSFP, steady-state free precession; TTE, transthoracic echocardiography.

400 Chapter 22  |  Pericardial Diseases TABLE 22-3 Utility of Different Imaging Modalities and Cardiac Catheterization in the Assessment of Pericardial Tamponade MODALITY

PROS

CONS/CAVEATS

Transthoracic Echocardiography

2D echocardiography • An excellent test to identify both the presence of pericardial fluid and its physiologic consequence • Useful signs include • An echolucent space around the heart = fluid • RA systolic collapse (>30% of the cardiac cycle)—a sensitive sign • RV diastolic collapse—a specific sign • IVC plethora consistent with elevated CVP (useful unless there is intravascular depletion) • A useful test to guide percutaneous drainage • Can identify some causes of tamponade (aortic dissection, myocardial infarction, myocardial rupture)

• Other echolucent materials that may be mistaken for pericardial fluid include • Epicardial fat • Intrapericardial thrombus • Purulent material • Edematous (“aqueous”) thickened pericardium

Doppler echocardiography: A useful, but overstated, method to determine the physiologic consequence of pericardial fluid, by noting exaggerated transmitral E-wave height variation (the E wave must be distinguished from the A wave)

• The observed variations of inflow depend on the mode of respiration/ventilation and the effort, and are confounded by the presence of concurrent pulmonary and pleural disease, which are common in tamponade cases. • Increased respiratory effort increases inflow variation; positive pressure ventilation tends to abolish inflow variation.

Transesophageal Echocardiography

Is readily able to identify pericardial effusions, and is better suited to differentiate pericardial fluid from clot than is TTE.

• Sedation to perform a TEE may be unusually hazardous if there is tight tamponade.

Cardiac CT

• (Chest CT): Can identify pericardial fluid, and approximate its “size” • (Chest CT): Probably the best test in existence to evaluate the thoracic and abdominal cavities for the presence of relevant disease. • A distended IVC and dye reflux into the IVC are reliable signs of right heart failure.

• A relatively poor test in determining the size of pericardial fluid—often times overestimating it, and without ECG-gating is almost useless in establishing the physiologic sequelae of pericardial effusion.

Cardiac MRI

SSFP sequences: SSFP sequencing detects effusions, although distinction from fat requires attention. (Chemical shift artifact indirectly reveals the presence of fluid, as do fat suppression sequences.)

NA

Nuclear

No role

Chest Radiography

Enlargement of the CPS in a globular fashion is consistent with the development of a moderate or large pericardial effusion. The ability to depict pleural effusions, lung masses and aortic enlargement is useful.

NA

Cardiac Catheterization

• The gold standard of recording intracavitary pressures, including intra-pericardial pressure • In a subset of cases that appear to lack echocardiographic manifestations of tamponade, cardiac catheterization may establish the presence of findings (elevated and equilibrated diastolic filling pressures), establishing the presence of cardiac compression/tamponade physiology.

• Seldom required in the routine evaluation of pericardial effusions • Respiratory effort engenders wide swings of intrathoracic pressure.

2D, two-dimensional; CPS, cardiopericardial silhouette; CVP, central venous pressure; ECG, electrocardiographic; IVC, inferior vena cava; NA, not applicable; RA, right atrial; RV, right ventricular; SSFP, steady-state free precession; TEE, transesophageal echocardiography; TTE, transthoracic echocardiography.

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TABLE 22-4 Utility of Different Imaging Modalities and Cardiac Catheterization in the Assessment of Pericardial Blood Clot MODALITY

PROS

CONS/CAVEATS

Transthoracic Echocardiography

2D echocardiography • Usually can distinguish pericardial clot from pericardial fluid • By its portability, it is well suited to ICU (typically post–open heart surgery) cases.

• Not always able to make the distinction between clot and fluid

Doppler echocardiography: NA

• Compressive physiology from clot usually lacks the characteristic spectral Doppler findings of tamponade.

Transesophageal Echocardiography

• Probably the single best test available to recognize intrapericardial clot, as the echocardiographic specular “texture” is characteristic • By its portability, well suited to ICU (typically post–open heart surgery) cases

Cardiac CT

• Detects material within the pericardial space, with attenuation characteristics similar to blood, not water • A rapid test that is readily performed on most ill patients

• Often will not distinguish intrapericardial blood clot from fluid

Cardiac MRI

NA

• Clinical instability generally precludes CMR scannning where monitoring is indirect and where the duration of the study is long.

Nuclear

NA

• Little role

Chest Radiography

NA

• Little role

Cardiac Catheterization

Detects the hemodynamic abnormalities due to compression

• The hemodynamic effects of intrapericardial clot are usually atypical of tamponade and more consistent with right heart obstruction, but it depends on where the clot has accumulated.

2D, two-dimensional; CMR, cardiac magnetic resonance; ICU, intensive care unit; NA, not applicable.

402 Chapter 22  |  Pericardial Diseases TABLE 22-5 Utility of Different Imaging Modalities and Cardiac Catheterization in the Assessment of Pericardial Constriction MODALITY

PROS

CONS/CAVEATS

Transthoracic Echocardiography

2D/M-mode echocardiography • The first contribution of 2D echocardiography is the elimination of alternative diagnoses, such as valvular heart disease and restrictive cardiomyopathy. • The demonstration of the following findings are useful: • Early diastolic septal shift • Late diastolic septal shift • Inspiratory septal shift (requires use of respirometry) • Pulmonic valve pre-systolic openning • In some cases, frankly thickened pericardium can be seen.

• Constriction may be concurrent with other disorders, including restrictive cardiomyopathy. • Variants of constriction abound (e.g., partial, transient, with normal pericardial thickness). • In most cases, pericardial thickening by TTE is notoriously ambiguous.

Doppler echocardiography • A useful method to determine the physiologic consequence of pericardial constriction • The demonstration of the following findings are useful: • Exaggerated transmitral E-wave velocities through the respiratory cycle (requires use of respirometry) • Increased hepatic expiratory D-wave reversal (60% sensitive, but 100% specific) • Increased inspiratory TR velocity • Pulmonic valve presystolic opening

• Observed variations of inflow depend on the mode of respiration/ventilation and the effort, and are confounded by the presence of concurrent pulmonary disease and mechanical ventilation. • Irregular cardiac rhythms confound the assessment, as does irregular breathing.

Transesophageal Echocardiography

Pericardial thickening can be identified by an experienced TEE operator.

• Sedation to perform a TEE may vary the respiratory effort and echocardiographic findings. • About 20% of constriction cases do not have unequivocal pericardial thickening because the substrate is stiff, minimally thickened pericardium.

Cardiac CT

• Can identify pericardial thickening • Exquisitely sensitive to pericardial or other calcification • Probably the best test in existence to evaluate the thoracic and abdominal cavities for the presence of relevant disease

• Without ECG-gating, CT is less likely to detect pericardial thickening. • CT has minimal ability to determine the physiology of constriction. • About 20% of constriction cases do not have unequivocal pericardial thickening because the substrate is stiff, minimally thickened pericardium. • Constriction is usually present without pericardial calcification. • Renal insufficiency complicates many cases of advanced constriction in older patients.

Cardiac MRI

T1-weighted black blood sequences: A very good test to detect pericardial thickening

• Determination of pericardial thickening by CMR requires either frank thickening or under- and overlying fat planes because the signal from the pericardium may be indistinguishable from that of myocardium.

SSFP sequences • SSFP sequencing detects effusions, although distinction from fat requires attention. (Chemical shift artifact indirectly reveals the presence of fluid, as do fat-suppression sequences.) • Free-breathing sequences can demonstrate an inspiratory septal shift.

• Irregular heart rhythms may reduce image quality. • Breath-holding may be difficult if pleural effusions or ascites are present.

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TABLE 22-5 Utility of Different Imaging Modalities and Cardiac Catheterization in the Assessment of Pericardial Constriction—cont’d MODALITY

PROS

CONS/CAVEATS

LGE sequences: Some cases of pericardial constriction are associated with LGE.

• Gadolinium enhancement is variably present.

Nuclear

NA

• Little role

Chest Radiography

• Pericardial calcification may be detectable by chest radiography, although both fluoroscopy and CT are more sensitive. • The presence of associated pleural effusion is usually unmistakable.

NA

Cardiac Catheterization

• The traditional standard of diagnosing con­ striction that improved considerably with the inclusion of ventricular interdependence and PCWP–LV pressure gradient parameters • Consistently useful; attention to respirometry helps very much. • Volume loading may be performed during the procedure to reestablish the disease physiology that diuresis may lessen. • Detects the physiology of constriction, which is present in all cases, whereas the substrate of constriction (stiff pericardium) may or may not have detectable thickening in only a majority of cases

• Many traditional catheterization-related parameters have limited predictiveness of constriction. • Irregular heart rhythms confound the assessment, but temporary transverse pacing can be used to regularize the R-R intervals.

2D, two-dimensional; CMR, cardiac magnetic resonance; ECG, electrocardiographic; LGE, late gadolinium enhancement; LV, left ventricular; NA, not applicable; PCWP, pulmonary capillary wedge pressure; SSFP, steady-state free precession; TEE, transesophageal echocardiography; TR, tricuspid regurgitation; TTE, transthoracic echocardiography.

404 Chapter 22  |  Pericardial Diseases TABLE 22-6 Utility of Different Imaging Modalities and Cardiac Catheterization in the Assessment of Pericardial Cysts MODALITY

PROS

CONS/CAVEATS

Transthoracic Echocardiography

2D echocardiography: Useful to detect cysts that contact the chest wall

• Seldom detects cysts that do not abut the wall

Doppler echocardiography: Useful to establish that there is no flow within the cyst Transesophageal Echocardiography

Will detect some cysts that do not abut the chest wall

• But they have to be in line with the heart from the TEE perspective

Cardiac CT

The depiction of the location, thin wall, shape of the cyst, and low attenuation of the material within it is often so typical that the likelihood of another diagnosis is very small.

• Contrary to some beliefs, CT does not delineate the wall of the cyst clearly enough to directly establish its nature.

Cardiac MRI

SSFP sequences: As with CT, the depiction of the location, thin wall, and shape of the cyst is often so typical that the likelihood of another diagnosis is very small.

NA

T2-weighted sequences: Are very useful in that they establish that the material within the cysts has a high signal (proton–water–content) Nuclear

No role

Chest Radiography

Surprisingly useful to prompt consideration of a cyst

NA

Cardiac Catheterization

NA

• No direct role, as compression of the heart does not occur

2D, two-dimensional; NA, not applicable; SSFP, steady-state free precession; TEE, transesophageal echocardiography.

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Figure 22-1.  Cardiac tamponade. Pericardial and left pleural effusions are present. The left atrial shape and size are consistent with underfilling. Upper images: Posterior long-axis views of systole (left) and diastole (right). Note the right ventricular outflow tract (RVOT) diastolic collapse (indentation). Middle images: Posterior short-axis views of systole (left) and diastole (right). There is RVOT diastolic collapse. The pericardial effusion appears large. This impression is in part true, but is in part enhanced by the small size of the heart and also by the absence of depth markers. Lower images: Apical four-chamber views of systole (left) and diastole (right). The right atrium is collapsed (inverted) in both phases of the cardiac cycle.

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Figure 22-2.  Pericardial tamponade. The upper images show posterior short-axis views at different phases of the respiratory cycle: expiration (upper left) and inspiration (upper right). With inspiration, there has been a shift of the septum toward the left ventricle (LV) (2D representation of ventricular inter-­ dependence). Lower left: M-mode study of the septum through several respiratory cycles (respirometer tracing at bottom) shows ventricular inter­dependence. In the second cardiac cycle during each inspiration (denoted by the upward deflection of the red respirometry tracing), the septum has shifted from the right to the left side Lower right: Doppler representation of ventricular inter-dependence. LV inflow is tracked through several respiratory cycles. With inspiration, there is a fall in in-flow velocity.

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Figure 22-3.  Constrictive pericarditis. Upper left: M-mode of septal motion. There is a prominent early-diastolic dip. Upper right: Tissue Doppler imaging of the lateral mitral annulus. The E′ velocity is normal, establishing normal myocardial relaxation and excluding diastolic abnormality of the myocardium, which would otherwise suggest infiltrative cardiomyopathy/restrictive cardiomyopathy. Lower left: M-mode of the inferior vena cava shows marked dilation and absence of respiratory variation (note the respirometry tracing) consistent with severely elevated central venous pressure. Lower right: Note the ascites over the liver and beneath the diaphragm.

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Figure 22-4.  Constrictive pericarditis in a terminal case with respiratory fatigue and failure from intractable ascites and anasarca. Upper left: The fivechamber view shows that the ventricles are normal sized. There is obvious thickening of the pericardium over the left ventricular (LV) lateral wall. Upper right: Spectral Doppler of LV inflow shows no appreciable variation of early filling velocities. However, the respirometer tracing demonstrates the shallow rapid pattern of breathing that is confounding assessment because the respiratory cycle is as short as the cardiac cycle. Middle left: Posterior short-axis M-mode study through the septum. There is no appreciable septal shift (“bounce”), but the respirometer again demonstrates lack of normal respiratory effort. Middle right: Posterior short-axis M-mode study with the patient coached to take breaths of normal depth. The septum does shift from the right to the left side. Lower left: Hepatic venous flow with the patient coached to breathe with a regular and normal depth: there is expiratory hepatic flow reversal. Lower right: Tissue Doppler imaging at the mitral annulus: the E′ velocity is low, likely due to the patient’s known, long history of hypertension. Alternatively, myocardial atrophy from the duration of the constriction also may have occurred. This case underscores the need not only to use respirometry, but to observe it and to coach the patient if necessary. Imaging in this case reveals concurrent myopathic disease, seen as low tissue Doppler imaging velocities.

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Figure 22-5.  Constrictive pericarditis in a 20-year-old patient with all typical findings present. Upper left: Posterior short-axis M-mode study through the septum. There is obvious septal shift (“bounce”) timed to inspiration, representative of ventricular interdependence. The respirometer demonstrates the normal respiratory effort and pattern. Upper right: Posterior short-axis high-sweep-speed M-mode shows the early diastolic dip, due to left ventricular diastolic pressure that is transiently lower than right ventricular diastolic pressures during very early diastole. This early diastolic septal dip is akin to the early pressure waveform dip. Middle left: The respiratory effort and pattern are normal, and there is marked variation of flow across the mitral valve with inspiratory fall far greater than 25%. Middle right: Hepatic venous flow: there is expiratory diastolic flow reversal. Lower left: Tissue Doppler imaging shows normal tissue velocity consistent with the absence of myocardial disease. Lower right: Abdominal aortic flow: there is the velocity equivalent of pulsus paradoxicus, which was present.

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Figure 22-6.  Constrictive pericarditis: hepatic venous flow. In this case, there is end-inspiratory increase in diastolic flow because of the length of inspiration. Usually, the diastolic flow reversal is seen in expiration.

Figure 22-7.  Upper images: A large pericardial effusion with prominent fibrous stranding due to hemopericardium. The lower images obtained from the subcostal position clearly demonstrate the right ventricular endocardial pacemaker. This was not the reason for the pleural effusion and tamponade, however, which is suggested by the right ventricular diastolic impression seen in both of the lower images. The patient had been anticoagulated for chronic atrial fibrillation, and a short course of antibiotics had increased the INR to a level of 9.5, resulting in the intrapericardial hemorrhage and tamponade.

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Figure 22-8.  Chest radiographs of the same case as Figure 22-7. The upper images were obtained before the intrapericardial hemorrhage; the lower images were obtained after the intrapericardial hemorrhage. The increase in the cardiopericardial silhouette as well as the more prominent globularity of the heart resulting from the accumulation of the intrapericardial blood are seen. These findings had prompted the echocardiogram.

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Figure 22-9.  Pericardial tamponade due to a large malignant effusion with prominent swinging of the heart. The apical four-chamber and short-axis images reveal the prominent swinging of the heart, which is under adrenergic stimulation due to the tamponade. There is abundant space for it to move within given the large fluid accumulation.

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Figure 22-10.  Pericardial tamponade. The upper images demonstrate the collapse of the right ventricular free wall in diastole, seen on both the parasternal long-axis and short-axis views. Middle left: Right ventricular free wall collapse on M-mode tracing. Middle right: Lack of respiratory motion of the inferior vena cava, consistent with severely elevated central venous pressure. The lower images, obtained as apical four-chamber views, reveal a large effusion, with small heart cavities, and prominent swinging motion of the heart. The swinging of the heart is responsible for the variation of electrical vectors–electrical alternans.

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Figure 22-11.  Off-axis apical views of a large pericardial effusion that contains a small, rounded, mobile lesion within it that was proven to be metastatic adenocarcinoma.

Figure 22-12.  An apical four-chamber view of a patient with a large pericardial effusion. Prominent depth of fluid is seen between the LV apex and the left ventricular apical parietal pericardium. The dimensional measurement of 4.36  cm that was measured here is consistent with greater safety by percutaneous drainage. The other useful measurement would be the distance of soft tissue to be traversed before entering the pericardial effusion.

Figure 22-13.  Subcostal long-axis view demonstrates the complex specular pattern typical of intrapericardial fat.

23

Right Heart Diseases

ECHOCARDIOGRAPHIC FINDINGS IN RIGHT HEART DISEASE Two-Dimensional Echocardiography Findings

Signs of right ventricular (RV) pressure overload r Right ventricular hypertrophy (RVH) r RVH dilation r ± Systolic dysfunction—global or regional. Regional SV systolic dysfunction is common in submassive pulmonary embolism (PE) Signs of RV volume overload r RV dilation r Vigorous systolic function Signs of RV systolic dysfunction r Causes of RV regional wall motion abnormalities • RV infarction • Submassive or massive PE • Arrhythmogenic right ventricular dysplasia • RV contusion Signs of RV diastolic failure or tricuspid regurgitation (TR) r Enlarged coronary sinus r Dilated inferior vena cava (IVC), hepatic veins Interatrial septum r For integrity (intact or not) • Atrial septal defect may be the cause of RV abnormalities. • Patent foramen ovale may open secondary to RV failure. r Position/curvature • Position (indicates relative pressures of the atria) Septal (“D”) shape and motion patterns consistent with the following: r Right-sided pressure overload • Systolic D shape • With or without diastolic D shape (if RV end-diastolic pressure [EDP] is elevated relative to LVEDP) r Right-sided volume overload • Diastolic D shape

Doppler Findings r TR r Pulmonic

insufficiency

r Right

ventricular systolic pressure (RVSP) calculated/estimated from TR. r Responsible shunt lesions r Right-to-left flow across a patent foramen ovale (PFO) prompted by RV flow. Recall that shunt le­ sions such as sinus venous atrial septal defects (ASDs) and anomalous pulmonary venous return are unlikely to be imaged by transthoracic echocardiography (TTE).

Occasional Findings r Emboli-in-transit

RIGHT VENTRICULAR HYPERTENSION AND PULMONARY HYPERTENSION As long as there is sufficient TR signal, the systolic RV– RA gradient can be calculated using the simple modified Bernouilli equation, and with the addition of an estimated mean RA pressure becomes the RVSP (which is thereby both a calculated and an estimated number). RVSP can be equated with systolic pulmonary artery pressure only when Doppler assessment of the right ventricular outflow tract and pulmonic valve excludes a gradient conferring stenosis. It is important to recall that changes in recorded RVSP may reflect normal daily variations of pulmonary artery pressure—in a given patient, variation of up to 30% in a 24-hour period may be seen. Echocardiography tends to overestimate lower RVSP and underestimate higher RVSP, but overall is generally accurate—as long as there is sufficient TR signal. Older, less commonly used, echocardiographic findings that have been associated with pulmonary hypertension include the following: r Pulmonary valve motion • Typically shows a reduced “a” wave and systolic notching of the pulmonary valve, but these signs are not specific for pulmonary hypertension. The “a” wave motion is affected by pulmonary artery diastolic pressure and also by atrial events, and midsystolic notching of the pulmonary valve motion is not specific for pulmonary hypertension (it is seen also in idiopathic pulmonary artery dilation). 415

416 Chapter 23  |  Right Heart Diseases r The



following older concepts all have correlations with pulmonary artery pressure but are no longer in use: • Ejection time indices (right ventricular preejection period/RV ejection time) • Pulmonary valve closure to tricuspid valve opening interval • Time to peak pulmonary artery pressure (acceleration time) • Ratio of acceleration time to RV ejection time

Causes of Right Ventricular/Pulmonary Artery Hypertension Apparent by Echocardiography

Pulmonary stenosis r Valvar r Subvalvar, with or without tetralogy or pentalogy r Supravalvar r Peripheral pulmonic stenosis is far harder to identify in adults using transthoracic echocardiography, Pulmonary hypertension r Loss of vasculature due to left-to-right shunts • Intracardiac • Atrial septal defect • Ventricular septal defect • Atrioventricular septal defect • Extracardiac • Surgical shunts • Patent ductus arteriosus (PDA) • Pulmonary emboli r Back-pressure from the left heart • Severe LV failure • Severe mitral valve disease • Cor triatriatum sinister

RIGHT VENTRICULAR HYPERTROPHY RV wall thickness correlates with RV systolic pressure: r = 0.92.1 RVH is identified on echocardiography only by an increase in RV wall thickness, because an accurate calculation of RV mass is not feasible by echocardiography. Measurement of RV wall thickness is challenging because of the exaggerated topography of the endocardial surface of the RV. Paradoxically, the better the RV endocardial detail achieved, the greater the uncertainty regarding where to measure. It is best to measure away from frank trabeculations, on whichever view gives the best detail of the RV free wall. Normal RV wall thickness is about 3 mm on autopsy and about 4 mm (4 ± 1 mm)2 by echocardiography. By convention, in the preharmonic era, RVH by echocardiography was 5 mm or greater. Thus, normal RV wall thickness and RVH are separated by only a narrow margin of 1 to 2 mm: r Normal RV wall thickness3: 3.3 ± 0.6 mm diastolic, 5.1 ± 1.5 mm systolic

r RVH

(on autopsy): 5.9 ± 0.9 mm diastolic, 9.1 ± 2.9 mm systolic For the diagnosis of RVH, there is a sensitivity of 90% and specificity of 94% for diastolic wall thickness of  5 mm or greater. There is sensitivity of 34% and specificity of 100% for systolic wall thickness of 10 mm or greater.

INFERIOR VENA CAVA DIMENSIONS AND COLLAPSE There is frankly poor correlation of IVC diameter with RA pressure and with RV systolic pressure r = 0.50, but the “collapsibility index” correlates somewhat better, at r = 0.714: Collapsibility index IVCDiameter Expiration − IVCDiameter Inspiration = IVCDiameter Expiration ×100

INTERVENTRICULAR SEPTAL SHAPE The normal interventricular septum configuration throughout the cardiac cycle is to be concave toward the left side—i.e., in a short-axis view, the LV remains symmetrically round throughout the cardiac cycle, and any orthogonal axes (diameters) are equal in dimension, for an “eccentricity index” of 1 (D1/D2).5 The basis of the preservation of the roundness of the septum in both diastole and systole is the LV-to-RV pressure gradient that are normally preserved in both diastole and systole. In RV systolic hypertension (“pressure overload”), with elevated RV systolic pressures, at end-diastole, the interventricular septum is, as it is normally, convex toward the LV. It becomes progressively flattened from end-diastole to end-systole. With suprasystemic RV systolic pressures, the interventricular septum is flattened at end-diastole and becomes concave toward the RV by end-systole. In RV volume overload, at end-diastole, the interventricular septum is flattened toward the left side. By endsystole, the interventricular septum configuration is normal. The RV dimensions are substantially increased.5

RIGHT VENTRICULAR VOLUME Determination of RV volume by echocardiography is difficult, time consuming, and not very accurate. The basic problem is the complex shape of the RV, which does not readily lend itself to reproduction with an equation, or to very reproducible measurement along arbitrary axes. Two methods have been suggested: r Method of disc summation (Simpson’s rule) • Entire RV volume: r = 0.85 versus biplane angiographic estimates.6

Right Heart Diseases  |  Chapter 23

• R  V “body” without RVOT (easier): r = 0.94; SEE = 10 mL • RV volumes by echocardiography correlate better with RV volumes by angiography than do any RV dimensional expressions of RV size. r Area plane method formula • 2⁄3 × area in one plane × area in another orthogonal plane (e.g., apical four-chamber view [A4CV], and SC at RVOT) • r = 0.95; SEE = 5 mL versus silicone autopsy casts7 • Areainflow × Lengthoutflow: pyramidal formula obtainable in only 64% of patients8 It is questionable whether the time and effort to calculate RV volume by echocardiography is worthwhile, as cardiac magnetic resonance is well-suited to the task.

TRICUSPID ANNULAR PLANE EXCURSION Tricuspid annular plane excursion (TAPSE), measured using M-mode from an apical 4CV and describing the longitudinal excursion of the lateral tricuspid annulus, is an objective and reproducible descriptor of RV systolic function, pulmonary artery pressure, and prognosis. TAPSE correlates directly with RV ejection fraction and behaves as a linear risk variable. The mean is 23 mm, and the lower reference value (mean minus 2 standard deviations) is 16 mm. TAPSE correlates inversely with pulmonary artery systolic pressure and also inversely with prognosis in heart failure, pulmonary hypertension, and chronic obstructive pulmonary disease. Confounding aspects of the use/interpretation of TAPSE are that (1) RV longitudinal systolic function is not less well-correlated with overall RV systolic function in the presence of RV regional wall motion abnormalities, (2) LV systolic function influences overall RV systolic function via septal function, and (3) severe TR decreases the correlation of TAPSE with RV ejection fraction.

RIGHT VENTRICULAR INFARCTION Significant RV infarction is seen predominantly in the setting of inferior infarction of the left ventricle, and rarely is seen in the absence of LV inferior and inferoseptal wall motion disturbances. Short-axis views of the RV and LV are the most helpful. The view often must be angulated to the right side to ensure visualization of the RV, especially when the RV dilates from infarction. The echocardiographic findings are as follows: r Posterior RV hypokinesia or akinesia if the right coronary artery is occluded before the posterior descending coronary artery but after the acute marginal branches. r Lateral and posterior RV hypokinesia if the right coronary artery is occluded before important acute marginal branches

417

r RV

dilation and engorgement of the IVC. TR is common. Complications of RV infarction that may be seen by echocardiography include the following: r RV or RA mural thrombi r RV papillary rupture r Right-to-left shunting across a patent foramen ovale, driven by high RV EDP from an RV myocardial infarction, may result in systemic arterial desaturation. 9–11 Inversion of the normal curvature of the interatrial septum may be seen in the setting of RV myocardial infarction, when the RA pressure exceeds LA pressure.12 RVH predisposes to RV myocardial infarction in the setting of first inferior infarction, as the imbalance of supply and demand is even more unfavorable.13 Mid-diastolic opening of the pulmonary valve may occur after RV infarction, due to RVEDP exceeding pulmonary artery diastolic pressure before RA systole.14

RIGHT VENTRICULAR DYSPLASIA RV dysplasia is a congenital disorder consisting of ­aplasia/hypoplasia with fibrofatty replacement exclusively or principally of the RV, in the presence of a structurally normal tricuspid valve. There is a spectrum of disease. Ventricular tachycardia of RV origin and rightsided heart failure are the principal consequences. The patient usually is young or middle-aged. The most severe cases occur in childhood, but milder cases may occur well into adult life. Familial cases have been described. Although the literature reports findings of RV dysplasia as seen on echocardiography, RV dysplasia is vastly better evaluated by cardiac magnetic resonance than by echocardiography. The following echocardiographic findings of RV dysplasia have been reported: r Enlarged RV: 30 of 30 patients r Generalized RV hypokinesia r Segmental RV hypokinesia/akinesia/dyskinesia, especially affecting the following: • The posterior wall beneath the tricuspid valve: 16 of 30 patients • The apex or the infundibular tract: 13 of 30 patients r Focal bulging in the areas just listed r Disarrangement of the RV trabecular pattern: 15 of 30 patients r “Conspicuously reflective” and shaped moderator band and papillary muscles: 20 of 30 patients r “Conspicuously reflective” RV myocardium15 r Enlarged RA, IVC

PULMONARY EMBOLISM The echocardiographic findings of PE are determined by the size and the hemodynamic burden of PE on the right heart.

418 Chapter 23  |  Right Heart Diseases With hemodynamically significant pulmonary embolism, the LV cavity (if otherwise normal) typically is small, as the pulmonary vascular obstruction results in underloading of the left heart. Doppler studies will reveal a low cardiac output, TR, and elevated RV systolic pressure. Rarely, a thrombus-in-transit has been visualized (in the IVC, RA, RV, main pulmonary artery, or branch pulmonary arteries) by transthoracic or transesophageal echocardiography. Following lysis of the thrombus, or surgical removal, right-sided chamber dimensions and interventricular septum configuration may normalize partially or entirely.16 The role of echocardiography in the assessment of PE is unclear. It appears to provide another objective means of establishing RV strain, as do physical diagnosis findings, elevated troponins, increased RV dimensions on CT scanning, and electrocardiographic changes. Echocardiography is only rarely able to make a direct diagnosis of PE (transesophageal echocardiographic visualization of central pulmonary artery thrombus). More commonly, echocardiography offers indirect evidence of PE by identifying RV strain features. Rarely, an embolus-in-transit is identified as a strong indirect evidence of PE. The presence of elevated RVSP is nonspecific as a sole feature and it is not adequate as an indirect sign of PE. RV strain, identified by any modality (e.g., troponin elevation, electrocardiographic abnormalities consistent with RV strain, echocardiographic identification of RV dilation or hypokinesis) is consistent with increased clinical risk from the PE, even if BP is not reduced (submassive PE) or shocky (massive PE). Therefore, the probable role for echocardiography is to assist with stratification of risk, rather than being a diagnostic test per se. Smaller pulmonary emboli that do not result in RV strain are exceedingly unlikely to result in abnormalities that echocardiography can identify; therefore, the sensitivity of RV echocardiographic findings of PE is heavily affected by the hemodynamic effect of the PE—in fact, it is dependent on it. The identification of emboli-in-transit is a matter of pure luck.

Echocardiographic Findings of Pulmonary Embolism

Direct evidence of PE r Transesophageal echocardiographic evidence of central pulmonary artery embolism, such as saddle emboli Indirect evidence of PE r RV hypokinesis, RV akinesis • The usual location of the RV wall motion abnormality is the site where the moderator band inserts into the lateral wall. The very apex of the RV typically still contracts. This finding, the McConnell sign, is quite good at distinguishing acute right heart strain from chronic pulmonary hypertension. Note

though that some PE cases occur in the context of chronic pulmonary hypertension—an unvalidated subset for this sign. r RV dilation r Embolus-in-transit • Hanging over the eustachian ridge • Hanging within tricuspid valve components • Stuck in a patent foramen ovale r Thrombus • In the IVC

PRIMARY PULMONARY HYPERTENSION The echocardiographic findings in primary pulmonary hypertension (PPH) are basically those of RV pressure overload, and reflect the severity of the pulmonary vascular disease. The pulmonary artery is almost invariably dilated, and pulmonary insufficiency is common. Pulmonary insufficiency, being under higher pressure than normal, is seen as being under higher velocity than normal. The following findings augur for significantly reduced survival,17 and may be apparent by echocardiography: r Severity of pericardial effusion r Heart rate >87 beats per minute r Pulmonary artery acceleration time 61 mm Hg r Pulmonary artery diastolic pressure >43 mm Hg A critical issue concerning echocardiography and pulmonary hypertension is that the lack of adequate TR signal (10–20% of cases) can conceal the findings of pulmonary hypertension until they are very far ­advanced.

REFERENCES 1. Prakash R, Matsukubo H. Usefulness of echocardiographic right ventricular measurements in estimating right ventricular hypertrophy and right ventricular systolic pressure. Am J Cardiol. 1983;51:1036–1040. 2. Gottdiener JS, Gay JA, Maron BJ, Fletcher RD. Increased right ventricular wall thickness in left ventricular pressure overload: echocardiographic determination of hypertrophic response of the “nonstressed” ventricle. J Am Coll Cardiol. 1985;6:550–555. 3. Prakash R, Umali SA. Comparison of echocardiographic and necropsy measurements of left ventricular wall thickness in patients with coronary artery disease. Am J Cardiol. 1984;53:838–841. 4. Moreno FL, Hagan AD, Holmen JR, et al. Evaluation of size and dynamics of the inferior vena cava as an index of right-sided cardiac function. Am J Cardiol. 1984;53:579–585. 5. Ryan T, Petrovic O, Dillon JC, et  al. An echocardiographic index for separation of right ventricular volume and pressure overload. J Am Coll Cardiol. 1985;5:918–927.

Right Heart Diseases  |  Chapter 23 6. Saito A, Ueda K, Nakano H. Right ventricular volume determination by two-dimensional echocardiography. J Cardiogr. 1981;11:1159–1168. 7. Levine RA, Gibson TC, Aretz T, et al. Echocardiographic measurement of right ventricular volume. Circulation. 1984; 69:497–505. 8. Starling MR, Crawford MH, Sorensen SG, O’Rourke RA. A new two-dimensional echocardiographic technique for evaluating right ventricular size and performance in patients with obstructive lung disease. Circulation. 1982;66:612–620. 9. Rietveld AP, Merrman L, Essed CE, et al. Right to left shunt, with severe hypoxemia, at the atrial level in a patient with hemodynamically important right ventricular infarction. J Am Coll Cardiol. 1983;2:776–779. 10. Bansal RC, Marsa RJ, Holland D, et al. Severe hypoxemia due to shunting through a patent foramen ovale: a correctable complication of right ventricular infarction. J Am Coll Cardiol. 1985;5:188–192. 11. Manno BV, Bemis CE, Carver J, Mintz GS. Right ventricular infarction complicated by right to left shunt. J Am Coll Cardiol. 1983;1(2 Pt 1):554–557. 12. Lopez-Sendon J, Lopez de Sa E, Roldan I, et al. Inversion of the normal interatrial septum convexity in acute myocardial infarction: incidence, clinical relevance and prognostic significance. J Am Coll Cardiol. 1990;15: 801–805. 13. Forman MB, Wilson BH, Sheller JR, et al. Right ventricular hypertrophy is an important determinant of right ventricular infarction complicating acute inferior left ventricular infarction. J Am Coll Cardiol. 1987;10: 1180–1187. 14. Doyle T, Troup PJ, Wann LS. Mid-diastolic opening of the pulmonary valve after right ventricular infarction. J Am Coll Cardiol. 1985;5(2 Pt 1):366–368. 15. Nava A, Thiene G, Canciani B, et  al. Familial occurrence of right ventricular dysplasia: a study involving nine families. J Am Coll Cardiol. 1988;12:1222–1228. 16. Dittrich HC, Nicod PH, Chow LC, et al. Early changes of right heart geometry after pulmonary thromboend­ arterectomy. J Am Coll Cardiol. 1988;11:937–943. 17. Eysmann SB, Palevsky HI, Reichek N, et  al. Twodimensional and Doppler-echocardiographic and cardiac catheterization correlates of survival in primary pulmonary hypertension. Circulation. 1989;80:353–360. 18. Douglas PS, Garcia MJ, Haines DE, et al. A report of the ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/ SCCM/SCCT/SCMR on the 2011 appropriate use criteria for echocardiography. J Am Coll Cardiol. 2011; 57(9):1126–1166. 19. Cheitlin MD, Armstrong WF, Aurigemma GP, et  al. ACC/AHA/ASE 2003 guideline update for the clinical application of echocardiography: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASE Committee to Update the 1997 Guidelines for the Clinical Application of Echocardiography). Circulation. 2003;108:1146–1162.

419

20. Cheitlin MD, Chair JS, Alpert JS, et  al. ACC/AHA guidelines for the clinical application of echocardiography: a report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines (Committee on Clinical Application of Echocardiography). Circulation. 1997;95:1686–1744. 21. Taylor AJ, Cerqueira M, Hodgson JM, et  al. ACCF/ SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/ SCMR 2010 appropriate use criteria for cardiac computed tomography. J Am Coll Cardiol. 2010;56(22): 1864–1894. 22. Hendel RC, Manesh PR, Kramer CM, Poon M. ACCF/ACR/SCCT/SCMR/ASNC/NASCI/SCAI/ SIR appropriateness criteria for cardiac computed tom­ ography and cardiac magnetic resonance imaging. J Am Coll Cardiol. 2006;48:1475–1497. 23. Pennell DJ, Sechtem UP, Higgins CB, et  al. Clinical indications for cardiovascular magnetic resonance (CMR): Consensus Panel report. J Cardiovasc Magn Reson. 2004;6: 727–765. 24. Klocke FJ, Baird MG, Bateman TM, et  al. ACC/ AHA/ASNC guidelines for the clinical use of cardiac radionuclide imaging: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASNC Committee to revise the 1995 Guidelines for the Clinical Use of Cardiac Radionuclide Imaging). Circulation. 2003;108: 1404–1418. 25. Douglas PS, Khandheria BK, Stainback RF, Weissman NJ. ACCF/ASE/ACEP/ASNC/SCAI/SCCT/SCMR 2007 appropriateness criteria for transthoracic and transesophageal echocardiography: a report of the American College of Cardiology Foundation Quality Strategic Directions Committee Appropriateness Working Group, American Society of Echocardiography, American College of Emergency Physicians, American Society of Nuclear Cardiology, Society for Cardiovascular Angiography and Interventions, Society of Cardiovascular Computed Tomography and the Society for Cardiovascular Magnetic Resonance. J Am Soc Echocardiogr. 2007; 20:787–805. 26. Hendel RC, Berman DS, Di Carli MF, et  al. ACCF/ ASNC/ACR/AHA/ASE/SCCT/SCMR/SNM 2009 appropriate use criteria for cardiac radionuclide imaging. J Am Coll Cardiol. 2009;53(23):2201–2229. 27. Vieira ML, Grinberg M, Pomerantzeff PM, et  al. Repeated echocardiographic examinations of patients with suspected infective endocarditis. Heart. 2004;90(9): 1020–1024.

420 Chapter 23  |  Right Heart Diseases BOX 23-1  Assessment Criteria and Indications for Cardiac Imaging Modalities for the Assessment of Right Heart Chamber Quantification TRANSTHORACIC ECHOCARDIOGRAPHY ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/ SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography18 Evaluation of Ventricular Function with TTE n Initial evaluation of ventricular function (e.g., screening) with no symptoms or signs of cardiovascular disease Appropriateness criteria: I; median score: 2 2003 ACC/AHA Guideline Update for the Clinical Application of Echocardiography19 n For pulmonary disease: pulmonary emboli and suspected clots in the right atrium or ventricle or main pulmonary artery branches* • Class IIa 1997 ACC/AHA Guidelines for the Clinical Application of Echocardiography 20 Pulmonary Disease n Suspected pulmonary hypertension • Class I n For distinguishing cardiac versus noncardiac etiology of dyspnea in patients in whom all clinical and laboratory clues are ambiguous* • Class I

n Follow-up of pulmonary artery pressures in patients with pulmonary hypertension to evaluate response to treatment • Class I n Lung disease with clinical suspicion of cardiac involvement (suspected cor pulmonale) • Class I n Measurement of exercise pulmonary artery pressure • Class IIa n Patients being considered for lung transplantation or other surgical procedure for advanced lung disease* • Class IIa n Lung disease without any clinical suspicion of cardiac involvement • Class III n Re-evaluation studies of RV function in patients with chronic obstructive lung disease without a change in clinical status • Class III

TRANSESOPHAGEAL ECHOCARDIOGRAPHY ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/ SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography 18 No specific entries CARDIAC COMPUTED TOMOGRAPHY ACCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/ SCMR 2010 Appropriate Use Criteria for Cardiac CT 21 Evaluation of Ventricular Morphology and Systolic Function n Quantitative evaluation of RV function Appropriateness criteria: A; median score 7

Assessment of RV Morphology n Suspected arrhythmogenic RV dysplasia Appropriateness criteria: A; median score: 727

CARDIAC MAGNETIC RESONANCE ACCF/ACR/SCCT/SCMR/ASNC/NASCI/SCAI/SIR 2006 Appropriateness Criteria for Cardiac Magnetic Resonance Imaging 22 No specific entries

SCMR Consensus Indication for Cardiac Magnetic Resonance Imaging 23 n For assessment of global (left and right) ventricular function • Class I

NUCLEAR ACC/AHA/ASNC 2003 Guidelines for the Clinical Use of Radionuclide Imaging 24 For Heart Failure: Fundamental Assessment n Initial assessment of LV and RV function at rest* • Test: Rest RNA • Class I (Level of evidence: A) n Routine serial assessment of LV and RV function at rest* • Test: Rest RNA • Class IIb (Level of evidence: B) n Initial or serial of ventricular function with exercise • Test: Exercise RNA • Class IIb (Level of evidence: B)

n For valvular heart disease: initial and serial assessment of LV and RV function • Test: Rest RNA • Class I (Level of evidence: B) n For adults with congenital heart disease: initial and serial assessment of LV and RV function • Test: Rest RNA • Class I (Level of evidence: B) n For specific causes of dilated cardiomyopathy: RV dysplasia • Test: Rest RNA • Class IIa (Level of evidence: B)   

Appropriateness criteria: A, appropriate; I, inappropriate; U, uncertain. LV, left ventricular; RNA, radionuclide angiography; RV, right ventricular; TEE, transesophageal echocardiography; TTE, transthoracic echocardiography. *TEE is indicated when TTE studies are not diagnostic.

Right Heart Diseases  |  Chapter 23

421

BOX 23-2  Appropriateness Criteria and Indications for Cardiac Imaging Modalities in the Assessment of Pulmonary Hypertension TRANSTHORACIC ECHOCARDIOGRAPHY ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/ SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography 18 Pulmonary Hypertension with TTE n Evaluation of suspected pulmonary hypertension, including evaluation of RV function and estimated pulmonary artery pressure Appropriateness criteria: A; median score: 9 n Routine surveillance (1 cm), pedunculated tumor that can occur anywhere on the ventricular endocardium or atrioventricular valves. Pathologically, it may look like a sea anemone. Clinically, it has embolic potential.

PRIMARY MALIGNANT CARDIAC TUMORS Rhabdomyosarcoma

Rhabdomyosarcoma occurs in infants and children.

Angiosarcoma r Includes

many histologic types, including Kaposi sarcoma r Is one of the most common primary cardiac malignancies, accounting for about one third of all primary cardiac malignancies r The gender ratio is male:female: 2–3:1. r Eighty to 97% originate in the RA wall or pericardium. r Angiosarcomas often are associated with a hemorrhagic pericardial effusion and may present as tamponade. r Angiosarcomas commonly obstruct right heart valves and right heart inflow or outflow. r Angiosarcoma presentations • Right-sided chamber or venous obstruction: 60% • Tamponade with right-sided obstruction: 40% r At surgery • Pericardial obliteration: 24% • Complete encasement of the heart: 31% Pericardial fluid cytology may be falsely negative. Angiosarcoma is highly aggressive, with pulmonary metastases present in half at the time of presentation. An echocardiographic RA mass or the presence of a pericardial peel following pericardiocentesis suggests angiosarcoma. Metastases to the heart are 20 to 40 times more common than are primary cardiac malignancies. Out of all patients dying of malignancy, 10% to 25% have cardiac involvement at autopsy. Pericardial involvement is far more common than is myocardial. Extension to the heart may occur by the following: r Hematogenous spread • Melanoma r Direct extension • Bronchogenic carcinoma, breast carcinoma, esoph­ ageal carcinoma, lymphoma r Caval extension • Renal cell carcinoma, hepatoma r Pulmonary venous extension • Bronchogenic carcinoma

INTRACARDIAC THROMBI LV thrombi occur overwhelmingly in the setting of coronary artery disease with infarction, but may also be seen in dilated cardiomyopathy, Chagas disease, and following contusion. LV thrombi vary morphologically between pedunculated and laminated, and have movement that varies between sessile and mobile. LV thrombi occur over dyskinetic or akinetic

Cardiac Masses  |  Chapter 24

segments, and are more likely to develop in the setting of low flow and heart failure. In a small number of patients with advanced malignancy, thrombus has occurred in normally contracting myocardium. Mural thrombi complicate 30% to 40% of (non-­ anticoagulated) transmural infarction. Thrombi form most commonly in the apex, which can be visualized in 90% of patients. Most (>80%) thrombi occur during the in-hospital phase following infarction. However, in a subset (~20%) of survivors with LF ejection fraction less than 35%, congestive heart failure, and persistent akinesia/dyskinesia, thrombi may form following hospital discharge (after about 14 days). Protuberant and mobile thrombi have been shown in some studies to have a weak predictive value of systemic embolization. In longitudinal studies, the morphology of thrombi has been documented to vary over time. For the diagnosis of intracavitary thrombus, the sensitivity of echocardiography is in the range of 90% to 95%, and the sensitivity is 85% to 90%. False-positive diagnoses arise from indistinct echoes at the apex, from misperception of LV bands, and from misinterpretation of trabeculae as thrombi. LV aneurysms are thin walled; therefore, visualization of normal wall thickness in a dyskinetic segment may suggest laminated thrombus within it. Two-dimensional echocardiographic features of thrombi include the following: r Echodensity (generally denser than underlying wall) distinct from the endocardium r Consistently present in multiple views r Overlie akinetic/dyskinetic myocardium Most emboli occur in patients who had documented thrombi, but some emboli occur in patients in whom thrombus was not detected.

Left Atrial Thrombi

LA thrombi usually accompany mitral disease, mainly mitral stenosis (because of the associated “low-flow” state within an often enlarged left atrium), and occur in the context of atrial fibrillation. They often arise in/from the LA appendage. Overall, transthoracic echocardiography is about 70% sensitive and more than 90% specific. The presence of a mitral valve prosthesis (which confers shadowing artifact) renders the assessment of the LA by transthoracic echocardiography invariably incomplete. Transesophageal echocardiography remains the best test to identify/exclude atrial appendage thrombosis.

Right Heart Thrombi

Right heart thrombi may be seen with the following: r Dilated cardiomyopathy and low output r Endomyocardial fibrosis, Loeffler’s endocarditis, hypereosinophilic syndrome r Following inferior myocardial or RV infarction r Cardiac contusion r Pulmonary hypertension with RV failure

r Catheter thrombosis r Embolus-in-transit (“popcorn”

443

shaped)

REFERENCES 1. McCarthy PM, Piehler JM, Schaff HV, et al. The significance of multiple, recurrent, and “complex” cardiac myxomas. J Thorac Cardiovasc Surg. 1986;91:389–396. 2. Carney JA, Gordon H, Carpenter PC, et al. The complex of myxomas, spotty pigmentation, and endocrine overactivity. Medicine (Baltimore). 1985;64:270–283. 3. Douglas PS, Garcia MJ, Haines DE, et al. A report of the ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/ SCCM/SCCT/SCMR on the 2011 appropriate use criteria for echocardiography. J Am Coll Cardiol. 2001;57(9): 1126–1166. 4. Cheitlin MD, Armstrong WF, Aurigemma GP, et  al. ACC/AHA/ASE 2003 guideline update for the clinical application of echocardiography: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASE Committee to Update the 1997 Guidelines for the Clinical Application of Echocardiography). Circulation. 2003;108:1146–1162. 5. Cheitlin MD, Chair JS, Alpert JS, et  al. ACC/AHA Guidelines for the Clinical Application of Echocardiography: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Clinical Application of Echocardiography). Circulation. 1997;95:1686–1744. 6. Douglas PS, Khandheria BK, Stainback RF, Weissman NJ. ACCF/ASE/ACEP/ASNC/SCAI/SCCT/SCMR 2007 appropriateness criteria for transthoracic and transesophageal echocardiography: a report of the American College of Cardiology Foundation Quality Strategic Directions Committee Appropriateness Working Group, American Society of Echocardiography, American College of Emergency Physicians, American Society of Nuclear ­Cardiology, Society for Cardiovascular Angiography and Interventions, Society of Cardiovascular Computed Tomography and the Society for Cardiovascular Magnetic Resonance. J Am Soc Echocardiogr. 2007;20:787–805. 7. Taylor AJ, Cerqueira M, Hodgson JM, et  al. ACCF/ SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/ SCMR 2010 appropriate use criteria for cardiac computed tomography. J Am Coll Cardiol. 2010;56(22): 1864–1894. 8. Hendel RC, Manesh PR, Kramer CM, Poon M. ACCF/ACR/SCCT/SCMR/ASNC/NASCI/SCAI/ SIR appropriateness criteria for cardiac computed tomography and cardiac magnetic resonance imaging. J Am Coll Cardiol. 2006;48:1475–1497. 9. Pennell DJ, Sechtem UP, Higgins CB, et al. Clinical indications for cardiovascular magnetic resonance (CMR): Consensus Panel report. J Cardiovasc Magn Reson. 2004; 6:727–765. 10. Klocke FJ, Baird MG, Bateman TM, et al. ACC/AHA/ ASNC guidelines for the clinical use of cardiac radionuclide imaging: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASNC Committee to revise the 1995 Guidelines for the Clinical Use of Cardiac Radionuclide Imaging). Circulation. 2003;108:1404–1418.

444 Chapter 24  |  Cardiac Masses BOX 24-1  Appropriateness Criteria and Indications for Cardiac Imaging Modalites for the Assesment of Suspected Cardiac Masses TRANSTHORACIC ECHOCARDIOGRAPHY ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/ SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography 3 TTE for Evaluation of Intracardiac and Extracardiac Structures and Chambers n Suspected cardiac mass Appropriateness criteria: A; median score: 9 n Suspected cardiovascular source of embolus Appropriateness criteria: A; median score: 9 ACC/AHA 2003 Guideline Update for the Clinical Application of Echocardiography 4 n No new or revised recommendations ACC/AHA 1997 Guidelines for the Clinical Application of Echocardiography 5 Indications for Echocardiography in Patients with Cardiac Masses and Tumors n Class I • Evaluation of patients with clinical syndromes and events suggesting an underlying cardiac mass

• Evaluation of patients with underlying cardiac disease known to predispose to mass formation for whom a therapeutic decision regarding surgery or anticoagulation will depend on the results of echocardiography • Follow-up or surveillance studies after surgical removal of masses known to have a high likelihood of recurrence (e.g., myxoma) • Patients with known primary malignancies when echocardiographic surveillance for cardiac involvement is part of the disease staging process n Class IIb • Screening persons with disease states likely to result in mass formation but for whom no clinical evidence for the mass exists n Class III • Patients for whom the results of echocardiography will have no impact on diagnosis or clinical decision making

TRANSESOPHAGEAL ECHOCARDIOGRAPHY ACCF/ASE/ACEP/ASNC/SCAI/SCCT/SCMR 2007 Appropriateness Criteria for Transesophageal Echocardiography 6 n TEE is used as an adjunct to TTE when suboptimal TTE images preclude obtaining a diagnostic study. n It is reasonable to use TEE as a first test when visualization of certain structures seen best by TEE is necessary to achieve the goals of the imaging test, including, but not limited to, evaluation of the mitral valve, atria, great vessels, and/or prosthetic valves. CARDIAC COMPUTED TOMOGRAPHY ACCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/SCMR 2010 Appropriate Use Criteria for Cardiac CT 7 n Initial evaluation of cardiac mass (suspected tumor or thrombus) Appropriateness criteria: I; median score: 3 n Evaluation of cardiac mass (suspected tumor or thrombus) Inadequate images from other noninvasive methods. Appropriateness criteria: A; median score: 8 CARDIAC MAGNETIC RESONANCE Appropriateness Criteria for the Use of Cardiac MRI for the Assessment of Cardiac Masses 8 n Evaluation of cardiac mass (suspected tumor or thrombus) Appropriateness criteria: A; median score: 9

SCMR Consensus Panel: Indication for Cardiac Magnetic Resonance Imaging 9 n For detection and characterization of cardiac and pericardiac tumors • Class I

NUCLEAR ACC/AHA/ASNC 2003 Guidelines for the Clinical Use of Radionuclide Imaging10 No    specific entries Appropriateness criteria: A, appropriate; I, inappropriate; U, uncertain. TEE, transesophageal echocardiography; TTE, transthoracic echocardiography.

Cardiac Masses  |  Chapter 24

445

TABLE 24-1 Primary Cardiac and Pericardial Tumors* TYPE

NO.

PERCENT

130

30.5

Lipoma

45

10.5

Papillary fibroelastoma

42

9.9

Rhabdomyoma

36

8.5

Fibroma

17

4.0

Hemangioma

15

3.5

Teratoma

14

3.3

Mesothelioma of AVN

12

2.8

319

75.1

Angiosarcoma

39

9.2

Rhabdomyosarcoma

26

6.0

Fibrosarcoma

14

3.3

Benign Myxoma

Total Malignant

Lymphoma Total

7

1.6

106

24.9

AVN, atrioventricular node. *0.0017–0.28%, autopsy series. From McAllister HA, McAllister H, Fenoglio JJ, Fenoglio JR. Atlas of Tumor Pathogy: Tumors of the Cardiovascular System. Washington, DC: U.S. Government Printing Office; 1990.

TABLE 24-2 Utility of Different Imaging Modalities and Cardiac Catheterization in the Assessment of Cardiac Masses MODALITY

PROS

CONS/CAVEATS

Transthoracic Echocardiography

Probably the best test overall to assess intracardiac masses, particularly small masses with random or oscillatory motion that would reduce imaging quality for cardiac CT or MRI

NA

Transesophageal Echocardiography

Likely the single best test to assess atrial level and valvular level lesions

NA

Cardiac CT

Chest CT and abdominal CT are enormously useful when assessing for other involvement of potentially metastatic disease and in finding the primary source.

NA

Cardiac MRI

SSFP sequences: Can identify many masses, as long as their signal differs from that of surrounding tissue

NA

LGE sequences: Demonstrate variable findings Gradient echo images: May assist in characterizing tumors (i.e., “salt-and-pepper” appearance of most myxomas) Nuclear

NA

• Affords little to the average cardiac masses case

Chest Radiography

Useful to depict pulmonary lesions, pleural effusions, and abnormal cardiac and mediastinal contours germane to cardiac masses

NA

Cardiac Catheterization

Provides the vehicle for endomyocardial biopsy of right heart lesions

NA

LGE, late gadolinium enhancement; NA, not applicable; SSFP, steady-state free precession.

446 Chapter 24  |  Cardiac Masses

Figure 24-1.  Transesophageal images. Upper left: Narrowing of the right pulmonary artery by soft tissue. Right image: Two large masses filling the right atrium and ventricle. Lower left: Flow acceleration in a pulmonary artery from compression by soft tissue. Lower middle image: Spectral image of accelerated flow from pulmonary artery compression. Lower right: Spectral flow from a compressed and narrowed pulmonary vein. Mediastinal and cardiac involvement by B-cell lymphoma.

Figure 24-2.  Left: Pleural metastases. Right: Liver metastases.

Cardiac Masses  |  Chapter 24

447

Figure 24-3.  Mediastinal masses (lymphoma). Left: Posterior short-axis image at the base of the heart. The right pulmonary artery is narrowed. Right: On the suprasternal image there is soft tissue under the aorta and around the right pulmonary artery.

Figure 24-4.  Multiple round masses of myeloma in the right atrium, interatrial septum, and right ventricle.

Figure 24-5.  Left atrial myxoma. Upper images: Soft tissue mass prolapsing into the mitral orifice is seen. Lower left: Apical two-chamber view shows flow acceleration around the soft tissue mass, resulting in a proximal isovelocity surface area. Lower right: Combined M-mode and phonocardiogram. The soft tissue mass fills the mitral orifice in diastole. The phonocardiogram demonstrates an early diastolic sound—the “tumor plop” of a left atrial myxoma.

Figure 24-6.  Large right atrial myxoma. Left: Posterior short-axis mid-ventricular level view obtained in diastole. The soft tissue mass has prolapsed into the right ventricle. Right: Posterior short-axis image obtained at the base of the heart. The large soft tissue mass nearly fills the right atrium and the proximal part of the right ventricle.

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449

Figure 24-7.  Mediastinal adenopathy and mass effect from metastatic breast carcinoma. Transesophageal echocardiographic views of a mass pinching the main pulmonary artery. The right panel demonstrates the flow acceleration across the pulmonary artery. There was a 60 mm Hg gradient.

Figure 24-8.  Transesophageal echocardiographic images of a papillary fibroelastoma on the atrial surface of the anterior leaflet of the mitral valve. The mass was slightly lobulated and mobile.

Figure 24-9.  Large pleural effusion in the left chest (note the descending aorta beside the heart). Left: A “tongue” of atelectatic lung is seen. Right: The large pleural-based soft tissue mass that is seen is metastatic adenocarcinoma from the gastrointestinal tract.

450 Chapter 24  |  Cardiac Masses

Figure 24-10.  Transesophageal echocardiographic views of a renal cell carcinoma extending via the inferior vena cava (IVC) into the right atrium. Left: Longaxis view shows the IVC dilated and filled with soft tissue. Middle: IVC junction to the right atrium seen on short-axis view. The soft tissue mass is circular in cross-section. Right: The entire right atrium is filled with a kidney-shaped soft tissue mass. The bulk of the mass in the right atrium indicates that it is more likely to be malignancy than thrombus.

Figure 24-11.  Hepatoma filling the right atrium as seen on a horizontal plane transesophageal echocardiographic view.

Figure 24-12.  Superior vena cava (SVC) syndrome/compression. A jet of flow into the right atrium from the SVC is seen. There is poorly defined soft tissue around and lateral to the SVC. Metastatic adenocarcinoma was the diagnosis.

Cardiac Masses  |  Chapter 24

Figure 24-13.  Papillary fibroelastoma on the right leaflet of the aortic valve.

Figure 24-14.  Presumed papillary fibroelastoma on the right leaflet of the aortic valve.

451

452 Chapter 24  |  Cardiac Masses

Figure 24-15.  Examples of thrombi in the heart. Upper left: Free-floating thrombus in the left atrium (LA). Upper right: Free-floating thrombus in the LA. As the mitral valve replacement has opened in diastole, the thrombus is floating toward the orifice. Lower left: Left atrial appendage thrombus. Lower right: Lobulated thrombus off the basal inferior wall of the left ventricle post-infarction.

25

Cardiac Trauma

ardiovascular trauma may be strongly suspected and sought immediately at the time of presentation, or, conversely, it may not be recognized at first because other trauma captures the attention. Cardiac wounds may be single or multiple. Transthoracic echocardiography (TTE) can be performed with adequate images in most patients, but for a substantial number, local chest wall pain will prohibit some aspects of transthoracic scanning, as may subcutaneous emphysema, and abdominal pain or distention may prevent subcostal imaging. A case can be made for transesophageal echocardiography (TEE) to identify or better define cardiac and aortic traumatic injuries that are not readily apparent on transthoracic scanning. Cardiac trauma should be suspected in any patient with a wound, penetrating but also nonpenetrating, to the chest, precordium, neck, or upper abdomen. Some penetrating wounds elsewhere in the body may result in cardiac trauma when a projectile travels or migrates within the body.

r Echocardiographic

BLUNT CARDIAC TRAUMA

Coronary Sequelae

C

Pericardial Sequelae r Pericardial r Pericardial

effusions tamponade • Should prompt consideration of rupture of the aorta or of a cardiac chamber r Pneumopericardium • Apparent as bright echoes with far-field shadowing, usually anteriorly (in a supine patient) seen in systole. • Pneumopericardium and subcutaneous emphysema often produce too much artifact for the heart to be visible from the chest wall surface— TEE may help as the esophagus courses between the pulmonary veins posteriorly and is partially extrapericardial, allowing visualization of the heart even with pneumopericardium. r Pericardial rupture, with/without herniation

Myocardial Sequelae r Myocardial

damage is produced in the area underlying the impact, but also may occur elsewhere in the heart, often on the opposite wall.

features of myocardial contusion include • Increased end-diastolic wall thickness (edema and hematoma) • Reduced systolic function r There is a spectrum of severity of myocardial contusion. Echocardiography is most likely to be sensitive to severe degrees of contusion, but some authors have questioned its sensitivity to less severe degrees of contusion.1 r Cardiac rupture may occur due to breakdown of myocardium post-contusion, due to violent compression of the heart, puncture by a rib, or coronary disruption or thrombosis from trauma. Ventricular septal defect,2 free wall rupture, tamponade, and pseudoaneurysms have all occurred.

Valvular Sequelae

r The aortic valve is most commonly injured,3 although

any valve may be involved. Insufficiency results from damage to leaflets, chordae, or papillary muscles, or semilunar leaflet avulsion or retroversion.

sequelae include thrombosis,4 dissection, aneurysm, and fistulous communication.5 r The left anterior descending and right coronary arteries are the most commonly affected. r Coronary

PENETRATING CARDIAC TRAUMA r In

the urban milieu, the missiles that most commonly penetrate the heart are knives and bullets. r Most (60–80%), but not all, of these wounds are fatal, often immediately. r The clinical presentation is usually tamponade or bleeding into the chest. r Left anterior stab wounds most often involve the right ventricle. Right anterior stab wounds may involve the right ventricle or atrium, and left lateral and posteriors stab wounds may involve the left ventricle. r Bullet wounds commonly involve the left ventricle. r Puncture of a cardiac chamber may result in the following: • Pericardial effusion • Pericardial tamponade 453

454 Chapter 25  |  Cardiac Trauma • Possible intracardiac communication/fistula • Valve disruption r Penetrating cardiac wounds often are multiple. r Shunt flow within the heart may have unusual color flow characteristics if caused by a knife, as on one plane the defect is seen as thin, and on another it is seen as wide. r Coronary artery laceration may occur, resulting acutely in tamponade and later in myocardial infarction.

• Pseudoaneurysm • Localized dissection r TEE has a major contribution to offer to the diagnosis of traumatic injury to the aorta.

INDICATIONS FOR TRANSESOPHAGEAL ECHOCARDIOGRAPHY IN CARDIAC TRAUMA r When

MISSILES WITHIN THE HEART Localization of a missile (e.g., bullet, bullet fragment, shotgun pellet, shrapnel) is important, because the decision to operate is based partly on its location. r Echocardiography may help localize a missile within the heart by imaging the location and motion6: • If the missile resides on the anterior surface of the heart and does not move, it is most likely in the pericardium or pericardial space • If it moves as the right ventricle moves, then it is most likely embedded in the right ventricle. r Some missiles may be free within a cardiac chamber. r Bullets and shotgun pellets are conspicuous by their tail of reverberations.

BLUNT AORTIC TRAUMA r As

many as one sixth of motor vehicle deaths are caused by aortic rupture. r Eighty percent of patients with aortic rupture die outright. r Twenty percent get to the hospital; of those who survive to the hospital, 70% may survive. r From 2% to 5% of patients with partial tears will develop pseudo-aneurysms (usually saccular), and half of those aneurysms will expand. r Any high-speed sudden deceleration may produce shearing at the junction of mobile and fixed portions of the aorta. Rarely, blast injury may cause aortic rupture. r Ninety percent of blunt injuries to the aorta involve either: • The isthmus at the insertion of the ligamentum arteriosum • The aorta at the level of the diaphragm • The origin of the innominate artery • The ascending portion of the aorta. r Lesions that may occur include the following: • Aortic transsection

the transthoracic echocardiographic study quality is not adequate r To exclude disruption of the aorta when other tests are equivocal TEE is validated for the detection of traumatic disruption, but performing TEE in the setting of trauma may carry additional difficulties (e.g., cervical collar) and risks (e.g., loosened or broken teeth, cervical spine injury, possible esophageal injury).

REFERENCES 1. Hossack KF, Moreno CA, Vanway CW, Burdick DC. Frequency of cardiac contusion in nonpenetrating chest injury. Am J Cardiol. 1988;61:391–394. 2. Boland MJ, Martin HF, Ball RM. Nonpenetrating traumatic ventricular septal defect: two-dimensional echocardiographic and angiographic findings. Am J Cardiol. 1985;55:1242–1243. 3. Rehr RB, Mack M, Firth BG. Aortic regurgitation and sinus of Valsalva-right atrial fistula after blunt thoracic trauma. Br Heart J. 1982;48:410–412. 4. Pandian NG, Skorton DJ, Doty DB, Kerber RE. Immediate diagnosis of acute myocardial contusion by twodimensional echocardiography: studies in a canine model of blunt chest trauma. J Am Coll Cardiol. 1983;2: 488–496. 5. Sareli P, Goldman AP, Pocock WA, et  al. Coronary artery-right ventricular fistula and organic tricuspid regurgitation due to blunt chest trauma. Am J Cardiol. 1984;54:697–699. 6. Hassett A, Moran J, Sabiston DC, Kisslo J. Utility of echocardiography in the management of patients with penetrating missile wounds of the heart. J Am Coll Cardiol. 1986;7:1151–1156. 7. Douglas PS, Garcia MJ, Haines DE, et  al. ACCF/ ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/ SCCT/SCMR 2011 appropriate use criteria for echocardiography. J Am Coll Cardiol. 2011;57(9):1126–1166. 8. Taylor AJ, Cerqueira M, Hodgson JM, et  al. ACCF/ SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/ SCMR 2010 appropriate use criteria for cardiac computed tomography. J Am Coll Cardiol. 2010;56(22): 1864–1894. 9. Hendel RC, Berman DS, Di Carli MF, et  al. ACCF/ ASNC/ACR/AHA/ASE/SCCT/SCMR/SNM 2009 appropriate use criteria for cardiac radionuclide imaging. J Am Coll Cardiol. 2009;53(23):2201–2229.

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BOX 25-1  Appropriateness Criteria and Indications for Cardiac Imaging Modalities for the Assessment of Cardiac Trauma TRANSTHORACIC ECHOCARDIOGRAPHY ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/ SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography7 Cardiac Trauma with TTE n Severe deceleration injury or chest trauma when valve injury, pericardial effusion, or cardiac injury are possible or suspected Appropriateness criteria: A; median score: 9 n Routine evaluation in the setting of mild chest trauma with no electrocardiographic changes or biomarker elevation Appropriateness criteria: I; median score: 2 ACC/AHA/ASE 2003 Guideline Update for the Clinical Application of Echocardiography Conditions and Settings in which TEE Provides the Most Definitive Diagnosis in the Critically Ill and Injured n The hemodynamically unstable patient with suboptimal TTE images n The hemodynamically unstable patient on a ventilator n Major trauma or postoperative patients (unable to be positioned for adequate TTE) n Suspected aortic dissection n Suspected aortic injury n Other conditions in which TEE is superior

• Mechanically ventilated multiple-trauma or chesttrauma patient • Suspected pre-existing valvular or myocardial disease in the trauma patient • The hemodynamically unstable multiple-injury patient without obvious chest trauma but with a mechanism of injury suggesting potential cardiac or aortic injury (deceleration or crush) • Widening of the mediastinum, postinjury suspected aortic injury (TEE) • Potential catheter, guidewire, pacer electrode, or pericardiocentesis needle injury with or without signs of tamponade n Class IIa • Evaluation of hemodynamics in multiple-trauma or chest trauma patients with pulmonary artery catheter monitoring and data disparate with clinical situation • Follow-up study on victims of serious blunt or penetrating trauma n Class III • Suspected myocardial contusion in the hemodynamically stable patient with a normal ECG who has no abnormal cardiac/thoracic physical findings and/or lacks a mechanism of injury suggesting ­cardiovascular contusion

Recommendations for Echocardiography in the Critically Injured* n Class I • Serious blunt or penetrating chest trauma (suspected pericardial effusion or tamponade) TRANSESOPHAGEAL ECHOCARDIOGRAPHY ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/ SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography7 n Suspected acute aortic pathology including, but not limited to, dissection/transsection CARDIAC COMPUTED TOMOGRAPHY ACCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/SCMR 2010 Appropriate Use Criteria for Cardiac CT 8 No specific entries NUCLEAR ACCF/ASNC/AHA/ASE/SCCT/SCMR/SNM 2009 Appropriate Use Criteria for Cardiac Radionuclide Imaging 9 No    specific entries Appropriateness criteria: A; appropriate; I, inappropriate; U, uncertain. TEE, transesophageal echocardiography; TTE, transthoracic echocardiography. *The use of TTE or TEE includes Doppler techniques when indicated and available and with appropriately trained and experienced sonographer and interpreter. TEE is indicated when TTE images are suboptimal. TEE often provides incremental information.

456 Chapter 25  |  Cardiac Trauma TABLE 25-1 Utility of Different Imaging Modalities and Cardiac Catheterization in the Assessment of Cardiac and Aortic Trauma MODALITY

PROS

CONS/CAVEATS

Transthoracic Echocardiography

2D echocardiography • Portability and general availability are high, especially at trauma centers. • A ready means by which to establish the presence of pericardial fluid and tamponade • A fair test to identify myocardial contusion • Can identify some intracardiac traumatic lesions

• Concurrent hypovolemia can alter the signs of tamponade. • The absence of a pericardial effusion does not exclude cardiac injury.

Doppler echocardiography: Is able to depict many cardiac flow disturbances (valvular disruption, VSDs, fistulae) secondary to penetrating and nonpenetrating trauma Transesophageal Echocardiography

• An excellent test for detection of the majority of cases of traumatic disruption of the aorta • Can identify most specific intracardiac traumatic lesions • Provides reliable imaging when TTE does not

• Concurrent maxillofacial trauma renders performing TEE more difficult, sometimes impossible.

Cardiac CT

NA

• Although CT is the workhorse of general trauma imaging, especially of the aorta, the role of cardiac CT in trauma is unclear.

Cardiac MRI

NA

• Affords little to most cases of cardiac trauma

Nuclear

NA

• Affords little to most cases of cardiac trauma

Chest Radiography

Standard initial test that yields considerable information

• Unlikely to recognize specific cardiac injury; more likely to recognize complications of cardiac injuries • Pulmonary contusion and aspiration findings may confound the recognition of heart failure. • Without a lateral view, it is difficult to localize projectiles within the heart. • Will not image nonradiopaque projectiles • Mediastinal hematomas are not synonymous with traumatic disruption of the aorta.

Cardiac Catheterization

• Contrast aortography is an established/ standard test to evaluate traumatic aortic disruption. • Catheterization and aortography are the vehicles by which to perform TEVAR for traumatic disruption of the aorta.

NA

2D, two-dimensional; NA, not applicable; TEE, transesophageal echocardiography; TEVAR, thoracic endovascular aortic repair; TTE, transthoracic echocardiography; VSD, ventral septal defect.

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Figure 25-1.  Stab wound in the apical area. The top images show parasternal long-axis views (diastole on the left, systole on the right). A small pericardial effusion is present. The diastolic image reveals a very small left atrium consistent with hypovolemia, possibly from the chest wound. In the middle images (diastole on the left, systole on the right), there is a thick pericardial clot under the left ventricle (LV). The LV cavity completely obliterates in systole. The lower images (diastole on the left, systole on the right) reveal a jet of flow at the very tip of the septum, seen in diastole and not in systole. Surgical inspection and review revealed a laceration of the left anterior descending coronary artery (LAD) at the apex, leading to intrapericardial hemorrhage and clot. LAD flow is more pulsatile in diastole, which is why the jet could be visualized in diastole, not systole.

458 Chapter 25  |  Cardiac Trauma

Figure 25-2.  Transesophageal echocardiographic image of a patient with stab wounds to the right and left anterior chest. The knife has sliced the mid-septum obliquely, resulting in a ventricular septal defect, revealed by color flow mapping. The right ventricle is dilated. There is no pericardial effusion, despite the penetrating trauma.

Figure 25-3.  Stab wound to the left parasternum. Left: Parasternal short-axis view with color flow mapping demonstrating a jet of flow across the septum into the right ventricle. Right: Spectral Doppler demonstrates high-velocity flow through the traumatic ventricular septal defect.

Figure 25-4.  Stab wound to the lower anterior left parasternum. Upper left: Posterior long-axis view shows a small- to moderate-sized pericardial effusion. Upper right: Parasternal short-axis image at the base of the heart. There is a turbulent jet in the posterior aortic root and part of the right atrium (RA). The RA is minimally compressed. Middle images: Apical four-chamber views (A4CVs) show a moderate-sized pericardial effusion with compression of the right ventricular (RV) wall, and a peculiar appearance to the RV free wall. Lower left: A4CV with color Doppler demonstrating a jet into the RA that extends into the RV. Lower right: The flow sampled in the jet is nearly continuous. A stab wound through the RV free wall, through the tricuspid orifice, and into the RA nicked the right sinus of Valsalva and produced an aortic-to-RA fistula with continuous flow.

Figure 25-5.  Stab wound to the left lateral chest, with the patient in shock. Transesophageal echocardiography images. Upper images: A soft tissue mass is seen moving in association with the anterior mitral leaflet. Middle images: A soft tissue mass is moving with the anterior mitral leaflet. The right middle image strongly suggests a decapitated papillary muscle. Lower images: View of the traumatically severed papillary muscle (left) and resultant severe mitral regurgitation (right).

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Figure 25-6.  Gunshot injury to the right lateral chest seen on a transesophageal image. There is a small pericardial effusion, and an epicardial rind of clot (containing specular echoes). There is a prominent reverberation artifact arising from a gunshot pellet. Figure 25-7.  Gunshot to the leg, with embolization of the bullet via the profunda femoris vein into the right heart. The bullet is seen as an echogenic mass along the right lateral wall of the right ventricular cavity.

Figure 25-8.  Stab wound to the mid–left anterior chest, resulting in left anterior descending coronary artery laceration/transaction and left-sided hemothorax. Left: Preoperative images; right: postoperative images. Upper images: diastolic; lower images: systolic. Note how preoperatively the septum does not thicken and the end-systolic cavity is large. Conversely, note how postoperatively the septum thickens and the end-systolic cavity size is small.

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26

Echocardiographic Guidance of Procedures STUART J. HUTCHISON, DEBORAH ISAAC, MARK JOHNSON, ROBERT MOSS, and BRAD MUNT

JUGULAR VENOUS CANNULATION Rationale and Role r To

simplify jugular venous access by direct visualization and guidance r To minimize complications such as hematomas due to jugular venous transfixion, carotid artery puncture, jugular venous to carotid arterial fistula, pneumothoraces, multiple puncture, and failed procedures

Sequence r Place

the patient in Trendelenburg position to increase the size of the neck veins. r With the skin cleaned and sterile, introduce the probe into a sterile plastic sheath. r Image from the anterior neck in the mid-portion, which overlies the internal jugular vein and the common carotid artery. The jugular vein, depending on the central venous pressure, may be (usually is) larger than the common carotid artery, but in volume-contracted or dehydrated patients, the vein may be smaller than the artery. The vein may lie to the side of, anterolateral to (this is its usual location in the mid-neck), anterior but slightly lateral to, or completely anterior to the artery. r The most desirable site for cannulation is where the vein is substantially at least lateral to the artery, so that inadvertent transfixion of the vein runs little risk of inadvertently puncturing the common carotid artery. Avoid locations where the jugular vein is directly anterior to the artery. r The vein is identified by the following: • Location • Distention with a partial Valsalva maneuver • Compressibility and anterior flattening by slight pressure application with the probe r If the vein is generously full, the needle is inserted carefully through the taut anterior wall of the vein until the tip is a few millimeters into the lumen.

r If

the vein is full but limp, have the patient make a partial Valsalva maneuver to distend the vein, providing a larger target for the needle puncture and a more taut anterior wall. r It is easiest if the patient is told to take a breath (inspire) before he or she is told to strain (perform a Valsalva maneuver). Guiding the patient in practicing the performance of a Valsalva maneuver before the procedure is helpful for patients who are not familiar with it. r Visualize the wire extending from the needle. r Visualize the sheath within the lumen following its insertion. r Be aware of the presence of jugular venous valves, a normal aspect of anatomy. Insertion beneath the valves may simplify the procedure. r Be aware of the appearance of jugular venous thrombus, a common residua of prior catheter and wire insertions

Pro

r With

practice and experience, a high degree of proficiency can be achieved.

Cons

r Few r Some

dexterity and proficiency with the technique of direct ultrasound imaging guidance are needed, resulting in a learning curve (Figs. 26-1 to 26-3).

ENDOMYOCARDIAL BIOPSY To reliably diagnose heart transplant rejection, right ventricular endomyocardial biopsy (percutaneous procurement of endomyocardial samples from the right ventricle1,2) remains the gold standard. Right ventricular endomyocardial biopsy also is a valuable way to assist with diagnosis and management of suspected myocarditis, infiltrative cardiomyopathy, or other unexplained ventricular dysfunction. 463

464 Chapter 26  |  Echocardiographic Guidance of Procedures Percutaneous right ventricular endomyocardial biopsy most commonly is performed using cannulation of the right internal jugular vein. In circumstances where this vessel is not usable, the femoral vein can be used for this purpose. Cardiologists traditionally have relied on fluoroscopic guidance for placement of the bioptome. Using frontal-plane fluoroscopic guidance, the bioptome is directed toward the right ventricular septum to obtain right ventricular samples. Bioptome contact with the right ventricular septum is confirmed by the presence of ventricular ectopic beats, and samples are taken from that site. Typically at least four biopsy samples are obtained, because a minimum of three adequate biopsy samples are required for histologic diagnosis. The use of fluoroscopy to guide right ventricular endomyocardial biopsy has a number of drawbacks: it provides only approximate bioptome placement information; exposes both the patient and physician to radiation; and requires use of the cardiac catheterization laboratory—a facility in high demand. Using fluoroscopic guidance, the complication rate ranges from 6% to 14%,3,4 with possible complications including myocardial perforation, tricuspid valve apparatus disruption, arrhythmias, coronary artery to right ventricular fistula, and inadvertent arterial punctures. A significant limitation of fluoroscopic guidance for right ventricular endomyocardial biopsies is that the bioptome placement and subsequent sampling area are limited due to inability to place the bioptome precisely, leading to repeated sampling from the same area. This contributes to biopsies that consist predominantly of scar from previous biopsy sites, which are inadequate for histologic assessment, and to reduced sensitivity due to the potentially focal nature of rejection or other cardiac histologic processes.

Rationale and Role

Real-time visualization r Of venipuncture to lessen access complications r Of bioptome placement/biopsy sampling • To lessen complications • To increase diagnostic yield

Sequence

r Echocardiographically

guided endomyocardial biopsy usually is performed in the echocardiography laboratory, with the assistance of an echosonographer and a nurse. r The person performing the biopsy procedure stands at the head of the bed, with the echosonographer and echocardiography machine to the patient’s left and the nurse and sterile tray to the patient’s right. r Echocardiographic images are obtained prior to venous cannulation to determine the optimal window and views for visualization of the right atrium and ventricle; to briefly assess left and right ventricular systolic function, the presence and amount of pericardial fluid present, and the presence and

degree of tricuspid regurgitation; and to estimate right ventricular systolic pressure. Preprocedure imaging also determines the ideal patient positioning. In many cases supine imaging is adequate, but patients may be moved into the left lateral lying position after initial insertion of the jugular venous sheath to optimize visualization of the right-sided cardiac structures. Ultrasound assessment of the right internal jugular vein may be done at this time, to assist in venous cannulation. r Venous access is obtained using standard Seldinger technique via the right internal jugular vein, with a sheath left in place. r The bioptome is then inserted through the venous sheath into the right atrium. r Using echocardiographic imaging to visualize the right-sided chambers and tricuspid valve and apparatus, the bioptome is then passed across the tricuspid valve into the right ventricle. The endocardial surfaces of the right ventricle are visualized, and the sonographer “follows” the advancement of the bioptome, keeping the forceps head of the bioptome clearly imaged throughout the procedure. The operator maneuvers the bioptome to the desired location, avoiding the moderator band and tricuspid apparatus. Once the bioptome is approximated next to the endomyocardial surface in the desired position, the jaws of the bioptome are opened, and the bioptome is advanced gently against the endomyocardium. Once in place, the jaws are closed and, with a very gentle tug, the biopsy sample is obtained. The bioptome is removed, the sample is placed in sterile saline, and the procedure is repeated until an adequate number of samples have been obtained. r Samples may be taken from the mid to distal right ventricular septum, apex, and free wall in post– cardiac transplant patients, but are usually restricted to the mid- to distal right ventricular septum in non–transplant patients. r Post-procedure echocardiographic imaging assesses for changes in the presence or degree of tricuspid regurgitation and/or pericardial fluid. Two decades ago, Miller published his successful results using echocardiographic guidance for right ventricular endomyocardial biopsy.5 Despite this and other reports of reduced costs and an improved safety profile using echocardiography to guide right ventricular endomyocardial biopsy in adults and children,6–10 this technique has not gained widespread popularity.

Pros

Echocardiographic guidance of right ventricular endomyocardial biopsy affords considerable benefits over traditional fluoroscopic guidance. r Improved safety • As well as elimination of radiation exposure, there is less likelihood of cardiac damage caused by poor visualization—such as inadvertently entering the coronary sinus or damage to tricuspid

Echocardiographic Guidance of Procedures  |  Chapter 26

apparatus—because of the superior means to identify anatomic cardiac landmarks. Intracardiac leads and catheters can be easily visualized and avoided for bioptome placement. • The uncommon complication of pericardial effusion development can be immediately identified and addressed if endomyocardial biopsy is performed under echocardiographic guidance. • Ultrasound guidance can be used to assist with difficult venous cannulation, which affords both a  safety and convenience advantage by reducing  inadvertent carotid artery punctures and repeated/multiple access attempts. r Provision of additional information • A brief assessment of left and right ventricular systolic function, valvular regurgitation, right ventricular/pulmonary artery systolic pressure, and presence of pericardial fluid can be performed to provide current and additional structural and functional information. r Portability • Although most patients will undergo right ventricular biopsy in the echocardiography laboratory, biopsies may be performed in the rooms of critically ill patients in the cardiac intensive care unit, saving staff time and eliminating the inconvenience of transporting the patient. r Improved sampling • An expanded endomyocardial sampling area improves the sensitivity for the diagnosis of rejection, which may be a focal process. In adequate samples may be obtained in up to 8% of biopsies performed under fluoroscopy and as low as 0%6 under echocardiographic guidance. • Using echocardiography, the bioptome can be directed away from scarred previous biopsy sites, and samples can be obtained safely from sites along the mid- to distal right ventricular septum and apex. • In patients who are more than 6 to 8 weeks post– cardiac transplantation, biopsies may be safely obtained from the patient’s right ventricular free wall by experienced operators.5 Biopsy samples should be limited to the right ventricular septum in patients who are within 6 to 8 weeks after cardiac transplantation, and in those with native hearts. r Directed biopsies • Echocardiographic biopsy guidance allows for targeted biopsy of intracardiac (i.e., within the right ventricle and right ventricular outflow tracts) masses due to the ability to clearly image the target area and the bioptome. r Reduced costs • Performance of right ventricular biopsy under echocardiographic guidance reduces costs up to 50%7 because it avoids the use of the cardiac catheterization laboratory, and it requires fewer staff resources—typically, one nurse and one echocardiography technician are needed, compared to

465

the need for a scrub nurse, a circulating nurse, and a monitoring technician in the catheterization laboratory. Despite valid and compelling benefits, there has been reluctance to adopt echocardiographically guided right ventricular biopsy. A typical argument against the technique is the perception that it is difficult to get adequate echocardiographic images in some patients. In 90% of patients, however, the standard apical four-chamber view can be used to view the bioptome head,6 although modifications of this view may be necessary to provide optimal imaging during bioptome manipulation.

Cons

r Learning curve r Need for the operator

26-4 to 26-10)

to develop confidence (Figs.

PERICARDIOCENTESIS Rationale and Role r Echocardiography

provides the most versatile means to guide pericardiocentesis by guiding access site selection and needle entry orientation, visual confirmation of needle entry into the pericardial space, avoidance of cardiac perforation, and verification of successful drainage.

Sequence

r Preprocedure

• S  tandard transthoracic study to establish the location and distribution of the pericardial fluid • Determination of the site that provides shortest distance to enter the pericardial fluid and the best orientation to minimize needle trauma to the heart (by orienting into the fluid space away from the heart chambers) r During the procedure • Visual identification of the needle orientation and entrance into the pericardial space • Visual confirmation of the wire within the pericardial space, with or without visual confirmation of the injection of agitated saline within the pericardial space • Visualization of reduction of the pericardial fluid r Unlike chest CT scan, real-time imaging by echocardiography of the heart’s motion within the pericardial space enables determination of the dimension of pericardial fluid throughout the cardiac cycle, which can vary considerably between diastole and systole. r During the procedure, use of a sterile sleeve to enable scanning immediately beside the site of puncture allows for real-time imaging.

Pros

r Portability: can be performed at any bedside r Real-time imaging during the procedure maximizes

procedural awareness.

466 Chapter 26  |  Echocardiographic Guidance of Procedures

Con

r Learning

eye–hand coordination to image the ­needle and wires requires willingness (Figs. 26-11 to 26-17).

TRANSSEPTAL PUNCTURE Rationale and Role r Visual

guidance by transesophageal echocardiography (TEE) of interatrial septal puncture to lessen risk of inadvertent puncture complications and identify any complications that do occur r Guidance of complex transseptal punctures in cases of kyphosis or scoliosis where the heart orientation (specifically that of the interatrial septum) within an abnormal chest cavity is unclear without imaging

Sequence

r Visualization

of the catheter and needle approaching the heart (inferior vena cava/bicaval view) r Visualization of the needle contacting the interatrial septum away from the margin of the septum r Visualization of the needle tenting the interatrial septum away from the margin of the septum r Visualization of the needle/catheter in the left atrium r Visualization of the catheter flush (small bubbles) in the left atrium

Pros

r Straightforward r Identification of

the presence of a patent foramen ovale alerts one that the interatrial septum may be inadvertently/quickly crossed.

Con

r Performing TEE on a supine patient requires atten-

tion and measures to protect the airway (Fig. 26-18).

CATHETER MITRAL BALLOON VALVULOPLASTY Rationale and Role r TEE

guidance of catheter balloon valvuloplasty affords a means by which to • Guide atrial septal puncture in difficult cases • Assess the degree of post–balloon inflation mitral insufficiency in cases of preprocedure moderate mitral regurgitation (MR) where there is concern about precipitating severe MR.

Sequence

r As described for r Color Doppler

atrial septal puncture guidance flow mapping and pulmonary venous sampling to determine the degree of mitral insufficiency incurred by balloon inflation

Pro

r Useful when contrast sparing is desirable (e.g., renal

insufficiency). Contrast ventriculography is otherwise used to assess the degree of mitral insufficiency post–balloon inflation.

Cons

r Not needed for the average case r Performing TEE on a supine patient requires atten-

tion and measures to protect the airway (Figs. 26-19 to 26-22).

PERCUTANEOUS AORTIC VALVULOPLASTY Rationale and Role

Traditional aortic valve replacement is performed via median sternotomy, cardiopulmonary bypass, aortotomy, resection of the native aortic valve, and insertion of a prosthetic aortic valve. Approximately 60,000 aortic valve surgeries are performed per year in North America; however, many patients in need of aortic valve surgery never undergo it due to prohibitive and generally noncardiac risks. Percutaneous aortic valve (PAV) replacement, as an alternative to open-chest aortic valve replacement, is emerging and is undergoing clinical investigation as an alternative to conventional surgery. Valves can be inserted percutaneously via retrograde aortic cannulation or anterogradely via a small thoracotomy. Two PAV prostheses currently are in clinical use: r The CoreValve prosthesis (Fig. 26-23) r The Edwards-Sapien prosthesis (Fig. 26-24) Echocardiography has an integral role in PAV implantation pre-, intra-, and post-procedurally, as two-dimensional imaging, especially by TEE, is generally very well-suited to delineate left ventricular outflow tract and aortic valve anatomy, and the hemodynamics of stenosis and insufficiency.

Sequence

Preprocedural Assessment Severity/morphology of aortic stenosis r Routine transthoracic echocardiography (TTE) is done to assess for aortic stenosis, including ensuring that the stenosis is valvular and determining, at a minimum, the valve gradient and aortic valve area. (Other values such as the dimensionless index may be helpful in some situations.) r Valve morphology • Tricuspid versus bicuspid valve • Aortic valve calcium distribution and extent Aortic root geometry TEE may be required to yield accurate root dimensions if TTE is technically difficult. The contribution of gated cardiac CT also should be considered for dimensional measurements

Echocardiographic Guidance of Procedures  |  Chapter 26

The number of key measurements depends on the PAV used: r For the CoreValve prosthesis • Aortic annulus diameter • Sinus of Valsalva diameter • Sinotubular junction diameter • Aortic annulus–coronary ostial distance (aortic valve area–ostial height) r For the Edwards-Sapien prosthesis • Aortic annulus diameter Aortic annulus The aortic annulus is a critical measurement in determining patient eligibility and is useful in device sizing. The aortic annulus is not a planar anatomic structure but, rather, a complex 3-dimensional “crown-like” configuration formed by the insertion of the aortic cusps into the aortic wall. Small variations in image plane can produce significantly differing annular measurements. Hence, careful alignment of the aortic root is essential in producing an accurate and reproducible measurement. r Parasternal long-axis view on TTE and the midesophageal long-axis view on TEE r Measure on a frozen zoomed end-diastolic frame (beginning of the QRS complex after closure of the mitral valve and before opening of the aortic valve). r Aortic root walls should be parallel and the aortic valve orifice central in a trileaflet valve. The crossplane (biplane) feature on three-dimensional probes can be helpful in aligning the aortic root. r Measured diameters are intraluminal, from aortic wall to aortic wall, ignoring any protuberant calcium from the measurement. r Annulus diameter is perpendicular to the long axis of the root, measured between the endocardial site that trisects the posterior aortic wall, noncoronary cusp hinge and the anterior mitral leaflet hinge, and the point that bisects the anterior aortic wall and the right coronary cusp hinge. Our recommendation is to obtain three reproducible measurements: r Sinus of Valsalva diameter • Perpendicular to the long axis of the root, parallel to the aortic annulus, the widest intraluminal distance within the sinuses. r Sinotubular junction diameter • Intraluminal diameter parallel to the sinus of Valsalva diameter, where the sinuses narrow and join the ascending aorta r Aortic valve area–ostial height • Distance of the right coronary ostium to the aortic annulus r These dimensions are critical for sizing the percutaneous prosthesis. Subaortic geometry r Assessment for noncompliant subaortic disease: protuberant calcium in the left ventricular outflow tract, moderate to severe septal hypertrophy

467

r CoreValve

recommends that implantation should not be performed if subaortic disease is sufficient to cause stenosis or if the septal wall thickness is 17 mm or more. r Hypertrophic cardiomyopathy with significant left ventricular outflow tract obstruction is a contraindication for both devices. • If the obstruction is subaortic, then, clearly, both devices are contraindicated. Other valve pathology/cardiac disease r Baseline assessment of left ventricular (LV) systolic and diastolic function, regional wall motion abnormalities, right ventricular (RV) function, and pulmonary artery pressure • Assess for significant mitral valve disease (MR and extensive mitral annular calcification are common). • The CoreValve is contraindicated if the severity of MR is greater than grade 2+. r Other test modalities that factor prominently into the preprocedural assessment of percutaneous aortic valve implantation procedures include • Cardiac catheterization for assessment of aortic stenosis severity assessment and detection of the presence of concurrent valvular problems and complications • Coronary angiography for the delineation of coro­ nary artery disease extent and severity • Electrocardiographically gated cardiac CT scan for assessment of dimensions Intraprocedural Role The CoreValve prosthesis often is implanted without intraoperative TEE guidance, whereas the EdwardsSapien valve usually is implanted under TEE guidance. r The long-axis view (~130 degrees) is used to guide deployment of the Edwards prosthesis. Ideally, the undeployed Edwards valve on the delivery system should be positioned across the aortic valve coaxial to the aorta. The ventricular end should be positioned up to 5 mm below the native aortic valve area, because there is a tendency for the percutaneous heart valve (PHV) deployment system to propagate incrementally toward the aortic root during deployment. The aortic end should be close to the tips of the native aortic valve leaflets to ensure full leaflet capture with deployment. r Identification of the ventricular and aortic rims of the prosthesis can be challenging, and knowledge of the PHV length (this may differ in the deployed and undeployed states), the use of high-frequency imaging, and manipulation of the probe are required to improve visualization. It should also be remembered that different iterations of the deployment systems have subtly different imaging characteristics. r Hemodynamic instability often is observed during device positioning. This may be due to critical output obstruction by the undeployed PHV, but is thought sometimes to be related to reflexive changes in vagal output. Correct deployment position of the Edwards

468 Chapter 26  |  Echocardiographic Guidance of Procedures valve is essential so that the fabric portion of the prosthesis is fully opposed to the aortic annulus. Deployment in a position that is too ventricular is serious; it may result in immediate and life-threatening aortic regurgitation; incomplete capture of native aortic valve leaflets and restriction of anterior mitral valve leaflet motion also may be seen. Deployment in a position that is too aortic can result in coronary artery obstruction and can compromise the stability of the valve, risking valve embolization. r Edwards-Sapien valves usually are implanted under TEE guidance: • To confirm valve annulus size • In assisting the crossing of the aortic valve with a wire • In assisting in positioning and monitoring aortic balloon valvuloplasty (performed prior to valve implantation) • To assess the degree of aortic regurgitation post– balloon valvuloplasty • To guide positioning of the prosthesis prior to balloon deployment • Assess PAV position stability, leaflet motion, and degree and location of aortic regurgitation (a  valve may be expanded further with another balloon inflation if more than mild paravalvular regurgitation is present) • To assist in determining the etiology of hypotension post–PAV deployment • In determining PAV gradients (from retroflexed transgastric views) r TEE can be helpful in assessing for aortic pathology that may occur during the procedure (e.g., dissection). Post-procedural Assessment r Immediate post-procedural assessment by TEE r PHV position and stability • When correctly positioned, the ventricular end of the PHV should lie 2 to 4 mm ventricular to the aortic annulus, while the aortic end should fully capture the aortic leaflets, displacing leaflet calcium into the aortic root. r Aortic regurgitation • Trivial or mild posterior paravalvular regurgitation often is noted and is of little concern. If there is greater than mild paravalvular regurgitation, the prosthetic valve may be expanded further with another balloon inflation. Trivial valvular aortic regurgitation also is commonly seen. r Unusual complications include the following: • Coronary ostial occlusion (displaced bulky calcium) • Cardiac trauma (pericardial effusion/tamponade) • Fragmented aortic debris or thrombus in relation to the PHV • Aortic root rupture during deployment, • Aortic dissection or rupture by the delivery system • Mitral valve dysfunction (this is unusual; functional MR often improves following PHV implantation)

r PHV

gradients (best obtained from deep transgastric views)

Post-procedural Follow-up by Transthoracic Echocardiography r TTE

for follow-up of PAV hemodynamics (gradients, area, regurgitation) r TTE for follow up of hemodynamic and morphologic response to PAV implantation (e.g., change in pulmonary artery pressure, LV mass changes) r TTE or TEE for assessment of symptoms that develop after valve implantation (e.g., imaging for suspected endocarditis; Figs. 26-25 to 26-30)

INTRA-AORTIC COUNTERPULSATION BALLOON TIP LOCALIZATION Rationale and Role r Identification

of the correct location of the intraaortic balloon in both intra-aortic and intra-cardiac assist devices

Sequence r The

tip of the intra-aortic counterpulsation balloon (IABP) is verified post-insertion by fluoroscopy or chest radiography. However, it is somewhat prone to movement, especially in patients who are transported. r TEE is readily able to verify the tip location of the balloon. It should be in the very proximal descending aorta.

Pros r A

practical means to use at the bedside to ensure correct placement of the IABP within the proximal descending aorta and to exclude misplacement, such as within the inferior vena cava r A practical means to identify some complications of IABP insertion such as iatrogenic dissection

Cons

r Few r F luoroscopy

generally is used to guide IABP placement, especially because most are placed in the cardiac catheterization laboratory. The role of TEE is limited to verification of correct placement without fluoroscopy (Figs. 26-31 and 26-32).

IMPELLA AND LEFT VENTRICULAR ASSIST DEVICE INSERTION* Rationale and Role r The

Impella percutaneous ventricular assist devices (Abiomed, Inc., Danvers, MA) typically are inserted percutaneously via the femoral artery (Impella 2.5) or via surgical cut-down (Impella 2.5 or 5). The device is advanced retrograde up the aorta, and

*This section was contributed by Gregory Schnell, MD.

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positioned across the aortic valve such that the intake is within the LV, and the output is above the aortic valve. The component of the device within the LV is best oriented along the long axis of the LV. The presence of significant aortic insufficiency would preclude the device achieving efficiency. r Echocardiography is useful to exclude significant aortic valve disease (i.e., aortic stenosis that would preclude delivery of the device into the left ventricle and aortic insufficiency that would impair efficiency). TEE usually is employed to verify the correct location/position of the intake component within the left ventricle and of the output component within the aorta. r Although these devices are deployed with fluoroscopic guidance, the combination of fluoroscopy and echocardiography—both two-dimensional and color Doppler—provides visualization of the wire and device (fluoroscopy and echocardiography) and the cardiac structures (echocardiography) such that the position and orientation of the device ensures optimal functioning

Sequence

Transthoracic echocardiography r To exclude significant aortic valvar stenosis r To exclude significant aortic valvar insufficiency r To exclude ‘mechanical’ complications of infarction Transesophageal echocardiography r After exclusion of significant aortic valve disease and mechanical complications of infarction • Obtain a suitable long-axis view of the left ventricle, left ventricular outflow tract, aortic valve, and aortic root. • Confirm that the guide wire has been advanced to and then across the aortic valve into the left ventricle. • Confirm that the device has been advanced a suitable distance into the left ventricle such that the intake is 4 to 5 cm beyond the aortic valve into the left ventricle. r The location of the intake can be determined as follows: • If the device is not on: by the bright reflections from the metallic body just distal to the actual intake • If the device is on: by color Doppler flow mapping that reveals continuous flow r Confirm that the device is oriented to have the distal part along the long axis of the left ventricle toward the apex, rather than toward the wall. r Confirm that the output component is ejecting blood within the aorta beyond the aortic valve.

Pros r A

practical means to use in the operating room or cardiac catheterization laboratory to ensure correct placement of the intake and the output components of the Impella device on their appropriate sides of the aortic valves

469

r TTE

may yield sufficient images, but TEE achieves more reliable visualization because most patients with cardiogenic shock are mechanically ventilated.

Cons

r Few r Visualization

of the length of the Impella 5 device within the LV necessitates obtaining a long-axis view along which the device falls. If the plane of the device varies from that of the imaging plane, visual misunderstanding about the location of the end of the device may occur because it may be assumed that the last visualized portion of the device is the end. r Familiarity with devices and with the two-dimensional and color Doppler imaging findings of their components is essential (Figs. 26-33 to 26-40).

SURGICAL VENTRICULAR ASSIST DEVICE PLACEMENT AND FUNCTION Rationale and Role r Identification

of the correct location of both intraaortic and intra-cardiac assist devices

Sequence r The

tip of the IABP is verified post-insertion by fluoroscopy or chest radiography. However, it is somewhat prone to movement, especially in patients who are transported. r TEE is readily able to verify the tip location of the balloon. It should be in the very proximal descending aorta.

Pros r A

practical means for use at the bedside to ensure correct placement of the IABP within the proximal descending aorta, and to exclude misplacement such as within the inferior vena cava r A practical means to identify some complications of IABP insertion, such as iatrogenic dissection

Cons

r Few r F luoroscopy

generally is used to guide IABP placement, especially because most are placed in the cardiac catheterization laboratory. The role of TEE is limited to verification of correct placement without fluoroscopy (Fig. 26-41).

REFERENCES 1. Caves PK, Stinson EB, Billingham M, Shumway NE. Percutaneous transvenous endomyocardial biopsy in human heart recipients. Experience with a new technique. Ann Thorac Surg. 1973;16(4):325–336. 2. Billingham M. Endomyocardial biopsy diagnosis of acute rejection in cardiac allografts. Prog Cardiovasc Dis. 2009;33:11–18.

470 Chapter 26  |  Echocardiographic Guidance of Procedures 3. Deckers JW, Hare JM, Baughman KL. Complications of transvenous right ventricular endomyocardial biopsy in adult patients with cardiomyopathy: a seven-year survey of 546 consecutive diagnostic procedures in a tertiary referral center. J Am Coll Cardiol. 1992;19(1): 43–47. 4. Sakakibara S, Konno S. Endomyocardial biopsy. Jpn Heart J. 1962;3:537–543. 5. Miller LW, Labovitz AJ, McBride LA, et  al. Echocardiography-guided endomyocardial biopsy. A 5-year experience. Circulation. 1988;78(5 Pt 2):III99–III102. 6. Blomstrom-Lundqvist C, Noor AM, Eskilsson J, Persson S. Safety of transvenous right ventricular endomyocardial biopsy guided by two-dimensional echocardiography. Clin Cardiol. 1993;16(6):487–492.

7. Weston MW. Comparison of costs and charges for fluoroscopic- and echocardiographic-guided endomyocardial biopsy. Am J Cardiol. 1994;74(8):839–840. 8. Williams GA, Kaintz RP, Habermehl KK, et al. Clinical experience with two-dimensional echocardiography to guide endomyocardial biopsy. Clin Cardiol. 1985;8(3): 137–140. 9. Ragni T, Martinelli L, Goggi C, et al. Echo-controlled endomyocardial biopsy. J Heart Transplant. 1990;9(5): 538–542. 10. Appleton RS, Miller LW, Nouri S, et al. Endomyocardial biopsies in pediatric patients with no irradiation. Use of internal jugular venous approach and echocardiographic guidance. Transplantation. 1991;51(2):309–311.

Positions of the internal jugular vein relative to the common carotid artery

Lateral

Anterolateral (most common)

Anterior, slightly lateral

Fully anterior

Ultrasound-guided internal jugular venipuncture

Figure 26-1.  Top: The different positions of the internal jugular vein (purple) relative to the common carotid artery (red) vary depending on the location of the neck and somewhat between patients. Bottom: Identification of the internal jugular vein and its venipuncture. Among other techniques, the internal jugular vein is identified by its compressibility in response to light pressure from the transducer, which flattens the near wall, and also by near-wall tenting/indentation in response to needle pressure.

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Figure 26-2.  Internal jugular venous cannulation guided by a transthoracic ultrasound probe, within a sterile sheath, for endomyocardial biopsy. Upper left: The internal jugular vein and the common carotid artery are seen in short-axis view. Upper right: With compression by the transducer, the jugular vein becomes partially flattened. Middle images: Before (left) and after (right) insertion of the needle through the anterior wall of the jugular vein. Lower left: The internal jugular vein is seen in longitudinal axis and the wire is seen along its oblique course through the overlying soft tissue and down and into the jugular vein. Lower right: The internal jugular vein is again seen in longitudinal axis and the Cordis catheter (Cordis Corporation) is seen within the lumen of the vein.

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Figure 26-3.  A venous valve within the internal jugular vein seen in longitudinal axis (upper images) and in short axis (lower images).

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Figure 26-4.  Upper images: Guidance of the internal jugular venipuncture is performed with ultrasound. Middle images: The sheath is advanced into the internal jugular vein and its position verified by ultrasound. Lower images: Bioptome in the closed (left) and open (right) positions. The ultrasonographic appearance of the bioptome tip can be expected to be more prominent when it is in the open position.

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Bioptome

Internal jugular vein

Clavicle

Apex

Figure 26-5.  Upper left: Internal jugular venous access is the preferred route to perform endomyocardial biopsy. Upper right: The bioptome is advanced under ultrasound guidance. Middle left: The bioptome is introduced through the sheath, down the superior vena cava. Middle right: The bioptome is introduced into the heart, and its tip can be seen within the right atrium. Lower left: The bioptome tip is being advanced into the right ventricle. Lower right: An endomyocardial biopsy sample.

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Figure 26-6.  Upper left: The bioptome tip has been advanced slightly past the tricuspid valve level. Upper right: The bioptome tip has been advanced toward the apical portion of the interventricular septum. Middle left: The bioptome has been opened, resulting in a more prominent appearance by two-dimensional ultrasound imaging. Middle right: Traction has been placed on the bioptome as the endomyocardial sampling is performed, slightly distorting the septal curvature. As the bioptome separates from the septum there is a slight but brisk motion of the septum as it assumes its normal curvature. Lower left: The bioptome with the endomyocardial biopsy sample has been withdrawn to the right atrium. Lower right: The bioptome with the endomyocardial biopsy sample has been withdrawn out of the heart.

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Figure 26-7.  Upper left: The bioptome tip can be seen within the right atrium. Upper right: The bioptome tip can be seen within the right ventricle, being advanced forward. Middle left: The bioptome tip is being advanced toward the apical portion of the interventricular septum. Middle right: The bioptome has been opened at the distal aspect of the right side of the interventricular septum. In its open position, the bioptome is more ultrasonographically obvious. Lower left: The bioptome, now with an endomyocardical biopsy sample, has been withdrawn into the body of the right ventricle. Lower right: The endomyocardial bioptome has been withdrawn out of the heart. Note the electrocardiographic tracing across the bottom of the images. At the time of contact of the bioptome during sampling, ventricular ectopy is generated.

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Figure 26-8.  Upper left: The bioptome has been inserted to the level of the tricuspid valve annulus. Upper right: The bioptome has been directed against the right ventricular freewall. Lower left: The bioptome has “bitten” the right ventricular freewall, and traction on it has retracted inward/tented the freewall. Lower right: The bioptome, now with a biopsy sample, has released the freewall, is located within the right ventricular cavity, and is being withdrawn.

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Figure 26-9.  Upper left: The bioptome has been applied against the distal septum. Upper right: The bioptome has engaged the mid-septum. Lower left: The bioptome has been opened, as indicated by the larger echo reflection, to acquire the biopsy. Lower right: The bioptome has been closed, as indicated by a smaller echo reflection.

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Figure 26-10.  Upper left: Before intracardiac insertion of the bioptome. Upper right: The bioptome has been advanced to the tricuspid valve level. Lower left: The bioptome has been advanced into the right ventricle toward the right ventricle’s freewall. Lower right: The bioptome, with sample, has been withdrawn into the right ventricular cavity.

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Figure 26-11.  Pericardiocentesis from an apical approach guided by transthoracic ultrasound (within a sterile sleeve) beside the puncture. Upper left: The optimal site and orientation of needle entry are established. From this site and with this orientation there is approximately 2 cm of soft tissue to traverse and approximately 2 cm of fluid over the apicolateral wall of the left ventricle. Upper right: The needle is visualized within the soft tissue having just entered the pericardial space. The orientation of the needle is actually more toward the heart than tangentially beside the heart, and the swinging motion of the apex has brought it within a few millimeters of the needle tip. Middle left: Shallow view demonstrating the bevel of the needle tip within the pericardial space. Middle right: The J-wire is visualized within the pericardial fluid. Lower left: The J-wire is has been advanced further into the fluid, as can be seen from the position of the J-shaped tip. Lower right: The catheter has been advanced over the wire into the pericardial space. Its appearance is different from that of the wire.

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Figure 26-12.  Pericardiocentesis from an apical approach guided by transthoracic ultrasound (within a sterile sleeve) beside the puncture. Upper left: The optimal site and orientation of needle entry are established; from this site and with this orientation there is approximately 2 cm of soft tissue to traverse and 3–4 cm of fluid over the apicolateral wall of the left ventricle. Upper right: Shallow view of the same are to “set up” the puncture. Middle left: The needle has been introduced into the pericardial space. A segment of needle is visualized in the more shallow soft tissue, but the tip and actual site of entry into the pericardial space are not seen on this plane of imaging. The bubbles from an agitated saline injection, however, corroborate entry of the needle tip into the pericardial space. Middle right: The wire is visualized within the pericardial space, and due to slight adjustment of the imaging plane, the entry of the wire into the pericardial space is seen. Lower left: The dilator over the wire is visualized within the pericardial space. Lower right: The drainage catheter is visualized within the pericardial space. Note the difference in the appearances of the wire, the dilator, and the drainage catheter.

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Figure 26-13.  Left: A shallow apical view to set up needle introduction into the pericardial space. There are only a few millimeters of fluid over the true apex; the safest site to enter is beside the apex, and the safest orientation is tangential to the apicolateral wall. Right: The needle has been introduced at the correct site and with the correct orientation.

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Figure 26-14.  Transthoracic echocardiographically guided pericardiocentesis. The plane of imaging perfectly follows the plane of the needle advancement, because the two are joined by a guide device. On these serial images the needle can be seen arriving at the parietal pericardium (upper right), tenting the parietal pericardium (middle left and right), entering the pericardial space (lower left), and having entered the pericardial space (lower left). Finally, the guidewire can be seen further entering the pericardial space (lower right).

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Figure 26-15.  Tenting of the parietal pericardium during pericardiocentesis. Left: Mild pressure with the needle has produced a shallow indentation/inversion of the curvature of the parietal pericardium. Right: Stronger pressure has resulted in more marked indentation/inversion of the parietal pericardium. In this case, the parietal pericardium was thickened from chronic pericarditis, and the effusion was effusoconstrictive.

Figure 26-16.  Left: Shallow apical view pretap/predrainage shows a large pericardial effusion. Right: Standard apical four-chamber view post-drainage: no fluid remains within the pericardial space, as seen on this plane of imaging.

Figure 26-17.  Transthoracic echocardiographic guidance during pericardiocentesis. Left: During insertion, the needle is ambiguously visualized, because there are four linear entities that all appear to enter the pericordial space from the orientation of the needle. Right: Injection of agitated saline clearly demonstrates that the needle is within the pericordial space despite the poor/ambiguous visualization of the needle.

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Figure 26-18.  Transesophageal guidance of the interatrial septal puncture to perform mitral valvuloplasty. Upper left: A superior cable view depicting the mid-portion of the inner atrial septum (septum primum) and the superior portion of the inner atrial septum (septum secundum). The superior vena cava is seen extending on the far side of the inner atrial septum toward the right side of the image. Upper right: A guidewire passed from the femoral vein to the heart has passed upward to the superior vena cava. Middle left: The Brockenbrough needle has been advanced into the lower mid–right atrium but is not in contact with the inner atrial septum. Middle right: The Brockenbrough needle is being pressed against the inner atrial septum and is tenting it prominently. The tip of the needle is a safe distance away from the superior margin of the left atrium. Lower left: The needle tip can be visualized within the left atrium Lower right: The saline flush can be seen to be within the left atrium.

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Figure 26-19.  Upper left: Transesophageal four-chamber view. The mitral valve morphology is clearly domed, and there is prominent thickening at the top of the anterior mitral leaflet in particular. There is right ventricular hypertrophy. A catheter is in the far interior part of the right ventricle. Upper right: A wire has been passed through the inner atrial septum and is visualized in the body of the left atrium and crossing the mitral valve. Middle left: Initial inflation of the balloon within the mitral valve orifice can be seen to widen the orifice slightly, but a long waist remains on the balloon. Middle right: Subsequent inflation of the balloon yields a smaller waist, indicative of better opening of the mitral valve. Lower left: Color Doppler flow mapping at the mitral stenosis orifice demonstrates a small to moderate sized proximal isovelocity surface area consistent with a gradient, but not a severe one. Lower right: Color Doppler flow mapping of mild mitral insufficiency.

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Figure 26-20.  These images were obtained following mitral valvuloplasty. Upper left: A zoom view from the peristernal long-axis orientation of the mitral valve. There are two jets of mitral insufficiency, one of which is highly eccentric and anterior. Upper right: Transesophageal view of the mitral valve shows a rupture of the anterior leaflet at its basal insertion into the mitral-aortic fibrosa. Lower views with color Doppler flow mapping demonstrate flow across the site of rupture of the anterior mitral leaflet and across the central mitral orifice.

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Figure 26-21.  Mitral valve gradients and the corresponding spectral Doppler display, which yields gradient calculation. MVG 19.8 mmHg MVA 0.93 cm2

PA 89/47 (65) 100

89

88

90

100

MVG 6.6 mmHg MVA 1.44 cm2 100

65 46

0

47

47

0

0

Figure 26-22.  Hemodynamic tracings performed during catheter balloon valvuloplasty. Left: The pulmonary artery (PA) tracing reveals systemic levels of pulmonary hypertension. Middle: The left ventricular and pulmonary venous capillary tracings yield the mitral valve gradient (MVG). The gradient is 20 mm, and the calculated mitral valve area (MVA) by the Gorlin relation is 0.9 cm2. Right: Following mitral valvuloplasty, the pulmonary capillary wedge to left ventricular gradient has fallen to 7 mm, and the area has increased to 1.4 cm2.

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Figure 26-24.  The Edwards-Sapien prosthesis. (Courtesy of Edwards Life-Sciences Inc., Irvine, California.)

Figure 26-23.  The CoreValve prosthesis. (Courtesy of CoreValve ReValving System, CoreValve Inc., Irvine, California.)

Figure 26-25.  Transesophageal echocardiographic midesophageal longaxis view of the aortic root at end-diastole, with measurements of the aortic annulus (A), sinus of Valsalva (B), sinotubular junction (C), and the sinus of Valsalva height (D).

Figure 26-26.  Three-dimensional transesophageal echocardiographic cross-plane midesophageal long- axis (left) and modified short-axis (right) view of the aortic valve during rapid ventricular pacing and aortic valvuloplasty. The right image is inverted in relation to the regular short-axis view, with the intra-atrial septum on the right. These images show a fully deployed aortic valvuloplasty balloon with no waisting of the balloon and displacement of the native aortic valve tissue into the sinuses of Valsalva.

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Figure 26-27.  Transesophageal echocardiographic midesophageal longaxis view of the aortic root pre-deployment of the Edwards-Sapien aortic prosthesis. The crimped Edwards-Sapien valve can be seen on its delivery system crossing the stenotic aortic valve. The ventricular and aortic ends of the crimped valve are marked by arrows. This image shows the correct positioning of the valve pre-deployment.

Figure 26-28.  Transesophageal echocardiographic midesophageal longaxis view of the aortic root pre-deployment of the Edwards-Sapien aortic prosthesis. The crimped Edwards-Sapien valve can be seen on its delivery system crossing the stenotic aortic valve. Blue arrows mark the ventricular and aortic ends of the crimped valve; a green arrow marks the level of the aortic annulus. This valve is positioned too ventricularly for deployment.

Figure 26-30.  Transesophageal echocardiographic color Doppler midesophageal long-axis view of the aortic root post-deployment of the Edwards-Sapien aortic prosthesis. There is mild posterior paravalvular aortic regurgitation. Trivial central aortic regurgitation also is present secondary to the guidewire across the aortic valve.

Figure 26-29.  Top: Transesophageal echocardiographic (TEE) color Doppler midesophageal long-axis view of the aortic root post-deployment of the Edwards-Sapien aortic prosthesis. Severe paravalvular aortic regurgitation secondary to a low valve deployment (i.e., too ventricular). Bottom: TEE color Doppler midesophageal short-axis view of the aortic root postdeployment of the Edwards-Sapien aortic prosthesis. Severe paravalvular regurgitation can be seen around the posterolateral border of the percutaneous heart valve.

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Figure 26-31.  Transesophageal echocardiographic (TEE) and chest radiograph images of a patient with an intra-aortic balloon pump. The short-axis (left) and long-axis (right) TEE images of the proximal descending aorta do not reveal the distal tip of the balloon pump, and the chest radiographs indicate a somewhat low placement in the thoracic aorta.

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Figure 26-32.  Transesophageal echocardiographic (TEE) images of a patient in cardiogenic shock. Upper left: The left main lumen is significantly narrowed. Upper right: Color Doppler flow mapping demonstrates flow acceleration in the mid-distal left mainstem artery. Middle left: Spectral Doppler recording at the site of flow acceleration reveals the diastolic dominant pattern typical of left coronary flow with elevation of flow velocity. Middle right: Cusp shot during coronary angiography prompted by the TEE findings reveals critical narrowing of the distal left main artery. Lower left: The ostial right coronary artery has a normal appearance. Lower right: The spectral Doppler display of flow recording of the right coronary artery is unremarkable in comparison to that of the left mainstem artery.

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Figure 26-33.  Chest fluoroscopy and radiography images of an Impella 5 device. Upper left: The transesophageal echocardiography probe is apparent in the fluoroscopy image as the heavy radiopaque motor and inlet components are obvious. The pigtail is evident, but less obvious. Upper right: With optimization of penetration on the radiograph, the Impella device components are more visible. Lower images: Migration of the device can be surmised by the motor housing having moved higher in the aorta (right versus left lower image).

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Figure 26-34.  Transesophageal echocardiographic images of an Impella 5 device. Upper images: The angulation of the device, which allows it to follow the long axes of the left ventricular outflow tract and of the left ventricle, can be seen. Middle and lower left images: Color Doppler flow mapping is useful to confirm the location of the intake and to allow measurement from the intake site (which is apparent as continuous color Doppler flow signal) to the aortic valve. Lower right image: Color Doppler flow imaging is useful to determine the output location in the aorta.

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Figure 26-35.  Transesophageal echocardiographic images of an Impella 5 device inserted too deeply into the left ventricle. Upper left: The distal extent of the device is indicated by the pigtail at the inferior aspect of the left ventricular apex. Upper right: The measurement from the intake to the aortic valve initially is 6.6 cm; subsequently, after withdrawal of the device (lower images), it is a more appropriate 5.1 cm.

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Figure 26-36.  Systolic (left images) and diastolic (right images) scans in long-axis (upper images) and short-axis (lower images) views of the Impella device across the aortic valve and into the left ventricular outflow tract (LVOT). In systole, little flow is depicted by color Doppler flow mapping ejected out the LVOT, due to the dominance of flow by the device. In diastole, a small central jet of aortic insufficiency can be seen, a common occurrence due to a small amount of coaptation failure imparted by the device. The prominent color flow Doppler mapping signal seen on the short-axis images between 6 and 9 o’clock is the flow within the device.

Figure 26-37.  Chest radiography and fluoroscopic images of an Impella unit. There is slight motion artifact on the fluoroscopic image. The detail afforded by the ideally penetrated chest radiograph is at least comparable to that of the fluoroscopic image. Also note the endotracheal tube and pulmonary artery catheter seen on the chest radiograph, and the transesophageal echocardiographic probe seen on the fluoroscopy image. The long radiopaque marker of the device can be seen along its length and down the aorta.

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Figure 26-38.  Transesophageal echocardiographic (TEE) and transthoracic measurements indicating the depth of the intake unit into the left ventricular cavity. The TEE images afford clear visualization of the device. The transthoracic image (lower right) is confounded by reverberation artifact, which happens to fall nearly along the line/axis of the device. The most echoreflective component is the metal housing by the intake. The device initially was inserted slightly too far, as seen in upper left image and the other TEE images. It was withdrawn so that the intake component was 4 to 5 cm beyond the aortic valve. Note that on all the images, the “hockey stick” angulation is misoriented, directing the distal component toward the posterior wall.

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Figure 26-39.  Diastolic (left) and systolic (right) views of a patient with massive infarction due to left main thrombosis. The fractional area change is minimal, as the ejection fraction was 10%. The Impella device has not yet been inserted.

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Figure 26-40.  Serial transesophageal echocardiographic imaging of the left ventricular outflow tract, aortic valve, and aortic root during insertion of the Impella device. Upper left: Baseline view. Upper right: The J-shaped guidewire has been advanced into the right aortic valve cusp/sinus. Middle left: The guidewire has been advanced across the aortic valve into the left ventricle. Middle right: The device has been advanced over the guidewire to the level of the aortic root. Lower left: The device has been advanced across the aortic valve into the left ventricular cavity. Lower right: Transthoracic view of unusually good quality demonstrates that the device is imperfectly oriented, as the hockey stick angulation is directing the distal component of the device against the posterior wall, rather than along the long axis of the left ventricle toward the apex.

500 Chapter 26  |  Echocardiographic Guidance of Procedures

Figure 26-41.  Malpositioning of an extracorporeal membrane oxygenation (ECMO) catheter. Upper left: Pre-insertion view of the right atrium. Color Doppler demonstrates a patent foramen ovale (PFO). Upper right: Eight days following insertion, this transesophageal echocardiographic view reveals that the inferior vena cava (IVC) catheter is pushing/pressing against the interatrial septum. Second row, left image: This long-axis view reveals the IVC catheter pushing/ pressing against the interatrial septum along its height. Second row, right image: Color Doppler reveals a jet of flow on the left atrial side of the septum, where the catheter has stretched/pressed open the PFO. Third row, left image: Color Doppler demonstrates that this jet pours along the roof of the left atrium and down and across the mitral valve to the left ventricle (right-to-left flow). Third row, right image: Spectral display confirms flow into the left atrium and ventricle from this jet. Lower left: After repositioning, the catheter has been retracted down toward the lower part of the interatrial septum and is no longer pressing on and distorting the interatrial septum PFO. Lower right: Color Doppler post repositioning demonstrates residual bidirectional/right-to-left flow across the PFO due to the right ventricular failure from protracted H1N1 pneumonitis.

INDEX Entries followed by b, f, or t indicate boxes, figures, or tables, respectively. A A (atrial) systole reversal wave, in pulmonary venous flow patterns, 257, 265f A wave, in diastole, 254, 256 Abdominal aorta retrograde holodiastolic flow in, 43–44 spectral profiles of, for aortic insufficiency, 57f Abscesses aortic root, 354 due to infective endocarditis, 157 myocardial, 157 perivalvar/valve ring, 158 TEE of, 171f, 327 AcuNav intravascular ultrasound catheter, 373f Adenosine stress echocardiography, 215, 222t Adolescents, congenital valvular heart disease in, 6b–7b Age-related changes in aortic valve, 3, 5b, 15f in left ventricular inflow patterns, 262t AI. See Aortic insufficiency (AI). Aliasing velocity, in proximal isovelocity surface area, 286–287 AMVL. See Anterior mitral valve leaflet (AMVL). Amyloidosis, cardiac, 228–229 echocardiographic findings of, 228–229, 249f imaging modalities for, 236b–237b, 244t Aneurysm false (pseudo-) from acute myocardial infarction, 203, 210f–211f contrast echocardiography of, 271 due to infective endocarditis, 169f–170f of interatrial septum, 328 left ventricular from acute myocardial infarction, 204–205 false, 203 apical, 194f–195f, 198f contrast echocardiography of, 276f, 282f Angiographic grading, of mitral stenosis, quantitative variables corre­ sponding to angiographic, 104t, 110f diagnostic value of, 105t Angiography, of LV volume, 176, 184t radionuclide, 188f, 176 Angiosarcoma, 442 Angle correction, for proximal isovelocity surface area, 285–286, 296f

Annular dehiscence, with prosthetic valve, 152f–154f due to infective endocarditis, 157 Anterior mitral valve leaflet (AMVL) fibrosis of, mitral regurgitation due to, 93 flail, 346–348, 358 fluttering of, with aortic insufficiency, 45 Anterolateral commissure, of mitral valve, 63 Anterolateral papillary muscle, of mitral valve, 63 Aorta, traumatic disruption of, 326 Aortic annulus, normal anatomy of, 1 Aortic arch, TEE of, 332t–333t Aortic associations, of bicuspid aortic valve, 3 distal, 11f proximal, 12f Aortic atheromatous debris, 326 Aortic balloon valvotomy, ACC/AHA recommendations for, 27b Aortic coarctation bicuspid aortic valve with, 11f, 17f TEE of, 326 Aortic diameter, in aortic stenosis, 18 Aortic disease, TEE of, 325–326 Aortic dissection aortography of, 330t computed tomography of, 330t contrast echocardiography of, 271, 278f MRI of, 330t TEE of, 325, 330t, 334f Aortic insufficiency (AI), 42–61 acute severe, 56f torrential, 45, 57f aortic valve replacement or repair for, ACC/AHA recommendations for, 48b cardiac catheterization for appropriateness of, 49b utility of, 52t cause(s) of, 42–43 aortic root, 42, 55f aortic valve, 42, 54f chest radiography of, 52t chronic moderate, 56f color flow Doppler mapping for, 57f of descending aorta, 44 of LVOT, 44, 51t problems with “quantification” from, 43 CT for appropriateness of, 49b utility of, 52t deceleration time in, 45 echocardiography of, goals of, 42

Aortic insufficiency (Cont.) effective regurgitant orifice method for, 44–45 end-diastolic velocity with, 56f–57f R-R intervals and, 58f due to endocarditis, 57f fluttering of anterior mitral leaflet in, 45 fluttering of aortic valve leaflets in, 56f grading of, 45t indexed to LVOT, 51t in hypertrophic cardiomyopathy, 227 imaging modalities for appropriateness of, 49b utility of, 52t LV parameters in, 42 LVEDP with, 45 LVOT in, 57f color flow Doppler mapping of, 44, 51t grading indexed to, 51t medical therapy for, 43, 48b mitral valve preclosure with, 45, 56f–57f, 61f moderate to severe, 59f MRI for appropriateness of, 49b steady-state free precession sequence for, 60f utility of, 52t velocity encoded phase contrast technique for, 59f nuclear imaging for appropriateness of, 49b utility of, 52t pressure half-time for, 45 proximal isovelocity surface area for, 44–45, 54f, 57f, 293f pros and cons of, 291t pulsed-wave Doppler of, 58f pulsed-wave mapping in LV of, 45 regurgitant fraction of, 45, 59f–60f regurgitant volume of, 44 reporting issues with, 43 required parameters to obtain for, 42 retrograde flow profiles in proximal thoracic descending aorta for, 44 retrograde holodiastolic flow in in abdominal aorta, 43–44 at aortic root level, 60f in lower thoracic aorta, 58f MRI velocity encoded phase contrast technique for, 59f due to rheumatic aortic valve disease, 54f R-R intervals in, 58f scanning issues with, 42 severe, 43, 58f, 60f acute, 56f

501

502 Index Aortic insufficiency (Cont.) severity of, 42–45 slope for, 45, 56f–57f R-R intervals and, 58f spectral profiles for, 43, 56f abdominal aortic, 57f TEE of, 45–46, 57f, 328 appropriateness of, 49b utility of, 52t time velocity interval in, 44 “trivial,” 43 TTE of appropriateness of, 49b utility of, 52t vegetations in, 159 velocity time interval in, 43 vena contracta width and area for, 44 volumetric techniques for, 43 Aortic root age-related changes in, 3 in aortic stenosis dimensions and appearance of, 21–22 narrow, 19 pressure recovery phenomenon at level of, 21 TEE of, 332t–333t Aortic root abscess, 354 Aortic root causes, of aortic insufficiency, 42, 55f Aortic root dilation, aortic insufficiency from, 42, 55f Aortic root dissection, aortic insufficiency from, 42 Aortic root level, retrograde holodiastolic flow at, 60f Aortic rupture, traumatic, 454 Aortic stenosis (AS), 18–41 aortic balloon valvotomy for, 27b aortic diameter in, 18 aortic root in dimensions and appearance of, 21–22 narrow, 19 pressure recovery phenomenon at level of, 21 aortic valve area in catheterization greater than echocardiography estimates of catheterization-responsible reasons for, 25 echocardiography-responsible reasons for, 23 catheterization less than echocardiography estimates of catheterization-responsible reasons for, 25 echocardiography-responsible reasons for, 23 continuity equation–derived issues related to, 21 in low-gradient severe disease, 22 LVOT measurement and, 18 aortic valve gradient in catheterization greater than echocardiography estimates of catheterization-responsible reasons for, 25 echocardiography-responsible reasons for, 23 catheterization less than echocardiography estimates of catheterization-responsible reasons for, 25

Aortic stenosis (Cont.) aortic valve gradient in (cont.) echocardiography-responsible reasons for, 23 heart rate and, 35f issues with, 20–21 and Gorlin equation, 24 in low-gradient severe disease, 22 as per-beat (volume) function, 20 R-R intervals and, 39f and stroke volume, 20 aortic valve replacement for, 27b with bicuspid aortic valve, 21, 41f cardiac catheterization for appropriateness of, 28b usual technique for, 24 utility of, 30t cardiac output with, 24 chest radiography of, 30t confounders in, 19 continuity equation for, 19 aortic valve area issues related to, 21 CT for appropriateness of, 28b utility of, 30t descriptors for, 21 discordance of catheterization and echocardiographic determination of severity of, 23–25 catheterization-responsible reasons for, 25 with catheterization greater than echocardiography estimates of aortic valve area, 25 with catheterization greater than echocardiography estimates of aortic valve gradient, 25 with catheterization less than echocardiography estimates of aortic valve area, 25 with catheterization less than echocardiography estimates of aortic valve gradient, 25 echocardiographic-responsible reasons for with echocardiography greater than catherization estimates of aortic valve area, 23 with echocardiography greater than catheterization estimates of aortic valve gradients, 23 with echocardiography less than catheterization estimates of aortic valve area, 23 with echocardiography less than catheterization estimates of aortic valve gradients, 23 Gorlin equation and, 24 CO issues with, 24 “constant” in, 24 gradient issues with, 24 heart rate with, 24 systolic ejection period with, 24 most common predictors of, 25 due to nonsimultaneous measurements, 23 possible reasons for, 23 usual catheterization technique and, 24 effective orifice area in, 23 equations for, 19 goals of echocardiography in, 18

Aortic stenosis (Cont.) heart rate and, 24, 35f imaging techniques for appropriateness of, 28b utility of, 30t infective endocarditis prophylaxis for, 27b intraventricular obstruction and, 38f–39f LV hypertrophy in, 22 concentric, 19 LV parameters in, 18–19 LV stroke work loss with, 19, 21 LVOT measurement in, 18 MRI for appropriateness of, 28b steady-state free precession images in, 41f utility of, 30t myocardial oxygen demand in, 19 nuclear imaging for appropriateness of, 28b utility of, 30t pathophysiology and findings of, 19 peak systolic velocity in, 21 and gradient issues, 20 pressure overload in, 19 progression of, 19 proximal isovelocity surface area in, 18 pros and cons of, 291t and subvalvar stenosis, 22 reporting issues with, 20–23 required parameters to obtain for, 18 aortic diameter as, 18 LV parameters as, 18 other, 18 valve parameters as, 18 R-R intervals in and aortic valve gradient, 39f and V2 measurement, 34f scanning issues in, 18–19 severe, 21 doubling of wall thickness in, 33f low-gradient, 22–23, 36f possibly, 21 stroke volume in, 18, 33f causes of larger, 20 mean gradient and, 19–20 subvalvar, 19, 22, 37f systolic ejection period with, 24 TEE of, 40f, 328 appropriateness of, 28b role for, 20 utility of, 30t TTE of appropriateness of, 28b utility of, 30t V1 measurement in, 18, 33f V2 measurement in, 19, 33f in atrial fibrillation, 34f and gradient issues, 20 R-R interval and, 34f type of probe and location of sampling in, 33f valve parameters in, 18 wall motion abnormalities in, 22 wall thickness in, 33f Aortic trauma, blunt, 454 Aortic valve, 1–17 age-related changes in, 3, 15f bicuspid, 2–3, 5b aortic stenosis with, 21, 41f with ascending aortic dilatation/ aneurysm, 3, 5b, 17f

Index Aortic valve (Cont.) bicuspid (cont.) with coarctation of aorta, 11f, 17f distal aortic associations and complications of, 11f echocardiographic recognition of, 3 examples of, 9f infective complications of, 11f infective endocarditis of, 354–356 proximal aortic associations and complications of, 12f steady-state free precession MRI of, 16f structural associations or complications of, 3 systolic doming motion of, 2–5 TEE of for aortic valve replacement, 354–355 thoracic vs., 13f, 16f true vs. “functionally,” 3, 9f causes of aortic insufficiency and, 42, 54f commissures of, 2 echocardiography of, 2 infective endocarditis of, 169f, 171f, 356 bicuspid, 354–355 intracardiac echocardiography of, 371–372, 375f–376f Lambl’s excrescences on, 3, 12f malformations of, 2–3, 6b–7b normal anatomy of, 1–2, 6b–7b quadricuspid, 2, 10f raphe of, 2, 9f in systole vs. diastole, 2, 14f unicuspid, 2, 10f systolic doming motion of, 2–5 vegetations of, 354–355 Aortic valve area (AVA) in aortic stenosis catheterization greater than ­echocardiography estimates of catheterization-responsible reasons for, 25 echocardiography-responsible reasons for, 23 catheterization less than echocardiography estimates of catheterization-responsible reasons for, 25 echocardiography-responsible reasons for, 23 continuity equation–derived issues related to, 21 in low-gradient severe disease, 22 LVOT measurement and, 18 with prosthetic valves bioprosthetic, 140 mechanical, 140 Aortic valve disease, TEE of, 328 Aortic valve gradient, in aortic stenosis with catheterization estimates greater than echocardiography catheterization-responsible reasons for, 25 echocardiography-responsible reasons for, 23 with catheterization estimates less than echocardiography catheterization-responsible reasons for, 25 echocardiography-responsible reasons for, 23

Aortic valve gradient, in aortic stenosis (Cont.) heart rate and, 35f issues with, 20–21 and Gorlin equation, 24 in low-gradient severe disease, 22 as per-beat (volume) function, 20 R-R intervals and, 39f and stroke volume, 20 Aortic valve leaflets, fluttering of, with aortic insufficiency, 56f Aortic valve repair, for aortic insufficiency, ACC/AHA recommendations for, 48b Aortic valve replacement (AVR) ACC/AHA recommendations for, 27b for aortic insufficiency, ACC/AHA recommendations for, 48b bioprosthetic, 140 mechanical, area issues with, 140 TEE in, 354–356 Aortic-to-RA fistula, due to stab wound, 459f Aortocoronary bypass, stress echocardiography after, 224f Aortography, of aortic dissection, 330t Aortomitral fibrosa, normal anatomy of, 1–2 Apical aneurysm, 194f–195f, 198f contrast echocardiography of, 276f, 282f Apical ballooning syndrome, 228 imaging modalities for, 235b–236b, 243t Apical thrombus, contrast echocardiography of, 271, 277f–278f Area plane method, for RV volume, 417 Arrhythmogenic right ventricular cardiomyopathy (ARVC), 423b, 428t, 433f AS. See Aortic stenosis (AS). Ascending aorta aneurysm of, with bicuspid aortic valve, 12f dilatation of, with bicuspid aortic valve, 3, 5b TEE of, 332t–333t ASDs. See Atrial septal defect(s) (ASDs). ASE equation, for LV mass, 174 Athletic heart strain imaging of, 319 tissue Doppler imaging of, 318 Atrial fibrillation and hepatic venous flow assessment, 135f mitral stenosis in, 86f pericardial constriction vs., 392 radiofrequency ablation for, intracardiac echocardiography in, 372, 385f tricuspid regurgitation with, 128f V2 measurement in, 34f Atrial septal defect(s) (ASDs) TEE of vs. cardiac catheterization, 331t vs. TTE, 326, 330t Atrial septal defect (ASD) device closure, intracardiac echocardiography of, 372 with AGA device, 384f with Amplatzer septal occluder device, 384f aortic knob rim in, 372, 382f for appropriate position and residual leak, 372, 383f during balloon test occlusion, 372, 383f

503

Atrial septal defect (ASD) device closure, intracardiac echocardiography of (Cont.) with encroachment on AV valves, 372, 383f with HELEX septal occluder device, 384f inferior rim in, 372, 382f superior rim in, 372, 383f Atrial septum, intracardiac echocardio­ graphy of, 372, 376f Atrial systole, in diastole, 254 Atrioventricular (AV) dyssynchrony, 299 Atrioventricular (AV) pacing, 304–305 ECG-derived algorithm for, 304 echocardiography algorithms for, 304 iterative method for, 304 Ritter method for, 304 simplified Doppler screening for, 304–305 using pulsed-wave Doppler, 316f Atrioventricular (AV) valves, intracardiac echocardiography of, 372, 377f AV. See Atrioventricular (AV). AVA. See Aortic valve area (AVA). AVR. See Aortic valve replacement (AVR). B Ball-in-cage valve, 146t–147t Balloon mitral valvuloplasty contraindications to, 73 suitability of, 70 vs. surgical mitral valve replacement, 82f TEE during, 88f Baloon valvotomy, for pulmonic stenosis, 122, 124b Barlow’s disease, mitral valve repair for, 342 B-cell lymphoma, cardiac mass due to, 446f Bernoulli equations, 253 “simplified” (modified), 254 Bicaval view, on TEE, 332t–333t Bileaflet occluder valve, 146t–147t pressure recovery in, 150f transesophageal views of, 154f Bioprosthetic valves aortic, 140 CE porcine, 148t dysfunction of, 140 echocardiographic and fluoroscopic findings with, 137, 146t–147t Hancock, 148t imaging modalities for appropriateness of, 143b utility of, 148t insufficiency of, 140 mitral area issues for, 139 torn leaflet of, 152f–153f stenosis of, 140 stented, 146t–147t stentless, 146t–147t Biventricular pacing, 305 Bjork-Shiley valve, 146t–147t Blood clot, intrapericardial, 389, 396b, 401t due to stab wound, 457f Blood flow, wall motion abnormalities and, 201 Blood pressure, stress echocardiography and, 214

504 Index Blunt trauma aortic, 454 cardiac, 453 coronary sequelae of, 453 myocardial sequelae of, 453 pericardial sequelae of, 453 valvular sequelae of, 453 Breast carcinoma, metastatic, 449f Bullet, within heart, 454, 461f Bullet wounds, 453, 461f C CABG (coronary artery bypass graft), mitral valve repair with, 362–363, 365 CAD. See Coronary artery disease (CAD). Carbomedics valve, 146t–147t Carcinoid right heart disease due to, 435f tricuspid regurgitation due to, 120, 130f, 136f Cardiac amyloidosis, 228–229 echocardiographic findings of, 228–229, 249f imaging modalities for, 236b–237b, 244t Cardiac arrest, pulmonary embolism with, 431f Cardiac catheterization for amyloidosis, 244t for aortic insufficiency appropriateness of, 49b utility of, 52t for aortic stenosis appropriateness of, 28b usual technique for, 24 utility of, 30t for apical ballooning, 243t for assessment of aortic valve morphology, 8t for atrial septal defects, 331t for cardiac masses, 445t for cardiac trauma, 456t for cardiomyopathy dilated, 231b–233b, 241t hypertrophic, 242t restrictive, 244t RV arrhythmogenic, 428t for hemodynamics, 263t for infective endocarditis appropriateness of, 163b–165b utility of, 168t for intrapericardial blood clot, 401t for LV assessment, 187t for mitral insufficiency appropriateness of, 101b utility of, 107t–109t for mitral stenosis, 72 appropriateness of, 77b–78b Gorlin equation for, 72 cardiac output issues with, 72 gradient issues with, 72 variables and constants with, 72 usual technique of, 72 utility of, 80t of mitral valve, 64b for myocarditis, 245t for pericardial constriction, 398t, 402t–403t for pericardial cysts, 404t for pericardial effusions, 399t for pericardial tamponade, 400t

Cardiac catheterization (Cont.) for prosthetic valves appropriateness of, 143b discordance of gradient assessment with, 139 utility of, 148t for pulmonary embolism, 429t for pulmonary hypertension, 426t for pulmonic valve disease, 125b for right heart chamber quantification, 425t for RV infarction, 427t for stress imaging, 218b for tricuspid valve disease, 126t utility of, 126t Cardiac chamber compression signs, in pericardial tamponade, 387 Cardiac hemochromatosis, 229 Cardiac imaging modalities, for assessment of aortic valve morphology appropriateness of, 6b utility of, 8t Cardiac index, in pericardial constriction, 390 Cardiac magnetic resonance (CMR) of amyloidosis, 236b–237b, 244t of aortic dissection, 330t of aortic insufficiency appropriateness of, 49b steady-state free precession sequence for, 60f utility of, 52t velocity encoded phase contrast technique for, 59f of aortic stenosis appropriateness of, 28b steady-state free precession images in, 41f utility of, 30t of apical ballooning, 235b–236b, 243t for assessment of aortic valve morphology appropriateness of, 6b utility of, 8t of cardiac masses, 444b, 445t of cardiac trauma, 455b, 456t of cardiomyopathy dilated, 231b–233b hypertrophic, 234b–235b, 242t, 250f–252f other forms of, 239b–240b restrictive, 236b–237b, 244t of coronary artery disease, 207b–208b for hemodynamics, 263t of infective endocarditis appropriateness of, 163b–165b utility of, 168t of intrapericardial blood clot, 396b, 401t of left ventricle, 178 appropriateness of, 182b–183b CT vs., 186t–187t echocardiography vs., 185t–186t real-time 3D, 186t–187t single breath-hold vs. multiple breath-hold in, 178, 185t of mitral insufficiency appropriateness of, 101b utility of, 107t–109t of mitral stenosis appropriateness of, 77b–78b utility of, 80t of mitral valve, 64b

Cardiac magnetic resonance (Cont.) of myocarditis, 238b, 245t of pericardial constriction, 397b, 402t–403t of pericardial cysts, 398b, 404t of pericardial effusions, 394b, 399t of pericardial tamponade, 395b, 400t of prosthetic valves appropriateness of, 143b utility of, 148t of pulmonary embolism, 424b, 429t of pulmonary hypertension, 421b, 426t of pulmonic valve disease, 125b for right heart chamber quantification, 420b, 425t of RV arrhythmogenic cardiomyopathy, 423b, 428t of RV infarction, 422b, 427t for stress imaging, 218b of tricuspid valve disease assessment of, 125b utility of, 126t Cardiac masses, 453–461 due to cardiac neoplasms. See Cardiac tumors. imaging modalities for, 444b, 445t due to intracardiac thrombi, 442–443 left atrial, 443 left ventricular, 442–443 right heart, 443 intravascular, 441, 450f TEE of, 327–328 thoracic (mediastinal), 441, 446f–447f Cardiac output (CO) in aortic stenosis, 24 in dilated cardiomyopathy, 226 echocardiography as pulmonary artery catheter for, 259–260 Doppler method assumptions for, 259 notes on, 259 pulmonary flow in, 260 in mitral stenosis, 72 in pericardial constriction, 390 Cardiac resynchronization therapy (CRT), 299–316 imaging modalities for, 308b indications for, 299 for LV dyssynchrony and narrow QRS complex, 305–306 optimization of, 304–305 atrioventricular, 304–305 ECG-derived algorithm for, 304 echocardiography algorithms for, 304 iterative method for, 304 Ritter method for, 304 simplified Doppler screening for, 304–305 using pulsed-wave Doppler, 316f biventricular, 305 pacing lead placement in, 304 patient selection for, 299 quantification of interventricular dyssynchrony prior to, 299–300, 309f quantification of intraventricular dyssynchrony prior to, 300 M-mode imaging techniques for, 300–301, 310f other techniques for, 303 strain and stress rate imaging for, 302 radial strain imaging as, 302–303, 314f

Index Cardiac resynchronization therapy (Cont.) quantification of intraventricular dyssynchrony prior to (cont.) tissue Doppler imaging techniques for, 301–303 apical 2-chamber view in, 311f apical 3-chamber view in, 312f apical 4-chamber view in, 313f color Doppler tissue analysis in, 301–302 radial strain, 302–303 tissue velocity imaging in, 301–303, 311f two-dimensional imaging technique for, 300 real-time 3D echocardiography to analyze dyssynchrony prior to, 303 dyssynchrony index in, 303, 315f Cardiac rupture, due to blunt cardiac trauma, 453 Cardiac sarcoidosis, 229 Cardiac tamponade, with pericardial and left pleural effusions, 405f Cardiac trauma, 463–500 blunt, 453 coronary sequelae of, 453 myocardial sequelae of, 453 pericardial sequelae of, 453 valvular sequelae of, 453 cardiac catheterization for, 456t chest radiography of, 456t CT of, 455b, 456t imaging modalities for, 455b, 456t due to missiles within heart, 454, 461f MRI of, 455b, 456t nuclear imaging of, 455b, 456t penetrating, 453–454 gunshot injury as, 453, 461f stab wound as, 453 aortic-to-RA fistula due to, 459f hemothorax due to, 461f intrapericardial hemorrhage and clot due to, 457f left anterior descending coronary artery laceration/transection due to, 461f mitral regurgitation due to, 460f pericardial effusion due to, 457f, 459f RV compression due to, 459f severed papillary muscle due to, 460f ventriculoseptal defect due to, 458f TEE of, 454, 455b, 456t tricuspid regurgitation due to, 120 TTE of, 455b, 456t Cardiac tumors benign, 441–442, 445t fibromas as, 442 hepatoma as, 450f myxomas as, 441 in Carney complex, 441 in Carney complex variants, 442 familial and complex, 441–442 left atrial, 441, 448f left ventricular, 441 right atrial, 441, 448f right ventricular, 441 papillary fibroelastoma as, 442, 449f, 451f papillary tumors of heart valves as, 442 rhabdomyomas as, 442

Cardiac tumors (Cont.) imaging modalities for, 444b, 445t malignant, 442, 445t angiosarcoma as, 442 lymphoma as, 446f–447f metastatic, 449f–450f myeloma as, 447f rhabdomyosarcoma as, 442 Cardiomyopathy(ies), 225–251 acquired, 225 arrhythmogenic RV, 423b, 428t, 433f cardiac hemochromatosis as, 229 cardiac sarcoidosis as, 229 Chagas disease as, 229 classification of, 225 dilated (congestive), 225–226 cardiac catheterization for, 231b–233b, 241t cardiac MRI of, 241t chest radiography of, 241t CT of, 231b–233b, 241t decreased systolic function in, 226 distortion of tricuspid and mitral apparatus in, 226 echocardiographic features of, 226 goals of echocardiography in, 225 hallmark findings in, 225 imaging modalities for, 231b–233b, 241t increased chamber dimensions in, 226 increased end-point to septal separation in, 226 increased ventricular mass in, 226 mild, 226 mitral regurgitation due to, 116f, 226 MRI of, 231b–233b mural thrombi in, 226 nuclear imaging of, 231b–233b, 241t reduced cardiac output in, 226 “restrictive pattern” of ventricular inflow in, 226 RV systolic pressure in, 226 TEE of, 231b–233b, 241t TTE of, 231b–233b, 241t hypertrophic, 226–228 aortic insufficiency in, 227 apical, 246f–247f, 250f–251f atypical distribution of, 247f cardiac catheterization for, 242t chest radiography of, 242t contrast echocardiography of, 271, 279f CT of, 234b–235b, 242t decreased septal movement in, 227 dyssynchronous LV relaxation in, 227 ECG of, 252f echocardiographic features of, 226–227 flow acceleration at base of LVOT in, 227 goals of echocardiography in, 226 imaging modalities for, 234b–235b, 242t increased RV wall thickness in, 227 LV hypertrophy in, 226 mitral morphologic abnormalities in, 227 mitral regurgitation in, 227 MRI of, 234b–235b, 242t, 250f–252f nuclear imaging of, 234b–235b, 242t obstructive, 227 echocardiography in surgical and catheter options for, 227

505

Cardiomyopathy(ies) (Cont.) hypertrophic (cont.) obstructive (cont.) intracavitary, 227 muscular outflow, 227 systolic anterior motion in, 248f TEE in surgical management of, 228, 368 septal, 247f–248f spectral profile of, 227 systolic anterior motion in, 227, 248f TEE of, 228, 234b–235b, 242t TTE of, 234b–235b, 242t, 251f mitral regurgitation due to, 112f, 116f mixed (genetic and nongenetic), 225 myocarditis as, 229–230 imaging modalities for, 238b, 245t other forms of, 239b–240b primary, 225 required parameters to obtain from scanning of, 225 restrictive and infiltrative, 228–229 cardiac amyloidosis as, 228–229 echocardiographic findings of, 228–229, 249f imaging modalities for, 236b–237b, 244t echocardiographic findings in, 228 endomyocardial fibrosis (eosinophilic endomyocardial disease) as, 228, 246f examples of, 228 imaging modalities for, 236b–237b, 244t tissue Doppler imaging of, 318 RV arrhythmogenic, 423b, 428t, 433f secondary, 225 strain imaging of, 319 stress. See Apical ballooning syndrome. wall motion abnormalities due to, 201 Cardiovascular central venous pressure, elevated, in pericardial constriction, 391 Carney complex, myxomas in, 441 Carney complex variants, myxomas in, 442 Carpentier-Edwards (CE) Physio Annuloplasty Ring, 343, 349, 360 Carpentier-Edwards (CE) porcine valve, 148t Catheter(s), for intracardiac echocardiography, 371 8F vs. 10F, 371 handle of, 371, 373f tip flexion of, 371, 374f Catheter balloon valvuloplasty (CBV) echocardiographic guidance of, 466 balloon inflation during, 486f color Doppler flow mapping in, 486f cons of, 466 gradient calculation in, 488f hemodynamic tracings during, 488f postoperative views of, 487f pros of, 466 rationale and role for, 466 sequence of, 466 transesophageal four-chamber view in, 486f for mitral stenosis contraindications for, 73 suitability for, 70 vs. surgical mitral valve replacement, 82f TEE during, 88f

506 Index Caval dilation, in pericardial constriction, 407f Caval distention, echocardiographic signs of, 388 CBV. See Catheter balloon valvuloplasty (CBV). CE (Carpentier-Edwards) Physio Annuloplasty Ring, 343, 349, 360 CE (Carpentier-Edwards) porcine valve, 148t Central venous pressure, elevated cardiovascular, in pericardial constriction, 391 Chagas disease, 229 CHD (congenital heart disease) infective endocarditis due to, 157 mitral valve repair with, 366 TEE of, 326 Chest radiography of amyloidosis, 244t of aortic insufficiency, 52t of aortic stenosis, 30t for assessment of aortic valve morphology, 8t of cardiac masses, 445t of cardiac trauma, 456t of cardiomyopathy dilated, 241t hypertrophic, 242t restrictive, 244t RV arrhythmogenic, 428t for hemodynamics, 263t of infective endocarditis, 168t of intrapericardial blood clot, 401t of left ventricle, 187t of mitral insufficiency, 107t–109t of mitral stenosis, 80t of mitral valve, 64b of myocarditis, 245t of pericardial constriction, 402t–403t of pericardial cysts, 404t of pericardial effusions, 399t, 411f of pericardial tamponade, 400t of prosthetic valves, 148t of pulmonary embolism, 429t of pulmonary hypertension, 426t of pulmonic valve disease, 125b for right heart chamber quantification, 425t of RV infarction, 427t of tricuspid valve disease, 126t CHF (congestive heart failure) due to infective endocarditis, 156–157 nuclear imaging with, 181b Children mitral valve repair in, 357–358 TEE in, 326 Chordae tendineae, of mitral valve, 62–63, 67f Chordae tendineae rupture mitral regurgitation due to, 114f mitral valve repair due to, 346–347, 349, 353 Chordal severing, in mitral valve replacement, 94, 104t Chordal sparing, in mitral valve replacement, 94, 104t Circumferential axis, in heart deformation coordinate system, 317, 320f Cleft mitral valve, 93, 112f–113f CMR. See Cardiac magnetic resonance (CMR).

CO. See Cardiac output (CO). Coarctation of aorta bicuspid aortic valve with, 11f, 17f TEE of, 326 Color Doppler flow mapping of aortic insufficiency, 57f of descending aorta, 44 of LVOT, 44, 51t problems with “quantification” from, 43 of infective endocarditis, 170f of mitral regurgitation, 95, 97 vs. proximal isovelocity surface area, 285 of tricuspid regurgitation, 119, 128f of proximal isovelocity surface area, 286–287 aliasing velocity in, 286–287 hemispheres of flow acceleration in, 286 radius of, 287 vena contracta in, 287 of tricuspid stenosis, 130f Color Doppler tissue analysis, 317 for dyssynchrony, 301–302 Color M-mode imaging, of prosthetic valves, 153f–154f Commissures, of mitral valve, 62–63, 67f Commissurotomy, for mitral stenosis, 70 Computed tomography (CT) of amyloidosis, 236b–237b, 244t of aortic dissection, 330t for aortic insufficiency appropriateness of, 49b utility of, 52t of aortic stenosis appropriateness of, 28b utility of, 30t of apical ballooning, 235b–236b, 243t for assessment of aortic valve morphology appropriateness of, 6b utility of, 8t of cardiac masses, 444b, 445t of cardiac resynchronization therapy, 308b of cardiac trauma, 455b, 456t of cardiomyopathy dilated, 231b–233b, 241t hypertrophic, 234b–235b, 242t other forms of, 239b–240b restrictive, 236b–237b, 244t of coronary artery disease, 207b–208b for hemodynamics, 263t of infective endocarditis appropriateness of, 163b–165b utility of, 168t of intrapericardial blood clot, 396b, 401t of left ventricle, 175, 182b–183b, 186t–187t ECG-gated, 178 of mitral insufficiency appropriateness of, 101b utility of, 107t–109t of mitral stenosis, 77b–78b of mitral valve, 64b of myocarditis, 238b, 245t of pericardial constriction, 397b, 402t–403t of pericardial cysts, 398b, 404t of pericardial effusions, 394b, 399t of pericardial tamponade, 395b, 400t

Computed tomography (Cont.) of prosthetic valves appropriateness of, 143b utility of, 148t of pulmonary embolism, 424b, 429t of pulmonary hypertension, 421b, 426t of pulmonic valve disease, 125b for right heart chamber quantification, 420b, 425t of RV arrhythmogenic cardiomyopathy, 423b, 428t of RV infarction, 422b, 427t for stress imaging, 218b for tricuspid valve disease assessment of, 125b utility of, 126t Congenital heart disease (CHD) infective endocarditis due to, 157 mitral valve repair with, 366 TEE of, 326 Congestive heart failure (CHF) due to infective endocarditis, 156–157 nuclear imaging with, 181b Constraint, in proximal isovelocity surface area, 285–286, 296f Constrictive pericarditis. See Pericardial constriction. Continuity equations for aortic stenosis, 19 aortic valve area issues related to, 21 for pulmonary venous flow patterns, 257–258 Continuity method, for mitral valve area, 70 Continuous wave Doppler measurements of mitral insufficiency, 294f of proximal isovelocity surface area, 287, 293f Contrast agents, 271, 275t contraindications to, 274b indications for, 271 safety issues with, 271–272, 274b side effects of, 274b Contrast echocardiography, 271–283 of aortic dissection, 271, 278f of apical hypertrophic cardiomyopathy, 271, 279f appropriateness of, 271 contraindications to, 274b for exercise and dobutamine stress echocardiography, 271, 277f of focal (discrete) apical aneurysm, 276f, 282f of intracardiac thrombi, 271, 277f–278f of LV noncompaction (noncompacted myocardium), 271, 279f for LV opacification, 272–273 contrast administration in, 272 echocardiographic system settings in, 272 imaging and scanning tips for, 272–273, 280f–282f supplies for, 272 of LV volumes and LVEF, 271, 276f microbubble contrast agents for, 271, 275t of myocardial perfusion, 273 of myocardial rupture, 271 overview of, 271, 275f of pseudoaneurysm, 271 of regional wall motion, 271, 276f safety issues with, 271–272, 274b side effects of, 274b

Index Contrast ventriculography of apical aneurysm, 282f of mitral regurgitation echocardiographic assessment differing from, 91–92 Sellers grade in, 97 Convective acceleration, and pressure drop across orifice, 253 Convergent flow, in proximal isovelocity surface area, 286, 292f Cor triatriatum sinister, 71 TEE of, 326 CoreValve prosthesis, percutaneous aortic valvuloplasty with, 489f Coronary artery(ies), LV wall motion and, 202 Coronary artery bypass graft (CABG), mitral valve repair with, 362–363, 365 Coronary artery disease (CAD), 201–212 acute myocardial infarction due to. See Myocardial infarction (MI), acute. dobutamine stress echocardiography for, 214, 222t imaging modalities for assessment of, 207b–208b with mitral valve repair, 362–365 stress echocardiography for. See Stress echocardiography. wall motion abnormalities in, 201 Coronary blood flow, and myocardial wall motion, 201 Coronary care unit, echocardiographic studies in, 202 reporting issues for, 202 required parameters to obtain from, 202 scanning issues for, 202 Coronary sequelae, of blunt cardiac trauma, 453 Cosgrove ring, 345, 358 Critically ill patients, 326–327 CRT. See Cardiac resynchronization therapy (CRT). CT. See Computed tomography (CT). Cyst, pericardial, 392, 398b, 404t D D (diastolic) wave, in pulmonary venous flow patterns, 257 DB (descent of base), of left ventricle, 177 Deceleration time (DT) in aortic insufficiency, 45 with LV filling pressures, 260, 266f–267f Descending aorta with aortic insufficiency color flow mapping of, 44 retrograde flow profiles in, 44 TEE of, 332t–333t Descent of base (DB), of left ventricle, 177 Diastasis, in diastole, 254 Diastole, phases of, 254 atrial systole as, 254 diastasis as, 254 early rapid filling as, 254 isovolumic relaxation time as, 254, 256 Diastolic dysfunction, 253–270 basic equations for, 253–254 categories of, 256 and heart failure, 254–256, 264f–266f hemodynamics of, 254–256, 264f–266f

Diastolic dysfunction (Cont.) impaired relaxation due to, 256 pseudonormal, 256 restrictive fixed, 256 restrictive reversible, 256 tissue Doppler imaging of, 318 Diastolic heart failure, 254–256, 264f–266f definite, 255 diagnostic criteria for, 255 Doppler vs. catheter-derived indices of, 255 possible, 255 probable, 255 Diastolic left ventricular (LV) inflow patterns, 256–257, 268f abnormal or delayed, 256, 269f normal, 256–257, 269f pseudonormal, 256, 269f restrictive, 256, 269f Diastolic pressure dips, in pericardial constriction, 390, 407f, 409f Diastolic pressure plateau, in pericardial constriction, 391 Diastolic stiffness, 265f Dipyridamole stress echocardiography, 214–215 comparison of, 215, 223t sensitivity of, 223t Disc summation method for LV volume, 177, 184t–185t, 193f for RV volume, 416–417 Dobutamine stress echocardiography, 214–215 comparison of, 215, 223t contrast agents in, 271 to detect coronary artery disease, 214, 222t to detect myocardial hibernation, 215, 215t, 223f for perioperative risk assessment, 214, 214t postinfarction to predict reversible myocardial dysfunction, 215, 222t for prognostication, 215, 215t for risk assessment, 215, 215t safety and tolerability of, 214 Doppler echocardiography of mitral stenosis, 86f pulsed-wave, 89f of pericardial tamponade, 406f of prosthetic valve infective ­endocarditis, 158 Doppler shift equation, 253 DT (deceleration time) in aortic insufficiency, 45 with LV filling pressures, 260, 266f–267f Duke criteria, for diagnosis of infective endocarditis, 155, 161b Dyssynchrony, 299–316 atrioventricular, 299 interventricular, 299–300, 309f intraventricular, 300 M-mode imaging techniques for, 300–301, 310f other techniques for, 303 strain and stress rate imaging for, 302 radial strain imaging as, 302–303, 314f tissue Doppler imaging techniques for, 301–303 apical 2-chamber view in, 311f

507

Dyssynchrony (Cont.) intraventricular (cont.) tissue Doppler imaging techniques for (cont.) apical 3-chamber view in, 312f apical 4-chamber view in, 313f color Doppler tissue analysis in, 301–302 radial strain, 302–303 tissue velocity imaging in, 301–303, 311f two-dimensional imaging technique for, 300 left ventricular, with narrow QRS complex, 305–306 real-time 3D echocardiography of, 303 dyssynchrony index in, 303, 315f Dyssynchrony index, 303, 315f E E wave deceleration time of, 256 in diastole, 254, 256 transmitral, 388 in ventricular interdependence, 390 E:A ratio, 256 with LV filling pressures, 260, 266f–267f Early rapid filling, in diastole, 254 Ebstein’s anomaly, tricuspid regurgitation due to, 120 ECG (electrocardiography) of hypertrophic cardiomyopathy, 252f of LV hypertrophy, 175, 184t ECG (electrocardiogram)-derived algorithm, for AV optimization, 304 Echocardiographic guidance, 463–500 of catheter mitral balloon valvuloplasty, 466 balloon inflation during, 486f color Doppler flow mapping in, 486f cons of, 466 gradient calculation in, 488f hemodynamic tracings during, 488f postoperative views of, 487f pros of, 466 rationale and role for, 466 sequence of, 466 transesophageal four-chamber view in, 486f of endomyocardial biopsy, 463–465 of apical portion of interventricular septum, 475f bioptome in closed and open positions in, 473f cons of, 465 of distal septum, 478f internal jugular vein access for, 474f position of probe in, 473f position verification in, 473f pros of, 464–465 rationale and role for, 464 at right side of interventricular septum, 476f of RV freewall, 477f, 479f sequence of, 464 of Impella and LVAD insertion, 468–469 across aortic valve and into LVOT, 496f angulation of device in, 494f chest fluoroscopy and radiography images of, 493f, 496f color Doppler flow mapping in, 494f

508 Index Echocardiographic guidance (Cont.) of Impella and LVAD insertion (cont.) cons of, 469 with malpositioning, 495f, 497f, 499f for massive infarction due to left main thrombosis, 498f pros of, 469 rationale and role for, 468–469 reverberation artifact in, 497f sequence of, 469 serial imaging in, 499f systolic and diastolic scans in, 496f, 498f transesophageal, 469, 494f–495f, 497f, 499f transthoracic, 469, 497f of intra-aortic counterpulsation balloon cons of, 468 pros of, 468 rationale and role for, 468 sequence of, 468 of intra-aortic counterpulsation balloon tip localization, 468, 491f–492f of jugular venous cannulation, 463, 471f–472f cons of, 463 identification of internal jugular vein in, 463, 470f most desirable site for cannulation in, 463 pros of, 463 rationale and role for, 463 sequence of, 463 of percutaneous aortic valvuloplasty, 466–468 with CoreValve prosthesis, 489f with Edwards-Sapien prosthesis, 489f postdeployment, 490f predeployment, 490f intraprocedure role in, 467–468 measurements in, 489f for postprocedural assessment, 468 for postprocedural follow-up, 468 for preprocedural assessment, 466–467 rationale and role for, 466 sequence of, 466–468 transesophageal views in midesophageal, 489f three-dimensional, 489f of pericardiocentesis, 465–466 from apical approach, 480f–481f with chronic pericarditis, 484f cons of, 466 optimal site and orientation of needle in, 480f–481f plane of imaging in, 483f poor/ambiguous visualization of needle in, 484f pre- and postdrainage views in, 484f pros of, 465 rationale and role for, 465 sequence of, 465 shallow apical view in, 482f, 484f tenting of pericardium in, 483f–484f of surgical ventricular assist device placement and function, 469 cons of, 469 malpositioning of, 500f pros of, 469 rationale and role of, 469 sequence of, 469

Echocardiographic guidance (Cont.) of trans-septal puncture, 466, 485f cons of, 466 pros of, 466 rationale and role for, 466 sequence of, 466 Echocardiography, of prosthetic heart valves, 146t–147t EDP (end-diastolic pressure), 265f EDPVR (end-diastolic pressure volume relationship), 255, 264f Edwards-Sapien prosthesis, percutaneous aortic valvuloplasty with, 489f postdeployment, 490f predeployment, 490f E/E’ method, for LV filling pressure, 260 Effective orifice area (EOA), in aortic stenosis, 23 Effective regurgitant orifice (ERO) for aortic insufficiency, 44–45 for mitral regurgitation, 95–96 in proximal isovelocity surface area, 287, 297f for tricuspid regurgitation, 120 Ejection fraction response, stress echocardiography for, 213 Electrocardiography (ECG) of hypertrophic cardiomyopathy, 252f of LV hypertrophy, 175, 184t Embolism cardiac sources of, 327–328 pulmonary. See Pulmonary embolism (PE). Embolus-in-transit, 430f–431f, 437f End-diastolic pressure (EDP), 265f End-diastolic pressure volume relationship (EDPVR), 255, 264f End-diastolic velocity, with aortic insufficiency, 56f–57f R-R intervals and, 58f Endocarditis aortic insufficiency due to, 57f infective. See Infective endocarditis (IE). mitral regurgitation due to, 93, 112f tricuspid regurgitation due to, 120 Endomyocardial biopsy, echocardiographic guidance of, 463–465 of apical portion of interventricular septum, 475f bioptome in closed and open positions in, 473f cons of, 465 of distal septum, 478f internal jugular vein access for, 474f position of probe in, 473f position verification in, 473f pros of, 464–465 rationale and role for, 464 at right side of interventricular septum, 476f of RV freewall, 477f, 479f sequence of, 464 Endomyocardial fibrosis, 228, 246f End-systolic diameter, with mitral regurgitation, 111f EOA (effective orifice area), in aortic stenosis, 23 Eosinophilic endomyocardial disease, 228, 246f Epicardial fat, 387 ERO. See Effective regurgitant orifice (ERO).

Exercise stress echocardiography, 214 comparison of, 215, 223t contrast agents in, 271, 277f in female patient, 214, 214t sensitivity and specificity of, 221t–222t F False aneurysm from acute myocardial infarction, 203, 210f–211f contrast echocardiography of, 271 Familial hypercholesterolemia, mitral valve repair with, 369 Fibroelastoma, papillary, 442, 449f, 451f Fibromas, 442 Fistulae aortic-to-RA, due to stab wound, 459f due to infective endocarditis, 157 TEE of, 327 Flail leaflets, mitral regurgitation due to, 93, 115f TEE of, 114f TTE of, 114f Flow, across restrictive orifice, 111f Flow acceleration hemisphere of, 285–286 in color Doppler measurement, 286 radius of, 287 schematic rendering of, 292f and pressure drop across orifice, 253 Flow convergence, in proximal isovelocity surface area, 286, 292f Flow convergence methods, 285–297 rationale for, 285 Flow propagation velocity (FPV), for LV filling pressures, 260 Flow-function relationship, 201 Fluoroscopy, of prosthetic heart valves, 146t–147t Foramen ovale, patent pulmonary embolism with, 430f, 437f pulmonary hypertension with, 434f TEE of, 328, 335f FPV (flow propagation velocity), for LV filling pressures, 260 Free wall rupture, from acute myocardial infarction, 203, 210f Full-volume acquisition (FVA), for intraventricular dyssynchrony, 303 G Gain dependency, of mitral insufficiency, 112f Gastrointestinal tract, metastatic adenocarcinoma from, 449f Gerbode defect, 1–2, 157 Gore-tex sutures, in mitral valve repair, 347–349, 358 Gorlin equation for aortic stenosis, 24 CO issues with, 24 “constant” in, 24 gradient issues with, 24 heart rate with, 24 systolic ejection period with, 24 for mitral stenosis, 72, 75b cardiac output issues with, 72 gradient issues with, 72 variables and constants with, 72

Index Gorlin equation (Cont.) for prosthetic valves flow and pressure dependence of, 139 general issues of correlation with, 139 Grayscale imaging, for proximal isovelocity surface area, 286 Gunshot injury, 453, 461f H Hancock valve, 148t Heart block, complete, left ventricle in, 199f Heart deformation coordinate system, 317, 320f Heart failure congestive due to infective endocarditis, 156–157 nuclear imaging with, 181b diastolic, 254–256, 264f–266f definite, 255 diagnostic criteria for, 255 Doppler vs. catheter-derived indices of, 255 possible, 255 probable, 255 strain imaging of, 319 Heart failure with normal systolic function (HFNSF), 254–256, 264f–266f definite, 255 possible, 255 probable, 255 Heart rate, and aortic stenosis, 24, 35f Heart valves, papillary tumors of, 442 Hematoma, intramural, 325 Hemi-disk occluders, 138 Hemochromatosis, cardiac, 229 Hemodynamics, 253–270 basic equations for, 253–254 Bernoulli, 253 “simplified” (modified), 254 Doppler shift, 253 of diastolic function and dysfunction, 254–256, 264f–266f of diastolic heart failure, 254–256, 264f–266f definite, 255 possible, 255 probable, 255 echocardiography as pulmonary artery catheter for, 258–260 cardiac output in, 259–260 Doppler method assumptions for, 259 notes on, 259 pulmonary flow in, 260 RA pressure in, 258–259, 262t RV systolic pressure in, 258–259 imaging modalities for, 263t of LV filling pressures, 260 deceleration time and E:A ratio in, 260, 266f–267f E/E’ method for, 260 Nagueh equation for, 260, 268f other findings with, 260 other formulas for, 260 of LV inflow patterns, 256–257, 268f abnormal or delayed, 256, 269f normal, 256–257, 269f pseudonormal, 256, 269f restrictive, 256, 269f

Hemodynamics (Cont.) of phases of diastole, 254 atrial systole as, 254 diastasis as, 254 early rapid filling as, 254 isovolumic relaxation time as, 254, 256 of pulmonary venous flow patterns, 257–258 continuity equations for, 257–258 D (diastolic) wave in, 257 S wave in, 257, 265f A (atrial) systole reversal wave in, 257, 265f tissue Doppler imaging of, 257, 270f summary of, 262b Hemolysis, after mitral valve repair, 358 Hemorrhage, intrapericardial, 410f–411f due to stab wound, 457f Hemothorax, due to stab wound, 461f Hepatic venous flow assessment, atrial fibrillation and, 135f Hepatic venous flow direction, 135f Hepatic venous flow pattern in pericardial constriction, 390–391, 408f–410f with pulmonary hypertension, 434f Hepatic venous systolic flow, retrograde, in tricuspid regurgitation, 119, 129f, 131f, 133f Hepatoma, 450f HFNSF. See Heart failure with normal systolic function (HFNSF). Hypercholesterolemia, familial, mitral valve repair with, 369 Hypertension pulmonary imaging modalities for, 421b, 426t primary, 418, 432f with RV hypertension, 415–416 terminal hepatic venous flow pattern in, 434f with patent foramen ovale, 434f RV apical thrombus in, 433f right ventricular, 415–416 due to pulmonary hypertension, 416 due to pulmonary stenosis, 416 systolic, 416 I ICE. See Intracardiac echocardiography (ICE). ICU (intensive care unit), TEE in, 326–327 IE. See Infective endocarditis (IE). IMH (intramural hematoma), 325 Impella device insertion, echocardiographic guidance of, 468–469 across aortic valve and into LVOT, 496f angulation of device in, 494f chest fluoroscopy and radiography images of, 493f, 496f color Doppler flow mapping in, 494f cons of, 469 with malpositioning, 495f, 497f, 499f for massive infarction due to left main thrombosis, 498f pros of, 469 rationale and role for, 468–469 reverberation artifact in, 497f sequence of, 469 serial imaging in, 499f systolic and diastolic scans in, 496f, 498f

509

Impella device insertion, echocardiographic guidance of (Cont.) transesophageal, 469, 494f–495f, 497f, 499f transthoracic, 469, 497f Infant, mitral valve repair in, 367 Infective endocarditis (IE), 155–172 of aortic valve, 169f, 171f TEE of, 354–356 cardiac catheterization for appropriateness of, 163b–165b utility of, 168t chest radiography of, 168t color Doppler mapping of, 170f combined aortic and mitral, 170f complications of, 156–157 cardiac, 156 abscesses as, 157–158, 171f aneurysm as, 169f–170f congestive heart failure as, 156–157 dehiscence as, 157 on echocardiography, 157 fistulae as, 157 leaflet rupture as, 169f–170f myocardial infarction as, 156–157 myocarditis as, 157 papillary muscle rupture as, 156 pericardial effusions as, 157 pericardial extension as, 156 valvular insufficiency as, 157 vegetations as, 169f, 171f. See also Vegetations. noncardiac, 156–157 metastatic infection as, 156 neurologic, 156 renal, 156–157 terminology for, 156 due to congenital heart disease, 157 CT of appropriateness of, 163b–165b utility of, 168t diagnosis of clinical, 156 modified Duke criteria for, 155, 161b echocardiographic criteria for, 156 echocardiographic hallmarks of, 156 goals of echocardiography in, 155 imaging modalities for appropriateness of, 163b–165b utility of, 168t of mitral valve, 169f, 171f MRI of appropriateness of, 163b–165b utility of, 168t native valve, 157 surgery for, 162b notes on, 156 nuclear imaging of appropriateness of, 163b–165b utility of, 168t prophylaxis for, 166t–167t with aortic stenosis, 27b with mitral stenosis, 76b with prosthetic valves, 142b prosthetic valve, 157–158 dehiscence with, 157 “early,” 156, 158 echocardiographic findings with, 157–158 Doppler, 158 M-mode, 157 notes on, 158

510 Index Infective endocarditis (Cont.) prosthetic valve (cont.) echocardiographic findings with (cont.) two-dimensional and real time, 157 “late,” 154, 158 surgery for, 162b recurrence of, 156 relapse of, 156 reporting issues with, 155–156 required parameters to obtain from scanning for, 155 due to rheumatic disease, 157 right-heart, 158 scanning issues with, 155 TEE of, 157–158 with abscess, 171f, 327 aortic and mitral, 170f appropriateness of, 163b–165b caveats for, 327 with fistula, 327 mitral, 171f, 353, 356 role of, 159 shortcomings of, 155 tricuspid, 172f utility of, 168t tricuspid, 170f, 172f TTE of appropriateness of, 163b–165b role of, 159 sensitivity and specificity of, 167t shortcomings of, 155 Inferior vena cava (IVC) dimensions and collapse of, 416 renal cell carcinoma extension into, 450f Intensive care unit (ICU), TEE in, 326–327 Interatrial septal puncture, echocardiographic guidance of, 466, 485f cons of, 466 pros of, 466 rationale and role for, 466 sequence of, 466 Interatrial septum in right heart disease, 415 TEE of, 332t–333t with aneurysm, 328 Internal jugular vein identification of, 463, 470f venous valve within, 472f Interventricular dyssynchrony, 299–300, 309f Interventricular septum, shape and motion patterns of, in right heart disease, 415–416, 432f Intra-aortic counterpulsation balloon tip localization, echocardiographic guidance of, 468, 491f–492f cons of, 468 pros of, 468 rationale and role for, 468 sequence of, 468 Intracardiac echocardiography (ICE), 371–385 of atrial septal defect device closure, 372 with AGA device, 384f with Amplatzer septal occluder device, 384f aortic knob rim in, 372, 382f for appropriate position and residual leak, 372, 383f during balloon test occlusion, 372, 383f with encroachment on AV valves, 372, 383f

Intracardiac echocardiography (Cont.) of atrial septal defect device closure (cont.) with HELEX septal occluder device, 384f inferior rim in, 372, 382f superior rim in, 372, 383f catheters for, 371 8F vs. 10F, 371 handle of, 371, 373f tip flexion of, 371, 374f of LVOT obstruction with prosthetic valves, 372, 377f of patent foramen ovale device closure, 372 with abnormalities of device position, 372, 381f with aneurysm of septum primum, 372, 378f with associated fenestrated defects, 372, 380f with Chiari malformation, 372, 378f contrast saline, 372, 379f during device delivery, 372, 379f with septum primum and septum secundum with left-to-right shunts, 372, 378f with thrombus formation, 372, 382f with trace residual leaks, 372, 380f in radiofrequency ablation for atrial fibrillation, 372, 385f standard image sweep in, 373t technique for, 371–372 clockwise rotation in, 371–372 home position in, 371–372, 375f image orientation in adjustment in unusual circumstances of, 371–372, 374f conventional, 371–372, 374f viewing of cardiac structures in, 371–372 aortic valve as, 371–372, 375f–376f atrial septum as, 372, 376f AV valves as, 372, 377f LA appendage as, 371–372, 375f left atrium as, 371–372, 375f–376f left pulmonary veins as, 375f mitral valve as, 371–372, 375f pulmonary valve as, 371–372, 375f right pulmonary artery as, 371–372, 376f right pulmonary veins as, 375f–376f tricuspid valve as, 371–372, 375f for trans-septal puncture, 372, 385f Intracardiac masses. See Cardiac masses. Intracardiac thrombi, 442–443, 452f contrast echocardiography of, 271, 277f–278f left atrial, 443, 452f TEE of, 327, 331t, 334f left ventricular, 442–443, 452f right heart, 443 Intracavitary thrombus, from acute myocardial infarction, 205 Intramural hematoma (IMH), 325 Intrapericardial blood clot, 389, 396b, 401t due to stab wound, 457f Intrapericardial fat, 387, 414f Intrapericardial hemorrhage, 410f–411f due to stab wound, 457f

Intravascular masses, 441, 450f Intraventricular dyssynchrony, 299–300, 309f M-mode imaging techniques for, 300–301, 310f other techniques for, 303 strain and stress rate imaging for, 302 radial strain imaging as, 302–303, 314f tissue Doppler imaging techniques for, 301–303 apical 2-chamber view in, 311f apical 3-chamber view in, 312f apical 4-chamber view in, 313f color Doppler tissue analysis in, 301–302 radial strain, 302–303 tissue velocity imaging in, 301–303, 311f two-dimensional imaging technique for, 300 Intraventricular obstruction, with aortic stenosis, 38f–39f Isovolumic relaxation time (IVRT), in diastole, 254, 256 Iterative method, for AV optimization, 304 IVC (inferior vena cava) dimensions and collapse of, 416 renal cell carcinoma extension into, 450f J Jugular venous cannulation, echocardiographic guidance of, 463, 471f–472f cons of, 463 identification of internal jugular vein in, 463, 470f most desirable site for cannulation in, 463 pros of, 463 rationale and role for, 463 sequence of, 463 K Kussmaul phenomena, in pericardial constriction, 390–391 L LA. See Left atrial (LA). LAMB syndrome, myxomas in, 442 Lambl’s excrescences, on aortic valve, 3, 12f Left anterior descending coronary artery, laceration/transection of, due to stab wound, 461f Left atrial appendage (LAA) intracardiac echocardiography of, 371–372, 375f TEE of, 332t–333t thrombus of, 331t, 452f Left atrial (LA) dimension, in mitral regurgitation, 96 Left atrial (LA) myxomas, 441, 448f Left atrial pressure (LAP) mean, 260 in mitral regurgitation, 96

Index Left atrial (LA) systole, and LV inflow, 254 Left atrial (LA) thrombus, 443, 452f TEE of, 327, 331t, 334f Left atrium (LA), intracardiac echo­ cardiography of, 371–372, 375f–376f Left pulmonary veins, intracardiac echocardiography of, 375f Left ventricle (LV), 173–200 assessment and quantification of, 173 cardiac catheterization for, 187t chest radiography for, 187t CT for, 175, 182b–183b, 186t–187t ECG-gated, 178 echocardiographic apical four-chamber view in, 176, 193f–194f apical two-chamber view in, 176, 193f biplane, 176 long-axis views in, 176, 190f LV volumes in, 176 real-time volumetric threedimensional, 177–178, 186t–187t reference limits and partition values in, 186t–187t required parameters to obtain from, 173 short-axis views in, 191f summary of, 180b imaging modalities for appropriateness of, 182b–183b pros and cons of, 187t LV mass in, 174 LV segmentation in, 175 LV wall thickness in, 173–174 autopsy vs. echocardiographic determination of, 184t echocardiographic error in measurement of, 184t LVEF and LV volume in, 175–176 MRI for, 178 appropriateness of, 182b–183b CT vs., 186t–187t echocardiography vs., 185t–186t real-time 3D echocardiography vs., 186t–187t single breath-hold vs. multiple breath-hold in, 178, 185t nuclear imaging for, 182b–183b TEE for, 182b–183b, 187t, 328, 332t–333t TTE for, 182b–183b in complete heart block, 199f descent of base of, 177 endocardial tip vs. blood pool techniques for, 192f with focal (discrete) apical aneurysm, 276f, 282f M-mode tracing of, 198f planar sampling of, 176, 198f pulsed-wave mapping of aortic insufficiency in, 45 17-segment bullet representation of, 190f–191f Left ventricular (LV) aneurysm from acute myocardial infarction, 204–205 false, 203 apical, 194f–195f, 198f contrast echocardiography of, 276f

Left ventricular assist device insertion, percutaneous, 468–469 across aortic valve and into LVOT, 496f angulation of device in, 494f chest fluoroscopy and radiography images of, 493f, 496f color Doppler flow mapping in, 494f cons of, 469 with malpositioning, 495f, 497f, 499f for massive infarction due to left main thrombosis, 498f pros of, 469 rationale and role for, 468–469 reverberation artifact in, 497f sequence of, 469 serial imaging in, 499f systolic and diastolic scans in, 496f, 498f transesophageal, 469, 494f–495f, 497f, 499f transthoracic, 469, 497f Left ventricular (LV) dimension, in mitral regurgitation, 96 Left ventricular (LV) dysfunction, mitral regurgitation due to, 92 Left ventricular (LV) dyssynchrony with narrow QRS complex, 305–306 with wide QRS complex, 299 Left ventricular ejection fraction (LVEF) assessment of, 175–176 algorithms for, 176–178 angiographic, 176, 184t descent of base of left ventricle in, 177 echocardiographic, 176, 188f interobserver variability in, 188f–189f real-time volumetric threedimensional, 177–178 suggested algorithm for, 176 Quinones methods for, 177 radionuclide angiography for, 176, 188f interobserver variability in, 188f–189f Simpson’s volumetric method (disc summation method) for, 177, 184t–185t visual estimates for, 177, 188f contrast echocardiography for, 271, 276f Left ventricular end-diastolic pressure (LVEDP), 260 with aortic insufficiency, 45 and A wave duration, 257, 265f Left ventricular (LV) end-diastolic volume, pulmonary capillary wedge pressure vs., 264f Left ventricular (LV) false aneurysm, from acute myocardial infarction, 203 Left ventricular (LV) filling pressures, 260 deceleration time and E:A ratio in, 260, 266f–267f E/E’ method for, 260 Nagueh equation for, 260, 268f other findings with, 260 other formulas for, 260 Left ventricular (LV) function, tissue Doppler imaging of, 318 Left ventricular (LV) geometry echocardiography reference limits and partition values of, 186t–187t mitral regurgitation due to, 92

511

Left ventricular (LV) hypertrophy, 174 in aortic stenosis, 22 apical four-chamber images of, 197f concentric, 19 assessment of, 174 LV mass calculation and equations for, 174–175 clinical risk of, 175 echocardiography vs. ECG for detection of, 175, 184t grading of, 174 in hypertrophic cardiomyopathy, 226 wall thickness and, 174 Left ventricular (LV) inflow LA systole and, 254 patterns of, 256–257, 268f abnormal or delayed, 256, 269f age-related differences in, 262t normal, 256–257, 269f pseudonormal, 256, 269f restrictive, 256, 269f Left ventricular (LV) mass assessment of, 174 calculation and equations for, 174 in dilated cardiomyopathy, 226 echocardiography of M-mode vs. two-dimensional, 174–175 reliability of differences in, 175 reproducibility of changes in, 175 reference limits and partition values for, 186t–187t index of, 174 grading of, 174 and LV hypertrophy, 174–175 normalization of, 174 Left ventricular (LV) myxomas, 441 Left ventricular (LV) noncompaction, contrast echocardiography of, 271, 279f Left ventricular (LV) opacification, contrast echocardiography for, 272–273 contrast administration in, 272 echocardiographic system settings in, 272 imaging and scanning tips for, 272–273, 280f–282f supplies for, 272 Left ventricular outflow tract (LVOT) in aortic insufficiency, 57f color flow Doppler mapping of, 44, 51t grading indexed to, 51t in aortic stenosis, 18 TEE of, 328, 332t–333t velocity time integral of, 304 Left ventricular outflow tract (LVOT) method, for cardiac output, 259 Left ventricular outflow tract (LVOT) obstruction dynamic, from acute myocardial infarction, 205, 212f with prosthetic valves, intracardiac echocardiography of, 372, 377f Left ventricular (LV) parameters in aortic insufficiency, 42 in aortic stenosis, 18–19 Left ventricular pre-ejection interval (LVPEI), 299–300 Left ventricular (LV) pressure-volume relationships, in mitral regurgitation, 96

512 Index Left ventricular (LV) pump failure, from acute myocardial infarction, 202–203 Left ventricular (LV) relaxation, dyssynchronous, in hypertrophic cardiomyopathy, 227 Left ventricular (LV) segmentation, 175–178 wall motion score and, 175 Left ventricular stroke work loss (LVSWL), with aortic stenosis, 19, 21 Left ventricular systolic dysfunction (LVSD), from acute myocardial infarction, 202–203, 208t Left ventricular (LV) thrombi, 442–443, 452f Left ventricular (LV) volume assessment of, 175–176 algorithms for, 176–178 angiographic, 176, 184t anterior oblique cine-angiography for, 184t catheter ventriculography for, 175–176 CT for, 175 descent of base of left ventricle in, 177 echocardiographic, 176 endocardial surface in, 175 foreshortening in, 176, 193f–195f planimetry in, 176, 198f real-time volumetric threedimensional, 177–178, 195f suggested algorithm for, 176 in systole vs. diastole, 175, 193f–194f, 196f trabeculation in, 175, 192f MRI for, 175–176 MUGA for, 175–176 Quinones methods for, 177 radionuclide angiography for, 176, 188f Simpson’s volumetric method (disc summation method) for, 177, 184t–185t, 193f visual estimates for, 177, 188f contrast echocardiography for, 271, 276f method of, for cardiac output, 259 Left ventricular (LV) wall motion, and coronary arteries, 202 Left ventricular (LV) wall thickness, 173–174, 184t autopsy vs. echocardiographic determination of, 184t echocardiographic error in measurement of, 184t Left ventriculography, quantitative, 197f Liver metastases, 446f Longitudinal axis, in heart deformation coordinate system, 317, 320f LV. See Left ventricle (LV). LVEDP (left ventricular end-diastolic pressure), 260 with aortic insufficiency, 45 and A wave duration, 257, 265f LVEF. See Left ventricular ejection fraction (LVEF). LVOT. See Left ventricular outflow tract (LVOT). LVPEI (left ventricular pre-ejection interval), 299–300 LVSWL (left ventricular stroke work loss), with aortic stenosis, 19, 21 Lymphoma, 446f–447f

M MAC (mitral annular calcification) mitral regurgitation due to, 93 mitral stenosis due to, 87f Magnetic resonance imaging (MRI), cardiac. See Cardiac magnetic resonance (CMR). Marantic vegetations, 158–159 McConnell sign, 418 Mean gradient, for aortic stenosis, 19–20 Mechanical prosthetic valves aortic, area issues with, 140 ball-in-cage, 146t–147t bileaflet occluder, 146t–147t pressure recovery in, 150f transesophageal views of, 154f Bjork-Shiley, 146t–147t Carbomedics, 146t–147t dysfunction of, 140 echocardiographic and fluoroscopic findings with, 137, 146t–147t insufficiency of, 140 Medtronic Hall, 146t–147t mitral area issues for, 139 transesophageal views of, 154f single tilting disk, 146t–147t St. Jude Medical, 146t–147t Starr-Edwards, 146t–147t stenosis of, 140 Medial commissure, of mitral valve, 63 Mediastinal masses, 441, 446f–447f Medtronic Hall valve, 146t–147t Mercedes-Benz sign, 2 Metastatic adenocarcinoma from gastrointestinal tract, 449f pericardial effusions with, 414f Metastatic infection, due to infective endocarditis, 156 Metastatic tumors, 449f–450f MI. See Myocardial infarction (MI). Microbubble contrast agents, 271, 275t contraindications to, 274b indications for, 271 safety issues with, 271–272, 274b side effects of, 274b Missiles, within heart, 454, 461f Mitral annular calcification (MAC) mitral regurgitation due to, 93 mitral stenosis due to, 87f Mitral annular dehiscence, with prosthetic valve, 152f–154f Mitral annular dilation, mitral regurgitation due to, 93 Mitral annulus, 63–64 Mitral inflow velocities, augmented respiratory variation of, in pericardial tamponade, 388 Mitral insufficiency, 90–117 cardiac catheterization for appropriateness of, 101b utility of, 107t–109t chest radiography of, 107t–109t CT of appropriateness of, 101b utility of, 107t–109t gain dependency of, 112f goals of echocardiography in, 90 imaging modalities for appropriateness of, 101b utility of, 107t–109t

Mitral insufficiency (Cont.) mitral leaflet angle quantification for, 92, 109f mitral repair and mitral replacement for end-systolic diameter as predictor of outcome of, 111f indications for, 100b notes on, 94 surgical repairability and, 92, 109f timing of, 97 MRI of appropriateness of, 101b utility of, 107t–109t nuclear imaging of appropriateness of, 101b utility of, 107t–109t reporting issues for, 91 required parameters to obtain from scanning for, 90 scanning issues for, 90–91 scanning notes on, 90 TEE of appropriateness of, 101b with mitral valve prolapse, 115f with papillary muscle rupture, 116f with repaired cleft leaflet, 113f role of, 91 with ruptured chords and flail posterior leaflet, 114f utility of, 107t–109t TTE of appropriateness of, 101b with ruptured chords and flail posterior leaflet, 114f utility of, 107t–109t zoom views for, 90 Mitral regurgitation (MR) causes of, 92–94 due to altered LV geometry (regional or global cavitary dilation), 92 due to cardiomyopathy, 112f, 116f dilated, 116f, 226 hypertrophic, 227 due to chordal rupture, 114f congenital (due to cleft), 93, 112f–113f due to endocarditis, 93, 112f, 170f due to fibrosis of medial half of anterior leaflet, 93 due to flail leaflets, 93, 115f TEE of, 114f TTE of, 114f due to ischemia alone, 93 due to LV dysfunction, 92 due to mitral annular calcification, 93 due to mitral annular dilation, 93 due to mitral valve prolapse, 93, 112f classical, 93 echocardiography for risk stratification in, 106t nonclassical, 93 TEE of, 115f due to myxomatous disease, 93, 113f due to papillary muscle rupture, 92–93, 115f–116f rheumatic, 93, 111f, 113f due to severe wall motion abnormality (infarction or stunning), 92 due to stab wound, 460f color Doppler flow mapping of, 95, 97 vs. proximal isovelocity surface area, 285 complex, 116f

Index Mitral regurgitation (Cont.) congenital, 93, 112f–113f contrast ventriculography of echocardiographic assessment vs., 91–92 Sellers grade in, 97 effective regurgitant orifice for, 95–96 “functional,” 92 due to acute myocardial infarction, 92, 205 grading of, 91 different on serial echocardiography studies, 91 PISA method for, 290t quantitative variables corresponding to angiographic, 104t, 110f diagnostic value of, 105t selected ranges for, 104t Sellers, 97 V-waves on pulmonary capillary wedge pressure tracing and, 92 hemodynamics of, 104t LV or LA dimension in, 96 “minor” signs of, 97 mitral leaf angle quantification for, 92, 109f mitral repair and mitral replacement for chordal sparing vs. chordal severing in, 94, 104t end-systolic diameter as predictor of outcome of, 111f indications for, 100b notes on, 94 surgical repairability and, 92, 109f timing of, 97 myocardial mass in, 110f pathophysiology of, 94 progression of, 94 with prosthetic valve, 152f–154f proximal isovelocity surface area for, 90, 95–96, 111f vs. color flow Doppler mapping, 285 continuous wave Doppler spectral display of, 294f in early, mid-, and late systole, 294f optimized, 293f, 296f pros and cons of, 291t rheumatic, 295f with underlying 2D grayscale views beside color Doppler flowmapping views, 296f well-formed, 293f proximal jet width in, 97, 111f–112f pulmonary artery pressure in, 96–97 pulmonary venous spectral Doppler for, 95 pulmonary venous systolic flow reversal in, 117f regurgitant fraction in, 96 and angiographic grade, 110f equation for, 90–91 two-dimensional Doppler method to determine, 96 regurgitant orifice area for, 96 regurgitant volume in, 90, 95–96 and angiographic grade, 110f equation for, 90–91 reporting issues with, 91 required parameters to obtain from scanning of, 90 scanning issues with, 90–91

Mitral regurgitation (Cont.) severity of echocardiography-catheterization discordance of assessment of, 91–92 methods to determine, 90, 103t equations for, 90–91 PISA as, 90, 95–96, 111f, 290t volumetric method as, 90 single best technique to describe, 94–97 TEE of, 328, 340 appropriateness of, 101b due to flail leaflet, 344, 346–347 with mitral valve prolapse, 115f due to myxomatous disease, 346, 349 with papillary muscle rupture, 116f with repaired cleft leaflet, 113f due to rheumatic disease, 357–358, 360 role of, 91 with ruptured chords and flail posterior leaflet, 114f utility of, 107t–109t TTE of appropriateness of, 101b with ruptured chords and flail posterior leaflet, 114f utility of, 107t–109t vena contracta width in, 97, 111f Mitral stenosis (MS), 68–89 in atrial fibrillation, 86f cardiac catheterization for, 72 appropriateness of, 77b–78b Gorlin equation for, 72 cardiac output issues with, 72 gradient issues with, 72 variables and constants with, 72 usual technique of, 72 utility of, 80t catheterization-echocardiographic discordance in, 72–73 for mitral valve area with echocardiography estimates greater than catheterization, 73 with echocardiography estimates less than catheterization, 73 for mitral valve gradient with echocardiography estimates greater than catheterization, 73 with echocardiography estimates less than catheterization, 73 reasons for, 73 for transmitral gradient, 73 chest radiography of, 80t commissurotomy for, 70 CT of, 77b–78b descriptors of severity of, 70 Doppler assessment of, 86f pulsed-wave, 89f etiologies of, 71 acquired, 71 congenital, 71 goals of echocardiography in, 68 imaging modalities for appropriateness of, 77b–78b utility of, 80t infective endocarditis prophylaxis for, 76b leaflet features of, 83f mass score for, 79t due to mitral annular calcification, 87f

513

Mitral stenosis (Cont.) mitral valve area measurement in, 70 catheterization-echocardiographic discordance in with echocardiography estimates greater than catheterization, 73 with echocardiography estimates less than catheterization, 73 continuity method for, 70 equation for, 72 methods for determining, 68 planimetry for, 69, 84f reporting issues with, 70 pressure half time for, 69 reporting issues with, 69–70 proximal isovelocity surface area for, 69 angle correction with, 82f reporting issues with, 70 real-time three-dimensional echocardiography for, 70 reporting issues related to, 69–70 mitral valve catheter balloon valvuloplasty for contraindications for, 73 suitability for, 70 vs. surgical mitral valve replacement, 82f TEE during, 88f mitral valve gradient measurement in catheterization-echocardiographic discordance in with echocardiography estimates greater than catheterization, 73 with echocardiography estimates less than catheterization, 73 and Gorlin equation, 72 mean, 69 reporting issues related to, 69 scanning notes on, 68 MRI of appropriateness of, 77b–78b utility of, 80t nuclear imaging of, 77b–78b pathophysiology of, 71 percutaneous mitral balloon valvotomy for echocardiographic prediction of outcome of, 79t indications for, 73, 75b proximal isovelocity surface area for, 287–288 pros and cons of, 291t rheumatic, 295f reporting issues with, 69–70 required parameters to obtain from scanning in, 68 rheumatic, 63, 83f–84f RV systolic pressure in, provocative testing to enhance, 71 scanning notes for, 68–69 in sinus rhythm, 86f due to submitral calcification, 89f with subvalvar disease, 83f, 85f, 87f surgical mitral valve replacement for catheter balloon valvuloplasty vs., 82f indications for, 73, 76b issues with, 70–71 TEE of, 328 appropriateness of, 77b–78b during mitral catheter balloon valvuloplasty, 88f

514 Index Mitral stenosis (Cont.) TEE of (cont.) role of, 71–72 utility of, 80t transmitral gradient in with catheterization estimates higher than echocardiography, 73 provocative testing to enhance, 71 TTE of appropriateness of, 77b–78b left atrium in, 85f role of, 71–72 utility of, 80t Mitral valve, 62–67 anatomy of, 62, 67f, 337f in TEE, 338f annulus of, 63–64 chordae tendineae of, 62–63, 67f cleft, 93, 112f–113f commissures of, 62–63, 67f diseases and dysfunction of, 62 in hypertrophic cardiomyopathy, 227 imaging techniques for, 64b infective endocarditis of, 169f, 171f intracardiac echocardiography of, 371–372, 375f myxomatous disease of mitral regurgitation due to, 93, 113f mitral stenosis due to, 63 mitral valve repair for, 63 papillary muscles of, 62–63, 67f physiology of, 62 schematic diagram based on Carpentier’s classification of, 338f surgical view of, 339f TEE of, 64b, 328, 332t–333t transgastric short-axis view of, 339f–341f ventricular myocardium and, 62 Mitral valve area (MVA) measurement, 70 catheterization-echocardiographic discordance in with echocardiography estimates greater than catheterization, 73 with echocardiography estimates less than catheterization, 73 continuity method for, 70 equation for, 72 methods for, 68 planimetry for, 69, 84f reporting issues with, 70 pressure half time for, 69 reporting issues with, 69–70 with prosthetic valves bioprosthetic, 139 mechanical, 139 proximal isovelocity surface area for, 69 angle correction with, 82f reporting issues with, 70 real-time three-dimensional echocardiography for, 70 reporting issues related to, 69–70 Mitral valve catheter balloon valvuloplasty contraindications for, 73 suitability for, 70 vs. surgical mitral valve replacement, 82f TEE during, 88f Mitral valve gradient measurement catheterization-echocardiographic discordance in with echocardiography estimates greater than catheterization, 73

Mitral valve gradient measurement (Cont.) catheterization-echocardiographic discordance in (cont.) with echocardiography estimates less than catheterization, 73 and Gorlin equation, 72 mean, 69 reporting issues related to, 69 scanning notes on, 68 Mitral valve leaflet(s) anatomy of, 62–63, 67f anterior fibrosis of, mitral regurgitation due to, 93 flail, 346–348, 358 fluttering of, with aortic insufficiency, 45 flail mitral regurgitation due to, 93, 115f TEE of, 114f TTE of, 114f TEE of anterior, 346–348, 358 posterior, 343–345, 352 in mitral stenosis, 83f nomenclature of, 93 posterior, flail, 343–345, 352 rupture of, due to infective endocarditis, 169f–170f Mitral valve leaflet angle quantification, for mitral insufficiency, 92, 109f Mitral valve preclosure with aortic insufficiency, 45, 56f–57f without aortic insufficiency, 61f Mitral valve prolapse (MVP), 93, 112f classical, 93 echocardiography for risk stratification in, 106t mitral valve repair for, 342, 349 nonclassical, 93 TEE of, 115f Mitral valve prosthesis bioarea issues for, 139 torn leaflet of, 152f–153f guidelines for selection of, 142b mechanical area issues for, 139 transesophageal views of, 154f Mitral valve repair for mitral insufficiency chordal sparing vs. chordal severing in, 94, 104t end-systolic diameter as predictor of outcome of, 111f indications for, 100b notes on, 94 surgical repairability and, 92, 109f timing of, 97 for myxomatous disease, 63 TEE in, 337–369 with Barlow’s disease, 342 with Carpentier-Edwards Physio Annuloplasty Ring, 343, 349, 360 with coronary artery disease, 362–365 with Cosgrove ring, 345, 358 with endocarditis, 353, 356 with familial hypercholesterolemia, 369 with flail leaflet anterior, 346–348, 358 posterior, 343–345, 352

Mitral valve repair (Cont.) TEE in (cont.) with Gore-tex sutures, 347–349, 358 with hemolysis, 358 with hypertrophic obstructive cardiomyopathy, 368 in infant, 367 with mitral valve prolapse, 342, 349 with multiple congenital heart pathology, 366 with myxomatous disease, 346, 349 with papillary muscle rupture, 361 pediatric, 357–358 with posterior annuloplasty ring, 340 with pulmonary edema, 342, 345 of pulmonary venous inflows, 347, 349 with rheumatic disease, 357–358, 360 with ruptured chorda tendinea, 346–347, 349, 353 with semi-rigid Carpentier ring, 343 with severe mitral regurgitation, 340 due to flail leaflet, 344, 346–347 due to myxomatous disease, 346, 349 due to rheumatic disease, 357–358, 360 with systolic anterior motion, 352 with vegetation, 353, 356 Mitral valve replacement (MVR) bioprosthetic area issues for, 139 torn leaflet of, 152f–153f color M-mode sampling of lateral sewing ring of, 153f–154f mechanical area issues for, 139 transesophageal views of, 154f for mitral insufficiency chordal sparing vs. chordal severing in, 94, 104t end-systolic diameter as predictor of outcome of, 111f indications for, 100b notes on, 94 surgical repairability and, 92, 109f timing of, 97 for mitral stenosis catheter balloon valvuloplasty vs., 82f indications for, 73, 76b issues with, 70–71 obstructed, 154f Mitral valve vegetations, 169f, 171f M-mode echocardiography of intraventricular dyssynchrony, 300–301, 310f for LV mass assessment, 174–175 of pericardial constriction, 390, 407f–409f of pericardial tamponade, 406f, 413f of prosthetic valve infective endocarditis, 157 of tricuspid regurgitation, 129f MR. See Mitral regurgitation (MR). MRI (magnetic resonance imaging), cardiac. See Cardiac magnetic resonance (CMR). MS. See Mitral stenosis (MS). Multi-gated acquisition (MUGA) scanning, of LV volume, 175–176 Mural thrombi, in dilated cardiomyopathy, 226

Index MVA measurement. See Mitral valve area (MVA) measurement. MVP. See Mitral valve prolapse (MVP). MVR. See Mitral valve replacement (MVR). Myeloma, 447f Myocardial abscess, due to infective endocarditis, 157 Myocardial contusion, due to blunt cardiac trauma, 453 Myocardial events, timing of, tissue Doppler imaging of, 318 Myocardial hibernation, dobutamine stress echocardiography of, 215, 215t, 223f Myocardial infarction (MI) acute complications of, 202–205 dynamic LVOT obstruction as, 205, 212f free wall rupture as, 203, 210f “functional” mitral regurgitation as, 92, 205 intracavitary thrombus as, 205 LV aneurysm as, 204–205 LV (or other) false aneurysm as, 203, 210f–211f LV systolic dysfunction and failure as, 202–203, 208t mechanical, 203–204 papillary muscle rupture as, 212f, 204, 212f due to pump failure, 202–203 RV infarction as, 203, 209f septal rupture as, 203–204, 209f echocardiographic studies in coronary care unit for, 202 reporting issues for, 202 required parameters to obtain from, 202 scanning issues for, 202 wall motion abnormalities in, 201, 208t dobutamine stress echocardiography after for prediction of reversible myocardial dysfunction, 215, 222t for prognostication, 215, 215t for risk assessment, 215, 215t due to infective endocarditis, 156–157 nuclear imaging of, 181b right ventricular, 203, 209f, 417, 432f imaging modalities for, 422b, 427t Myocardial ischemia, mitral regurgitation due to, 93 Myocardial mass, in mitral regurgitation, 110f Myocardial oxygen demand, with aortic stenosis, 19 Myocardial perfusion, contrast echocardiography for, 273 Myocardial rupture, contrast echocardiography of, 271 Myocardial sequelae, of blunt cardiac trauma, 453 Myocardial stunning, mitral regurgitation due to, 92 Myocardial viability, strain and strain rate imaging of, 319 Myocarditis, 229–230 imaging modalities for, 238b, 245t due to infective endocarditis, 157

Myxomas, 441 in Carney complex, 441 in Carney complex variants, 442 familial and complex, 441–442 left atrial, 441, 448f left ventricular, 441 right atrial, 441, 448f right ventricular, 441 Myxomatous disease of mitral valve mitral regurgitation due to, 93, 113f mitral stenosis due to, 63 mitral valve repair for, 63, 346, 349 tricuspid regurgitation due to, 120 N Nagueh equation, 260, 268f NAME syndrome, myxomas in, 442 Neurologic complications, of infective endocarditis, 156 Node of Arantius, normal anatomy of, 1 Noncompacted myocardium, contrast echocardiography of, 271, 279f Nuclear imaging of amyloidosis, 236b–237b, 244t of aortic insufficiency appropriateness of, 49b utility of, 52t of aortic stenosis appropriateness of, 28b utility of, 30t of apical ballooning, 235b–236b, 243t for assessment of aortic valve morphology, 6b of cardiac masses, 444b, 445t of cardiac resynchronization therapy, 308b of cardiac trauma, 455b, 456t of cardiomyopathy dilated, 231b–233b, 241t hypertrophic, 234b–235b, 242t other forms of, 239b–240b restrictive, 236b–237b, 244t RV arrhythmogenic, 423b, 428t of coronary artery disease, 207b–208b of heart failure, 181b for hemodynamics, 263t of infective endocarditis appropriateness of, 163b–165b utility of, 168t of intrapericardial blood clot, 396b, 401t of left ventricle, 181b for left ventricular assessment and quantification, 182b–183b of mitral insufficiency appropriateness of, 101b utility of, 107t–109t of mitral stenosis, 77b–78b of mitral valve, 64b of myocardial infarction, 181b, 218b of myocarditis, 238b, 245t of pericardial constriction, 397b, 402t–403t of pericardial cysts, 398b, 404t of pericardial effusions, 394b, 399t of pericardial tamponade, 395b, 400t of prosthetic valves appropriateness of, 143b utility of, 148t of pulmonary embolism, 424b, 429t of pulmonary hypertension, 421b, 426t

515

Nuclear imaging (Cont.) of pulmonic valve disease, 125b for right heart chamber quantification, 420b, 425t of RV infarction, 422b, 427t of tricuspid valve disease assessment of, 125b utility of, 126t O Occluders, 138 Open surgical commissurotomy, for mitral valve replacement catheter balloon valvuloplasty vs., 82f indications for, 73, 76b issues with, 70–71 P PA. See Pulmonary artery(ies) (PAs). Pacemaker stress echocardiography with, 224f tricuspid regurgitation due to, 120 Pacing lead placement, 304 Pannus, of prosthetic valve, 138 Papillary fibroelastoma, 442, 449f, 451f Papillary muscle(s) of mitral valve, 62–63, 67f severed, due to stab wound, 460f TEE of, 332t–333t Papillary muscle rupture (PMR) from acute myocardial infarction, 204, 212, 212f complete, 204 due to infective endocarditis, 156 mitral regurgitation due to, 92–93, 115f–116f mitral valve repair with, 361 partial, 204 severe, 204 tricuspid regurgitation due to, 120 Papillary tumors, of heart valves, 442 Paravalvar insufficiency, with prosthetic valves, 137, 152f color M-mode imaging of, 153f–154f reporting of, 138 TEE of, 138 Patent foramen ovale pulmonary embolism with, 430f, 437f pulmonary hypertension with, 434f TEE of, 328, 335f Patent foramen ovale device closure, intracardiac echocardiography of, 372 with abnormalities of device position, 372, 381f with aneurysm of septum primum, 372, 378f with associated fenestrated defects, 372, 380f with Chiari malformation, 372, 378f contrast saline, 372, 379f during device delivery, 372, 379f with septum primum and septum secundum with left-to-right shunts, 372, 378f with thrombus formation, 372, 382f with trace residual leaks, 372, 380f Patient-prosthesis mismatch (PPM), 139 PAV replacement. See Percutaneous aortic valve (PAV) replacement.

516 Index PCWP. See Pulmonary capillary wedge pressure (PCWP). PE. See Pulmonary embolism (PE). Peak systolic velocity, in aortic stenosis, 21 and gradient issues, 20 Pediatric patients mitral valve repair in, 357–358 TEE in, 326 Penetrating cardiac trauma, 453–454 gunshot injury as, 453, 461f stab wound as, 453 aortic-to-RA fistula due to, 459f hemothorax due to, 461f intrapericardial hemorrhage and clot due to, 457f left anterior descending coronary artery laceration/transection due to, 461f mitral regurgitation due to, 460f pericardial effusion due to, 457f, 459f RV compression due to, 459f severed papillary muscle due to, 460f ventriculoseptal defect due to, 458f Penn formula, for LV mass, 174 Percutaneous aortic valve (PAV) replacement, echocardiographic guidance of, 466–468 with CoreValve prosthesis, 489f with Edwards-Sapien prosthesis, 489f postdeployment, 490f predeployment, 490f intraprocedure role in, 467–468 measurements in, 489f for postprocedural assessment, 468 for postprocedural follow-up, 468 for preprocedural assessment, 466–467 rationale and role for, 466 sequence of, 466–468 transesophageal views in midesophageal, 489f three-dimensional, 489f Percutaneous heart valve (PHV) CoreValve, 489f Edwards-Sapien, 489f postdeployment, 490f predeployment, 490f Percutaneous mitral balloon valvotomy, for mitral stenosis echocardiographic prediction of outcome of, 79t indications for, 73, 75b Pericardial blood clot, 389, 396b, 401t due to stab wound, 457f Pericardial constriction, 389–392 vs. atrial fibrillation, 392 cardiac catheterization for, 398t, 402t–403t cardiac output/index in, 390 chest radiography of, 402t–403t CT of, 397b, 402t–403t echocardiographic appearance of, 407f–410f echocardiographic signs of, 390–392 caval dilation as, 407f early diastolic pressure dips as, 390, 407f, 409f early diastolic pressure plateau as, 391 elevated cardiovascular central venous pressure as, 391 elevated RV diastolic pressure as, 391–392

Pericardial constriction (Cont.) echocardiographic signs of (cont.) hepatic venous flow pattern as, 390–391, 408f–410f inspiratory fall in LV early diastolic inflow velocities as, 390 inspiratory increase in RV systolic pressure as, 391 inspiratory septal shift as, 390, 408f–409f Kussmaul phenomena as, 390–391 late diastolic septal dip as, 391 normal underlying heart as, 391 pericardial thickening as, 391, 408f reduced RV (extrinsic) compliance as, 391 ventricular interdependence as, 389–390, 409f imaging modalities for appropriateness of, 397b pros and cons of, 402t–403t M-mode echocardiography of, 390, 407f–409f MRI of, 397b, 402t–403t nuclear imaging of, 397b, 402t–403t required parameters to obtain from scanning of, 389–390 respiratory cycle vs. cardiac cycle in, 390, 408f respirometry in, 389, 408f–409f stroke volume in, 390 surgical risk and outcomes for, 392 TEE of, 397b, 402t–403t tissue Doppler imaging of, 318, 407f–408f tricuspid regurgitation in, 390 TTE of, 397b, 402t–403t valid means to make diagnosis of, 392 Pericardial cyst, 392, 398b, 404t Pericardial disease, 387–414 intrapericardial blood clot as, 389 pericardial constriction as, 389–392 pericardial cyst as, 392 pericardial effusions as, 387 pericardial tamponade as, 387–389 TEE of, 327 Pericardial effusions, 387 cardiac catheterization for, 399t cardiac tamponade with, 405f chest radiography of, 399t, 411f CT of, 394b, 399t goals of echocardiography of, 387 imaging modalities for appropriateness of, 394b utility of, 399t due to infective endocarditis, 157 due to intrapericardial hemorrhage, 410f–411f malignant, pericardial tamponade due to, 412f with metastatic adenocarcinoma, 414f MRI of, 394b, 399t nuclear imaging of, 394b in pericardial tamponade, 388 vs. pleural effusion, 387 size of, 387, 414f due to stab wound, 457f, 459f TEE of, 394b, 399t TTE of, 394b, 399t Pericardial extension, of infective endocarditis, 156 Pericardial fat, 387, 414f

Pericardial sequelae, of blunt cardiac trauma, 453 Pericardial space, echolucent material within, 387, 414f Pericardial tamponade, 387–389 due to blunt cardiac trauma, 453 cardiac catheterization for, 400t causes seen or suggested by echocardiography of, 389 chest radiography of, 400t CT of, 395b, 400t Doppler imaging of, 406f early postoperative, 389 echocardiographic images of, 406f, 412f–413f echocardiographic signs of, 388–389 augmented respiratory variation of mitral inflow velocities as, 388 cardiac chamber compression signs as, 387 caval distention as, 388 notes on, 388–389 pericardial effusion as, 388 RA collapse as, 388 right heart obstruction sign as, 388 RV diastolic collapse as, 388, 413f ventricular interdependence as, 388, 406f echocardiography used to guide periocentesis in, 389 imaging modalities for appropriateness of, 395b utility of, 400t due to malignant effusion, 412f M-mode echocardiography of, 406f, 413f MRI of, 395b, 400t nuclear imaging of, 395b, 400t with pulsus paradoxus, 389 required parameters to obtain from scanning of, 387–388 with swinging of heart, 412f–413f TEE of, 395b, 400t TTE of, 395b, 400t Pericardial thickening, in pericardial constriction, 391, 408f Pericardiocentesis echocardiographic guidance of, 465–466 from apical approach, 480f–481f with chronic pericarditis, 484f cons of, 466 optimal site and orientation of needle in, 480f–481f plane of imaging in, 483f poor/ambiguous visualization of needle in, 484f pre- and postdrainage views in, 484f pros of, 465 rationale and role for, 465 sequence of, 465 shallow apical view in, 482f, 484f tenting of pericardium in, 483f–484f echocardiography used to guide, 389 Pericarditis, constrictive. See Pericardial constriction. Perioperative risk assessment, dobutamine stress echocardiography for, 214, 214t Perivalvar abscess, due to infective endocarditis, 158 PHT. See Pressure half-time (PHT). PHV. See Percutaneous heart valve (PHV). PI (pulmonic insufficiency), 122 imaging modalities for, 125b

Index PISA. See Proximal isovelocity surface area (PISA). Planimetry, for mitral valve area measurement, 69, 84f reporting issues with, 70 Pleural effusions cardiac tamponade with, 405f pericardial vs., 387 Pleural metastases, 446f PMR (papillary muscle rupture). See Papillary muscle rupture (PMR). Pneumopericardium, due to blunt cardiac trauma, 453 Posterior annuloplasty ring, 340 Posterior mitral valve leaflet, flail, 343–345, 352 Posteromedial papillary muscle, of mitral valve, 63 Postsystolic shortening, strain and strain rate imaging of, 319 PPM (patient-prosthesis mismatch), 139 Pressure half-time (PHT) with aortic insufficiency, 45 for mitral valve area measurement, 69 reporting issues with, 69–70 Pressure overload, in aortic stenosis, 19 Pressure recovery phenomenon in aortic stenosis, 21 with prosthetic valves, 138–139, 150f, 151f Prosthetic valves, 137–154 aortic bioprosthetic, 140 mechanical, area issues with, 140 area issues with, 139–140 with aortic valve replacement bioprosthetic, 140 mechanical, 140 flow and pressure dependence of Gorlin and continuity as, 139 general issues of correlation as, 139 with mitral valve replacements bioprosthetic, 139 mechanical, 139 assumptions inherent in modified Bernoulli equation for, 139 bioprosthetic aortic, 140 CE porcine, 148t dysfunction of, 140 echocardiographic and fluoroscopic findings with, 137, 146t–147t Hancock, 148t insufficiency of, 140 mitral area issues for, 139 torn leaflet of, 152f–153f stenosis of, 140 stented, 146t–147t stentless, 146t–147t cardiac catheterization for appropriateness of, 143b discordance of gradient assessment with, 139 utility of, 148t chest radiography of, 148t CT for appropriateness of, 143b utility of, 148t dysfunction of, 140 bioprosthetic, 140 mechanical, 140

Prosthetic valves (Cont.) expected areas and gradients for, 138 Gorlin equation for flow and pressure dependence of, 139 general issues of correlation with, 139 gradient issues with, 138 hemi-disk occluders of, 138 imaging modalities for appropriateness of, 143b utility of, 148t infective endocarditis of, 157–158 dehiscence with, 157 “early,” 156, 158 echocardiographic findings with, 157–158 Doppler, 158 M-mode, 157 notes on, 158 two-dimensional and real time, 157 “late,” 157, 158 prophylaxis for, 142b surgery for, 162b LVOT obstruction with, intracardiac echocardiography of, 372, 377f mechanical aortic, area issues with, 140 ball-in-cage, 146t–147t bileaflet occluder, 146t–147t pressure recovery in, 150f transesophageal views of, 154f Bjork-Shiley, 146t–147t Carbomedics, 146t–147t dysfunction of, 140 echocardiographic and fluoroscopic findings with, 137, 146t–147t insufficiency of, 140 Medtronic Hall, 146t–147t mitral area issues for, 139 transesophageal views of, 154f single tilting disk, 146t–147t St. Jude Medical, 146t–147t Starr-Edwards, 146t–147t stenosis of, 140 mitral bioprosthetic area issues for, 139 torn leaflet of, 152f–153f color M-mode sampling of lateral sewing ring of, 153f–154f mechanical area issues for, 139 transesophageal views of, 154f obstructed, 154f MRI of appropriateness of, 143b utility of, 148t “normal appearance” of, 138 nuclear imaging of appropriateness of, 143b utility of, 148t obstruction of, 137, 154f occluders of, 138 pannus of, 138 paravalvar insufficiency with, 137, 152f color M-mode imaging of, 153f–154f reporting of, 138 TEE of, 138 patient-prosthesis mismatch with, 139 pressure recovery phenomenon with, 138–139, 150f, 151f range of design of, 137, 146t–147t

517

Prosthetic valves (Cont.) reporting issues with, 137–139 required parameters to obtain from scanning of, 137 retroverted leaflet of, 138 scanning issues with, 137 scanning notes for, 137 sewing ring of, 138 color M-mode sampling of, 153f–154f TEE of, 140, 154f, 328 appropriateness of, 143b description of paravalvar leaks on, 138 utility of, 148t terminology for, 137–138 thrombosis of, 142b thrombus of, 138 torn leaflet of, 138, 152f–153f transvalvar insufficiency with, 137 TTE of appropriateness of, 143b utility of, 148t vegetations of, 138 Proximal isovelocity surface area (PISA), 285–297 aliasing velocity in, 286–287 angle correction for, 285–286, 296f for aortic insufficiency, 44–45, 54f, 57f, 293f pros and cons of, 291t for aortic stenosis, 18 pros and cons of, 291t and subvalvar stenosis, 22 color Doppler measurements of, 286–287 aliasing velocity in, 286–287 hemispheres of flow acceleration in, 286 radius of, 287 vena contracta in, 287 constraint in, 285–286, 296f continuous wave Doppler measurements of, 287, 293f with mitral insufficiency, 294f convergent flow in, 286, 292f derivations of, 287 effective regurgitant orifice in, 287, 297f equations for, 287–288 flow rate in, volumetric, 287 for grading of valvular insufficiency, 288, 290t hemisphere of flow acceleration in, 285–286 in color Doppler measurement, 286 radius of, 287 schematic rendering of, 292f for mitral regurgitation, 90, 95–96, 111f vs. color Doppler flow mapping, 285 continuous wave Doppler spectral display of, 294f in early, mid-, and late systole, 294f optimized, 293f, 296f pros and cons of, 291t rheumatic, 295f with underlying 2D grayscale views beside color Doppler flowmapping views, 296f well-formed, 293f for mitral stenosis, 287–288 pros and cons of, 291t rheumatic, 295f for mitral valve area measurement, 69 angle correction with, 82f reporting issues with, 70

518 Index Proximal isovelocity surface area (Cont.) parameters needed for, 286 pros and cons of, 291t rationale for, 285 regurgitant volume in, 287, 297f for rheumatic mixed mitral stenosis/ insufficiency, 295f scanning parameters for, 286–288 simplified methods for, 288 summary of, 291t technical points on, 288 for tricuspid regurgitation, 119 in two-dimensional and grayscale imaging, 286 Proximal jet width, in mitral regurgitation, 97, 111f–112f Pseudoaneurysm from acute myocardial infarction, 203, 210f–211f contrast echocardiography of, 271 Pulmonary artery(ies) (PAs), TEE of, 332t–333t Pulmonary artery (PA) catheter, echocardiography as, 258–260 cardiac output in, 259–260 Doppler method assumptions for, 259 notes on, 259 pulmonary flow in, 260 RA pressure in, 258–259, 262t RV systolic pressure in, 258–259 Pulmonary artery (PA) pressure, in mitral regurgitation, 96–97 Pulmonary artery wedge pressure (PWP) deceleration time and, 267f E:A ratio and, 267f Pulmonary capillary wedge pressure (PCWP) deceleration time and, 257, 266f E:A ratio and, 257, 266f vs. left ventricular end-diastolic volume, 264f for LV filling pressures, 260 with mitral stenosis, 72 systolic fraction and, 257, 265f V-waves on, and mitral regurgitation grading, 92 Pulmonary edema, mitral valve repair with, 342, 345 Pulmonary embolism (PE), 417–418 apical four-chamber view of, 430f–431f with cardiac arrest, 431f cardiac catheterization for, 429t chest radiography of, 429t CT of, 424b, 429t direct evidence of, 418 with embolus-in-transit, 430f–431f, 437f imaging modalities for, 424b, 429t indirect evidence of, 418 interatrial septum in, 430f MRI of, 424b, 429t nuclear imaging of, 424b, 429t with patent foramen ovale, 430f, 437f posterior short-axis view of, 430f, 432f repeated, 437f with RV failure, 430f, 432f RV inflow view of, 430f with RV strain, 418, 431f, 436f severe RV dysfunction and dilation due to, 436f TEE of, 424b, 429t, 431f thromboembolic specimens of, 430f TTE of, 424b, 429t, 431f

Pulmonary flow, 260 Pulmonary hypertension imaging modalities for, 421b, 426t primary, 418, 432f with RV hypertension, 415–416 terminal hepatic venous flow pattern in, 434f with patent foramen ovale, 434f RV apical thrombus in, 433f tricuspid regurgitation due to, 128f, 136f Pulmonary stenosis. See Pulmonic stenosis. Pulmonary valve. See Pulmonic valve. Pulmonary veins, TEE of, 332t–333t Pulmonary venous flow patterns, 257–258 continuity equations for, 257–258 D (diastolic) wave in, 257 S wave in, 257, 265f A (atrial) systole reversal wave in, 257, 265f tissue Doppler imaging of, 257, 270f Pulmonary venous inflows, in mitral valve repair, 347, 349 Pulmonary venous spectral Doppler, in mitral regurgitation, 95, 117f Pulmonary venous systolic flow reversal, in mitral regurgitation, 95, 117f Pulmonic insufficiency (PI), 122 imaging modalities for, 125b Pulmonic stenosis, 121–122 grading of, 121 imaging modalities for, 125b indications for balloon valvotomy for, 122, 124b indications for evaluation of, 122, 124b RV/pulmonary artery hypertension due to, 416 Pulmonic valve, intracardiac echocardiography of, 371–372, 375f Pulmonic valve disease imaging modalities for, 125b TEE of, 125b, 332t–333t Pulmonic valve motion, in pulmonary hypertension, 415 Pulsed-wave Doppler of aortic insufficiency, 58f in left ventricle, 45 of mitral stenosis, 89f Pulsed-wave tissue Doppler imaging, 317 Pulsus paradoxus, pericardial tamponade with, 389 Q QRS complex, LV dyssynchrony with narrow, 305–306 wide, 299 Quinones method, for LV volume, 177 R RA. See Right atrial (RA). RAA (right atrial appendage), TEE of, 332t–333t Radial axis, in heart deformation coordinate system, 317, 320f Radial speckle tracking, for intraventricular dyssynchrony, 302–303, 314f Radial strain imaging, of intraventricular dyssynchrony, 302–303, 314f Radiofrequency ablation, for atrial fibrillation, intracardiac echocardiography in, 372, 385f

Radionuclide angiography, of LV volume, 176, 188f Radionuclide imaging. See Nuclear imaging. RAP (right atrial pressure), in tricuspid regurgitation, 120 RCC (renal cell carcinoma), cardiac mass due to extension of, 450f Real-time three-dimensional echocardiography (RT3DE) of dyssynchrony, 303 index of, 303, 315f of left ventricle, 177–178, 186t–187t for mitral valve area measurement, 70 of prosthetic valve infective endocarditis, 157 Regional wall motion, contrast echocardiography of, 271, 276f Regurgitant fraction (RF) of aortic insufficiency, 45, 59f–60f in mitral regurgitation, 96 and angiographic grade, 110f equation for, 90–91 two-dimensional Doppler for, 96 in pulmonary venous flow calculations, 258 Regurgitant orifice area (ROA), for mitral regurgitation, 96 Regurgitant volume (RV) in aortic insufficiency, 44 in mitral regurgitation, 90, 95–96 and angiographic grade, 110f equation for, 90–91 in proximal isovelocity surface area, 287, 297f in pulmonary venous flow calculations, 258 Renal cell carcinoma (RCC), cardiac mass due to extension of, 450f Renal complications, of infective endocarditis, 156–157 Respirometry, in pericardial constriction, 389, 408f–409f Restrictive orifice, components of flow across, 111f Retrograde flow profiles, in aortic insufficiency, 44 Retrograde holodiastolic flow, in aortic insufficiency in abdominal aorta, 43–44 at aortic root level, 60f in lower thoracic aorta, 58f MRI velocity encoded phase contrast technique for, 59f Retroverted leaflet, of prosthetic valve, 138 RF. See Regurgitant fraction (RF). Rhabdomyomas, 442 Rhabdomyosarcoma, 442 Rheumatic disease aortic insufficiency due to, 54f of chordae of mitral valve, 63 infective endocarditis due to, 157 mitral regurgitation due to, 93, 111f, 113f mitral stenosis due to, 63, 83f–84f mitral valve repair due to, 357–358, 360 mixed mitral stenosis/insufficiency due to, 295f tricuspid regurgitation due to, 120 Right atrial appendage (RAA), TEE of, 332t–333t Right atrial (RA) collapse, in pericardial tamponade, 388

Index Right atrial (RA) myxomas, 441, 448f Right atrial (RA) pressure, echocardiography as pulmonary artery catheter for, 258–259, 262t Right atrial pressure (RAP), in tricuspid regurgitation, 120 Right chamber quantification, 420b, 425t Right coronary artery, ostium to, 440f Right heart disease(s), 415–440 arrhythmogenic RV cardiomyopathy as, 423b, 428t, 433f carcinoid, 435f echocardiographic findings in, 415 Doppler, 415 occasional, 415 two-dimensional, 415 infective endocarditis as, 158 inferior vena cava dimensions and collapse in, 416 interatrial septum in, 415 interventricular septal shape and motion patterns in, 415–416, 432f ostium to right coronary artery in, 440f pulmonary embolism as, 417–418 apical four-chamber view of, 430f–431f with cardiac arrest, 431f cardiac catheterization for, 429t chest radiography of, 429t CT of, 424b, 429t direct evidence of, 418 with embolus-in-transit, 430f–431f, 437f imaging modalities for, 424b, 429t indirect evidence of, 418 interatrial septum in, 430f MRI of, 424b, 429t nuclear imaging of, 424b, 429t with patent foramen ovale, 430f, 437f posterior short-axis view of, 430f, 432f repeated, 437f with RV failure, 430f, 432f RV inflow view of, 430f with RV strain, 418, 431f, 436f severe RV dysfunction and dilation due to, 436f TEE of, 424b, 429t, 431f thromboembolic specimens of, 430f TTE of, 424b, 429t, 431f pulmonary hypertension as imaging modalities for, 421b, 426t primary, 418, 432f with RV hypertension, 415–416 terminal hepatic venous flow pattern in, 434f with patent foramen ovale, 434f RV apical thrombus in, 433f right chamber quantification in, 420b, 425t RV diastolic failure in, 415, 432f RV dysplasia as, 417 in arrhythmogenic RV cardiomyopathy, 433f RV endocardial pacer lead for, 440f RV hypertension as, 415–416 due to pulmonary hypertension, 416 due to pulmonary stenosis, 416 systolic, 416 RV hypertrophy as, 416, 432f RV infarction as, 417, 432f imaging modalities for, 422b, 427t RV moderator band in, 438f

Right heart disease(s) (Cont.) RV pressure overload in, 415 RV septal thickness in, 439f RV systolic dysfunction in, 415, 436f RV trabeculation in, 439f RV volume in, 416–417 overload in, 415–416 tricuspid regurgitation in, 415, 432f, 435f Right heart obstruction sign, in pericardial tamponade, 388 Right heart thrombi, 443 Right pulmonary artery, intracardiac echocardiography of, 371–372, 376f Right pulmonary veins, intracardiac echocardiography of, 375f–376f Right ventricle (RV), TEE of, 332t–333t Right ventricular (RV) apical thrombus, in pulmonary hypertension, 433f Right ventricular (RV) arrhythmogenic cardiomyopathy, 423b, 428t, 433f Right ventricular (RV) compliance, reduced, in pericardial constriction, 391 Right ventricular (RV) compression, due to stab wound, 459f Right ventricular (RV) diastolic collapse, in pericardial tamponade, 388, 413f Right ventricular (RV) diastolic failure, 415, 432f Right ventricular (RV) diastolic pressure, in pericardial constriction, 391–392 Right ventricular (RV) dysplasia, 417 in arrhythmogenic RV cardiomyopathy, 433f Right ventricular (RV) endocardial pacer lead, 440f Right ventricular (RV) failure, pulmonary embolism with, 430f, 432f Right ventricular (RV) hypertension, 415–416 due to pulmonary hypertension, 416 due to pulmonary stenosis, 416 systolic, 416 Right ventricular hypertrophy (RVH), 416, 432f Right ventricular (RV) infarction, 203, 209f, 417, 432f imaging modalities for, 422b, 427t Right ventricular (RV) moderator band, 438f Right ventricular (RV) myxomas, 441 Right ventricular (RV) outflow tract, TEE of, 332t–333t Right ventricular pre-ejection interval (RVPEI), 299 Right ventricular (RV) pressure overload, 415 Right ventricular (RV) regurgitant fraction, in mitral regurgitation, 96 Right ventricular (RV) septal thickness, 439f Right ventricular (RV) strain, pulmonary embolism with, 418, 431f, 436f Right ventricular (RV) systolic dysfunction, 415, 436f Right ventricular systolic pressure (RVSP) in dilated cardiomyopathy, 226 echocardiography as pulmonary artery catheter for, 258–259 in mitral stenosis, 71

519

Right ventricular systolic pressure (Cont.) in pericardial constriction, 391 in RV hypertension, 415 in tricuspid regurgitation, 119–121, 132f with pericardial constriction, 390 and pulmonary hypertension, 120 and pulmonary stenosis, 120 Right ventricular (RV) trabeculation, 439f Right ventricular (RV) volume, 416–417 overload in, 415–416 Right ventricular (RV) wall thickness in hypertrophic cardiomyopathy, 227 in RV hypertrophy, 416, 432f Right ventricular–to–right atrial (RV-to-RA) gradient, 259 in tricuspid regurgitation, 120 Right-sided valve disease pulmonic imaging modalities for, 125b pulmonic insufficiency as, 122 pulmonic stenosis as. See Pulmonic stenosis. TEE of, 125b, 332t–333t tricuspid anatomy and, 119 imaging modalities for, 125b, 126t TEE of, 125b, 328, 332t–333t tricuspid regurgitation as. See Tricuspid regurgitation (TR). tricuspid stenosis as. See Tricuspid stenosis (TS). Ritter method, for AV optimization, 304 ROA (regurgitant orifice area), for mitral regurgitation, 96 R-R intervals in aortic insufficiency, 58f in aortic stenosis and aortic valve gradient, 39f and V2 measurement, 34f in tricuspid regurgitation, 128f RT3DE. See Real-time three-dimensional echocardiography (RT3DE). RV. See Regurgitant volume (RV); Right ventricle (RV). RVH (right ventricular hypertrophy), 416, 432f RVPEI (right ventricular pre-ejection interval), 299 RVSP. See Right ventricular systolic pressure (RVSP). S S wave, in pulmonary venous flow patterns, 257, 265f SAM (systolic anterior motion), in hypertrophic cardiomyopathy, 227, 248f TEE of, 352 Sarcoidosis, cardiac, 229 SDI (systolic dyssynchrony index), 303, 315f Segmental wall motion analysis, stress echocardiography for, 213 Sellers grade, for mitral regurgitation, 97 Semi-rigid Carpentier ring, TEE of, 343 SEP (systolic ejection period), with aortic stenosis, 24 Septal dip, late diastolic, in pericardial constriction, 391 Septal rupture, from acute myocardial infarction, 203–204, 209f

520 Index Septal shift, inspiratory, in pericardial constriction, 390, 408f–409f Sewing ring, of prosthetic valve, 138 color M-mode sampling of, 153f–154f Simpson’s volumetric method for LV volume, 177, 184t–185t, 193f for RV volume, 416–417 Single tilting disk valve, 146t–147t Sinotubular junction, normal anatomy of, 1 Sinus rhythm, mitral stenosis in, 86f SJM (St. Jude Medical) valve, 146t–147t Slope, for aortic insufficiency, 45, 56f–57f Speckle tracking echocardiography, 319, 322f Spectral profiles for aortic insufficiency, 43, 56f abdominal, 57f for tricuspid regurgitation, 119, 128f–129f, 132f–133f for tricuspid stenosis, 130f St. Jude Medical (SJM) valve, 146t–147t Stab wound, 453 aortic-to-RA fistula due to, 459f hemothorax due to, 461f intrapericardial hemorrhage and clot due to, 457f left anterior descending coronary artery laceration/transection due to, 461f mitral regurgitation due to, 460f pericardial effusion due to, 457f, 459f RV compression due to, 459f severed papillary muscle due to, 460f ventriculoseptal defect due to, 458f Starr-Edwards valve, 146t–147t Strain, 302, 318–319, 321f Strain imaging, 318–319, 321f of athletic heart, 319 of cardiomyopathy, 319 of heart failure, 319 of myocardial viability, 319 Strain rate, 318, 321f imaging of, 318–319 of intraventricular dyssynchrony, 302 radial strain imaging as, 302–303, 314f of myocardial viability, 319 step-by-step approach to, 318–319, 321f Stress echocardiography, 213–224 adenosine, 215, 222t and blood pressure, 214 contrast agents in, 271, 277f dipyridamole, 214–215 comparison of, 215, 223t sensitivity of, 223t dobutamine, 214–215 comparison of, 215, 223t contrast agents in, 271 of coronary artery disease, 214, 222t of myocardial hibernation, 215, 215t, 223f for perioperative risk assessment, 214, 214t postinfarction for predicting reversible myocardial dysfunction, 215, 222t for prognostication, 215, 215t for risk assessment, 215, 215t safety and tolerability of, 214 equipment for, 213

Stress echocardiography (Cont.) exercise, 214 comparison of, 215, 223t contrast agents in, 271, 277f in female patient, 214, 214t sensitivity and specificity of, 221t–222t imaging modalities for, 218b limitations of, 215 for noninvasive risk stratification, 218b postaortocoronary bypass with ventricular pacemaker, 224f segmental wall motion analysis in, 213 transesophageal, 215 uses of images in, 213 wall thickening/ejection fraction response in, 213 Stroke volume in aortic stenosis, 18, 33f causes of larger, 20 mean gradient and, 19–20 echocardiographic calculation of, 259 in pericardial constriction, 390 Submitral calcification, mitral stenosis due to, 89f Subvalvar aortic stenosis, 19, 22, 37f Subvalvar disease, mitral stenosis with, 83f, 85f, 87f Superior vena cava (SVC) syndrome/ compression, 450f Surgical mitral valve replacement catheter balloon valvuloplasty vs., 82f indications for, 73, 76b issues with, 70–71 Swinging of heart, in pericardial tamponade, 412f–413f Systolic anterior motion (SAM), in hypertrophic cardiomyopathy, 227, 248f TEE of, 352 Systolic dyssynchrony index (SDI), 303, 315f Systolic ejection period (SEP), with aortic stenosis, 24 Systolic fraction, and pulmonary capillary wedge pressure, 257, 265f Systolic function in dilated cardiomyopathy, 226 LV assessment for, 175–178 T Tako-tsubo. See Apical ballooning syndrome. TDA (traumatic disruption of aortic), 326 TDI. See Tissue Doppler imaging (TDI). TEE. See Transesophageal echocardiography (TEE). Thoracic aorta, retrograde holodiastolic flow in, 58f Thoracic masses, 441, 446f–447f Three-dimensional (3D) echocardiography real-time of dyssynchrony, 303 index in, 303, 315f of left ventricle, 177–178, 186t–187t for mitral valve area measurement, 70 Thrombosis, of prosthetic heart valves, 142b Thrombus(i) intracardiac contrast echocardiography of, 271, 277f–278f left atrial, 443, 452f TEE of, 327, 331t, 334f

Thrombus(i) (Cont.) intracardiac (cont.) left ventricular, 442–443, 452f right heart, 443 intracavitary, from acute myocardial infarction, 205 of prosthetic valve, 138 Time velocity interval (TVI), in aortic insufficiency, 44 Tissue displacement, 302 Tissue Doppler imaging (TDI), 317–318, 320f of athletic heart, 318 clinical applications of, 318 color, 317 of constrictive pericarditis vs. restrictive cardiomyopathy, 318 of diastolic function, 318 for dyssynchrony, 301–303 apical 2-chamber view in, 311f apical 3-chamber view in, 312f apical 4-chamber view in, 313f color Doppler tissue analysis in, 301–302 radial strain, 302–303 tissue velocity imaging in, 301–303, 311f of LV function, 318 of pericardial constriction, 318, 407f–408f pulsed-wave, 317 of timing of myocardial events, 318 Tissue synchronization imaging (TSI), 302 Tissue tracking, 302 Tissue velocity imaging (TVI) for dyssynchrony, 301–303, 311f for pacing lead placement, 304 Torn leaflet, of prosthetic valve, 138, 152f–153f TR. See Tricuspid regurgitation (TR). Transesophageal echocardiography (TEE), 323–335 of amyloidosis, 236b–237b, 244t of aortic arch, 332t–333t of aortic atheromatous debris, 326 of aortic disease, 325–326 of aortic dissection, 325, 330t, 334f of aortic insufficiency, 45–46, 57f, 328 appropriateness of, 49b utility of, 52t of aortic root, 332t–333t of aortic stenosis, 40f, 328 appropriateness of, 28b role for, 20 utility of, 30t of aortic valve disease, 328 in aortic valve replacement, 354–356 of apical ballooning, 235b–236b, 243t of ascending aorta, 332t–333t for assessment of aortic valve morphology appropriateness of, 6b utility of, 8t of atrial septal defects, 326, 330t–331t bicaval view on, 332t–333t of cardiac masses, 444b, 445t of cardiac resynchronization therapy, 308b of cardiac sources of embolism, 327–328

Index Transesophageal echocardiography (Cont.) of cardiac trauma, 454, 455b, 456t of cardiomyopathy dilated, 231b–233b, 241t hypertrophic, 228, 234b–235b, 242t restrictive, 236b–237b, 244t RV arrhythmogenic, 423b, 428t caveats with, 324 of coarctation of aorta, 326 complications of, 324–325 of congenital heart disease, 326 contraindications to, 323 of cor triatriatum, 326 of coronary artery disease, 207b–208b in critically ill patients, 326–327 of descending aorta, 332t–333t equipment for, 323 getting lost and finding your bearings in, 324 indications for, 330b of infective endocarditis, 327 with abscess, 171f, 327 aortic, 354–356 aortic and mitral, 170f appropriateness of, 163b–165b caveats for, 327 with fistula, 327 mitral, 171f, 353, 356 role of, 159 shortcomings of, 155 tricuspid, 172f utility of, 168t of interatrial septum, 332t–333t with aneurysm, 328 of intracardiac masses, 327–328 of intramural hematoma, 325 of intrapericardial blood clot, 396b, 401t of LA appendage, 332t–333t of LA thrombus, 327, 331t, 334f of left ventricle, 182b–183b, 187t, 328, 332t–333t of LVOT lesions, 328, 332t–333t medications for, 323 of mitral regurgitation, 328 appropriateness of, 101b with mitral valve prolapse, 115f with papillary muscle rupture, 116f with repaired cleft leaflet, 113f role of, 91 with ruptured chords and flail posterior leaflet, 114f utility of, 107t–109t of mitral stenosis, 328 appropriateness of, 77b–78b during mitral catheter balloon valvuloplasty, 88f role of, 71–72 utility of, 80t of mitral valve, 64b, 328, 332t–333t in mitral valve repair, 337–369 with Barlow’s disease, 342 with Carpentier-Edwards Physio Annuloplasty Ring, 343, 349, 360 with coronary artery disease, 362–365 with Cosgrove ring, 345, 358 with endocarditis, 353, 356 with familial hypercholesterolemia, 369 with flail leaflet anterior, 346–348, 358 posterior, 343–345, 352 with Gore-tex sutures, 347–349, 358

Transesophageal echocardiography (Cont.) in mitral valve repair (cont.) with hemolysis, 358 with hypertrophic obstructive cardiomyopathy, 368 in infant, 367 with mitral valve prolapse, 342, 349 with multiple congenital heart pathology, 366 with myxomatous disease, 346, 349 with papillary muscle rupture, 361 pediatric, 357–358 with posterior annuloplasty ring, 340 with pulmonary edema, 342, 345 of pulmonary venous inflows, 347, 349 with rheumatic disease, 357–358, 360 with ruptured chorda tendinea, 346–347, 349, 353 with semi-rigid Carpentier ring, 343 with severe mitral regurgitation, 340 due to flail leaflet, 344, 346–347 due to myxomatous disease, 346, 349 due to rheumatic disease, 357–358, 360 with systolic anterior motion, 352 with vegetation, 353, 356 of myocarditis, 238b, 245t of papillary muscles, 332t–333t of patent foramen ovale, 328, 335f in pediatric patients, 326 of pericardial constriction, 397b, 402t–403t of pericardial cysts, 398b, 404t of pericardial diseases, 327 of pericardial effusions, 394b, 399t of pericardial tamponade, 395b, 400t probe insertion for, 323–324 procedure for, 323 of prosthetic valves, 140, 154f, 328 appropriateness of, 143b description of paravalvar leaks on, 138 utility of, 148t of pulmonary arteries, 332t–333t of pulmonary embolism, 424b, 429t, 431f of pulmonary hypertension, 421b, 426t of pulmonary veins, 332t–333t of pulmonic valve disease, 125b, 332t–333t of RA appendage, 332t–333t for right heart chamber quantification, 420b, 425t of right ventricle, 332t–333t of RV infarction, 422b, 427t of RV outflow tract, 332t–333t safety with, 324–325 standard protocol for, 332t–333t for stress imaging, 215, 218b of traumatic disruption of aorta, 326 of tricuspid valve disease, 328, 332t–333t assessment of, 125b utility of, 126t of valve disease, 328 of vegetations, 167t, 169f–171f vs. TTE, 331t Transient apical ballooning. See Apical ballooning syndrome. Transmitral E wave, 388 Transmitral gradient, in mitral stenosis with catheterization estimates higher than echocardiography, 73 provocative testing to enhance, 71

521

Trans-septal puncture echocardiographic guidance of, 466, 485f cons of, 466 pros of, 466 rationale and role for, 466 sequence of, 466 intracardiac echocardiography for, 372, 385f Transthoracic echocardiography (TTE) of amyloidosis, 236b–237b, 244t of aortic insufficiency appropriateness of, 49b utility of, 52t of aortic stenosis appropriateness of, 28b utility of, 30t of apical ballooning, 235b–236b, 243t for assessment of aortic valve morphology appropriateness of, 6b utility of, 8t of atrial septal defects, 330t of cardiac masses, 444b, 445t of cardiac resynchronization therapy, 308b of cardiac trauma, 455b, 456t of cardiomyopathy dilated, 231b–233b, 241t hypertrophic, 234b–235b, 242t, 251f other forms of, 239b–240b restrictive, 236b–237b, 244t RV arrhythmogenic, 423b, 428t of coronary artery disease, 207b–208b for hemodynamics, 263t of infective endocarditis appropriateness of, 163b–165b role of, 159 sensitivity and specificity of, 167t shortcomings of, 155 of intrapericardial blood clot, 396b, 401t of left atrial and left atrial appendage thrombus, 331t of left ventricle, 182b–183b of mitral regurgitation appropriateness of, 101b with ruptured chords and flail posterior leaflet, 114f utility of, 107t–109t of mitral stenosis appropriateness of, 77b–78b left atrium in, 85f role of, 71–72 utility of, 80t of mitral valve, 64b of myocarditis, 238b, 245t of pericardial constriction, 397b, 402t–403t of pericardial cysts, 398b, 404t of pericardial effusions, 394b, 399t of pericardial tamponade, 395b, 400t of prosthetic valve appropriateness of, 143b utility of, 148t of pulmonary embolism, 424b, 429t, 431f of pulmonary hypertension, 421b, 426t of pulmonic valve disease, 125b for right heart chamber quantification, 420b, 425t of RV infarction, 422b, 427t for stress imaging, 218b

522 Index Transthoracic echocardiography (Cont.) of tricuspid valve disease assessment of, 125b utility of, 126t of vegetations, 167t, 169f vs. TEE, 331t Transvalvar insufficiency, with prosthetic valves, 137 Traumatic disruption of aortic (TDA), 326 Traumatic injury. See Cardiac trauma. Tricuspid atresia, 121 tricuspid stenosis due to, 121 Tricuspid bioprosthesis, obstruction from large vegetations of, 134f–135f Tricuspid insufficiency due to carcinoid, 136f due to pulmonary hypertension, 136f summary of, 122 Tricuspid regurgitation (TR), 119–121 with atrial fibrillation, 128f causes of, 120 carcinoid as, 120, 130f, 136f congenital, 120 Ebstein’s anomaly as, 120 endocarditis as, 120, 170f functional, 120 myxomatous disease as, 120 “organic,” 120 pacemakers as, 120 pulmonary hypertension as, 128f, 136f rheumatic, 120 RV papillary muscle rupture as, 120 trauma as, 120 tricuspid valve dysplasia as, 120 tricuspid valve prolapse as, 120 color Doppler flow mapping of, 119, 128f effective regurgitant orifice with, 120 imaging modalities for, 125b management of, 121, 123b M-mode echocardiography of, 129f in pericardial constriction, 390 proximal isovelocity surface area in, 119 RA pressure in, 120 reporting issues with, 119–120 retrograde hepatic venous systolic flow in, 119, 129f, 131f, 133f in right heart disease, 415, 432f, 435f R-R interval in, 128f RV systolic pressure in, 119–121, 132f and pulmonary hypertension, 120 and pulmonary stenosis, 120 RV-to-RA gradient in, 120 scanning issues with, 119 scanning notes for, 119 severity of, 119 spectral recording in, 119, 128f–129f, 132f–133f “trivial,”119 volume overload in, 129f, 131f Tricuspid stenosis (TS), 121 causes of, 121 tricuspid atresia as, 121 color Doppler imaging of, 130f concerns with, 121 imaging modalities for, 125b scanning issues with, 121 spectral profiles in, 130f summary of, 122

Tricuspid valve infective endocarditis of, 170f, 172f intracardiac echocardiography of, 371–372, 375f Tricuspid valve apparatus, anatomy of, 120 Tricuspid valve disease imaging modalities for assessment of, 125b utility of, 126t TEE of, 125b, 328, 332t–333t Tricuspid valve dysplasia, tricuspid regurgitation due to, 120 Tricuspid valve prolapse tricuspid regurgitation due to, 120 Tricuspid valve repair or replacement, 121, 123b Tricuspid valve vegetations, 170f TS. See Tricuspid stenosis (TS). TSI (tissue synchronization imaging), 302 TTE. See Transthoracic echocardiography (TTE). TVI (time velocity interval), in aortic insufficiency, 44 TVI (tissue velocity imaging) for dyssynchrony, 301–303, 311f for pacing lead placement, 304 Two-dimensional echocardiography for dyssynchrony, 300 for LV mass assessment, 174–175 of prosthetic valve infective endocarditis, 157 for proximal isovelocity surface area, 286 V V1 measurement, in aortic stenosis, 18, 33f V2 measurement in aortic stenosis, 19, 33f with aortic stenosis in atrial fibrillation, 34f and gradient issues, 20 R-R interval and, 34f type of probe and location of sampling in, 33f Valve ring abscess, due to infective endocarditis, 158 Valvular heart disease congenital, in adolescents and young adults, 6b–7b TEE of, 328 Valvular insufficiency grading of, 288, 290t due to infective endocarditis, 157 Valvular sequelae, of blunt cardiac trauma, 453 Vector velocity imaging, for intraventricular dyssynchrony, 303 Vegetations aortic valve, 355 limitations on identifying, 159 localization of, 159 marantic (noninfective), 158–159 mitral valve, 169f, 171f TEE of, 353, 356 notes on, 158–159 of prosthetic valve, 138 serial assessment of, 159 significance and size of, 159 TEE of, 167t, 169f–171f, 327 vs. TTE, 331t

Vegetations (Cont.) tricuspid valve, 170f, 327 TTE of, 167t, 169f vs. TEE, 331t Velocity ratio (VR) equation, for aortic stenosis, 19 Velocity time integral (VTI) in aortic insufficiency, 43 of LV outflow tract, for AV optimization, 304 Vena contracta, in proximal isovelocity surface area, 287 Vena contracta width in aortic insufficiency, 44 in mitral regurgitation, 97, 111f Ventricular assist device insertion percutaneous, 468–469 across aortic valve and into LVOT, 496f angulation of device in, 494f chest fluoroscopy and radiography images of, 493f, 496f color Doppler flow mapping in, 494f cons of, 469 with malpositioning, 495f, 497f, 499f for massive infarction due to left main thrombosis, 498f pros of, 469 rationale and role for, 468–469 reverberation artifact in, 497f sequence of, 469 serial imaging in, 499f systolic and diastolic scans in, 496f, 498f transesophageal, 469, 494f–495f, 497f, 499f transthoracic, 469, 497f surgical, 469 cons of, 469 malpositioning of, 500f pros of, 469 rationale and role of, 469 sequence of, 469 Ventricular interdependence in pericardial constriction, 389–390, 409f in pericardial tamponade, 388, 406f signs of, 389–390 Doppler, 390 early diastolic pressure dips as, 390 inspiratory fall in LV early diastolic inflow velocities as, 390 inspiratory septal shift as, 390 Ventricular myocardium, and mitral valve, 62 Ventricular pacemaker, stress echocardiography with, 224f Ventricular septal rupture, from acute myocardial infarction, 203–204, 209f Ventricular-ventricular (V-V) pacing, 305 Ventriculography, contrast, of mitral regurgitation echocardiographic assessment differing from, 91–92 Sellers grade in, 97 Ventriculoseptal defects (VSDs), due to stab wound, 458f VFR (volumetric flow rate), in proximal isovelocity surface area, 287 Viscous friction, and pressure drop across orifice, 253

Index Visual estimates, of LV volume, 177, 188f Volume overload, in tricuspid regurgitation, 129f, 131f Volumetric flow rate (VFR), in proximal isovelocity surface area, 287 Volumetric method for aortic insufficiency, 43 for mitral regurgitation, 90, 95–96 and angiographic grade, 110f equation for, 90–91 VR (velocity ratio) equation, for aortic stenosis, 19 VSDs (ventriculoseptal defects), due to stab wound, 458f VTI (velocity time integral) in aortic insufficiency, 43 of LV outflow tract, for AV optimization, 304

V-V (ventricular-ventricular) pacing, 305 V-waves, on pulmonary capillary wedge pressure tracing, and mitral regurgitation grading, 92 W Wall motion, regional, contrast echocardiography of, 271, 276f Wall motion abnormalities (WMAs) in acute myocardial infarction, 201, 208t echocardiographic view of, 202 apical five-chamber, 202 apical two-chamber, 202 parasternal long-axis, 202 parasternal short-axis, 202 in aortic stenosis, 22 and coronary blood flow, 201 mitral regurgitation due to, 92

523

Wall motion analysis, segmental, stress echocardiography for, 213 Wall motion score (WMS), 175 with acute myocardial infarction, 201 Wall motion score index (WMSI), 175 Wall thickening in aortic stenosis, 33f in cardiac amyloidosis, 229 stress echocardiography for, 213 WMAs. See Wall motion abnormalities (WMAs). WMS (wall motion score), 175 with acute myocardial infarction, 201 WMSI (wall motion score index), 175 Z Zoom views, of mitral regurgitation, 90

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