Cardiac CT Made Easy An Introduction to Cardiovascular Multidetector Computed Tomography [2 ed.] 9781482214239

Table of contents :
Front Cover
Contents
Foreword
Contributors
Part 1: Basics of Multidetector Computed Tomography (MDCT)
Chapter 1: Introduction to cardiovascular MDCT imaging
Chapter 2: CT perspective of normal cardiovascular anatomy
Chapter 3: Technical aspects of multi-detector row computed tomography
Part 2: Clinical Cardiovascular Applications
Chapter 4: Cardiac Chambers and Myocardial Disease
Chapter 5: Pericardial disease
Chapter 6: Valvular heart disease
Chapter 7: CT planning and guidance for transcatheter interventions
Chapter 8: Coronary arterial and venous disease
Chapter 9: Pulmonary circulation
Chapter 10: Aortic disease
Chapter 11: Peripheral artery disease
Chapter 12: Cardiac masses
Chapter 13: Adult congenital heart disease
References
List of Videos
Index
Back Cover

Citation preview

S ec ond E d i t i o n

Easy Made CT Cardiac An Introduction to Cardiovascular Multidetector Computed Tomography

S ec ond E d i t i o n

Easy Made CT Cardiac An Introduction to Cardiovascular Multidetector Computed Tomography Edited by

Paul Schoenhagen , MD

Cleveland Clinic, Cleveland, Ohio, USA

Carl J. Schultz , MD

Erasmus Medical Center, Rotterdam, The Netherlands Royal Perth Hospital and School of Medicine and Pharmacology University of Western Australia, Perth, Western Australia

Sandra S. Halliburton , MD

Cleveland Clinic, Cleveland, Ohio, USA

Boca Raton London New York

CRC Press is an imprint of the Taylor & Francis Group, an informa business

CRC Press Taylor & Francis Group 6000 Broken Sound Parkway NW, Suite 300 Boca Raton, FL 33487-2742 © 2014 by Taylor & Francis Group, LLC CRC Press is an imprint of Taylor & Francis Group, an Informa business No claim to original U.S. Government works Version Date: 20140108 International Standard Book Number-13: 978-1-4822-1423-9 (eBook - PDF) This book contains information obtained from authentic and highly regarded sources. While all reasonable efforts have been made to publish reliable data and information, neither the author[s] nor the publisher can accept any legal responsibility or liability for any errors or omissions that may be made. The publishers wish to make clear that any views or opinions expressed in this book by individual editors, authors or contributors are personal to them and do not necessarily reflect the views/opinions of the publishers. The information or guidance contained in this book is intended for use by medical, scientific or health-care professionals and is provided strictly as a supplement to the medical or other professional’s own judgement, their knowledge of the patient’s medical history, relevant manufacturer’s instructions and the appropriate best practice guidelines. Because of the rapid advances in medical science, any information or advice on dosages, procedures or diagnoses should be independently verified. The reader is strongly urged to consult the drug companies’ printed instructions, and their websites, before administering any of the drugs recommended in this book. This book does not indicate whether a particular treatment is appropriate or suitable for a particular individual. Ultimately it is the sole responsibility of the medical professional to make his or her own professional judgements, so as to advise and treat patients appropriately. The authors and publishers have also attempted to trace the copyright holders of all material reproduced in this publication and apologize to copyright holders if permission to publish in this form has not been obtained. If any copyright material has not been acknowledged please write and let us know so we may rectify in any future reprint. Except as permitted under U.S. Copyright Law, no part of this book may be reprinted, reproduced, transmitted, or utilized in any form by any electronic, mechanical, or other means, now known or hereafter invented, including photocopying, microfilming, and recording, or in any information storage or retrieval system, without written permission from the publishers. For permission to photocopy or use material electronically from this work, please access www.copyright.com (http://www.copyright.com/) or contact the Copyright Clearance Center, Inc. (CCC), 222 Rosewood Drive, Danvers, MA 01923, 978-750-8400. CCC is a not-for-profit organization that provides licenses and registration for a variety of users. For organizations that have been granted a photocopy license by the CCC, a separate system of payment has been arranged. Trademark Notice: Product or corporate names may be trademarks or registered trademarks, and are used only for identification and explanation without intent to infringe. Visit the Taylor & Francis Web site at http://www.taylorandfrancis.com and the CRC Press Web site at http://www.crcpress.com

Contents

Foreword ix Contributors xi

Part 1 Basics of Multidetector Computed Tomography (MDCT) 1.

Introduction to cardiovascular MDCT imaging

3

2.

CT perspective of normal cardiovascular anatomy

7

2.1 Cardiac chambers

7

2.2 Central venous and pulmonary venous return

8

3.

2.3 Pulmonary artery

10

2.4 Aorta

11

2.4.1 Aortic root

11

2.4.2 Aorta

18

2.5 Coronary arteries

19

2.6 Extracardiac structures: lungs and mediastinum

20

Technical aspects of multi-detector row computed tomography

29

3.1 Data acquisition

29

3.1.1 Current CT systems

29

3.1.2 ECG referencing

30

v

vi Contents

3.1.3 Acquisition mode

31

3.1.4 Tube current modulation

32

3.1.5 Special image reconstruction techniques to improve temporal resolution

32

3.1.6 Radiation exposure

34

3.1.7 Contrast media

34

3.1.8 Control of heart rate: beta-blocker

37

3.1.9 Control of vessel tone: nitroglycerine

37

3.1.10 Imaging protocols

37

3.2 Image reformation and interpretation

37

3.2.1 Axial CT images

38

3.2.2 Image artifacts

45

Part 2  Clinical Cardiovascular Applications 4.

Cardiac chambers and myocardial disease

53

4.1 Cardiomyopathies

54

4.1.1 Non-ischemic cardiomyopathies

54

4.1.2 Ischemic cardiomyopathy

65

4.2 Other cardiac and myocardial conditions 4.2.1 Myocarditis

67 67

4.2.2 Non-ischemic atrial and ventricular aneurysms and diverticula 69

5. 6. 7. 8.

4.2.3 Atrial and ventricular thrombus formation

70

4.2.4 Lipomatous hypertrophy Pericardial disease Valvular heart disease CT planning and guidance for transcatheter interventions Coronary arterial and venous disease

71 85 103 123 141

8.1 Coronary artery disease

145

8.1.1 Atherosclerotic coronary artery disease 8.2 Myocardial stress/rest perfusion

145 164

8.2.1 Static and dynamic CT perfusion imaging

164

8.2.2 Artifacts in CT myocardial perfusion imaging

166

Contents  vii

8.2.3 CT myocardial perfusion protocols

166

8.2.4 Interpretation of CT myocardial perfusion studies

172

8.2.5 Systematic evaluation of perfusion

173

8.2.6 Quantitation of perfusion findings

175

8.3 Coronary veins and coronary sinus 8.3.1 Other applications 9.

10.

182 185

Pulmonary circulation

197

9.1 Pulmonary artery

197

9.2 Pulmonary veins

197

Aortic disease

205

10.1 Acute aortic syndromes

205

10.1.1 Definition

205

10.1.2 Morphologic classification

207

10.1.3 Location and extent

209

10.1.4 Diagnostic consideration

210

10.1.5 Differential diagnosis (triple rule-out)

212

10.1.6 Therapeutic implications

213

10.2 Aortic aneurysmal disease

215

10.3 Endovascular stent graft

216

10.4 Aortic surgery

218

10.5 Non-aortic pre-operative imaging

219

10.6 Other conditions

220

Peripheral artery disease

277

11.1 Lower-extremity CT angiography

277

12.

Cardiac masses

283

13.

Adult congenital heart disease

297

13.1 Cardiac chambers and myocardium

297

13.2 Pericardial disease

299

13.3 Valvular heart disease

299

13.4 Coronary arteries

301

13.5 Coronary veins and coronary sinus

304

13.6 Pulmonary veins

305

11.

viii Contents

13.7 Aortic disease

305

13.8 Arteriovenous shunt defects

317

References

323

List of Videos

357

Index 361

Foreword

Computed tomography has established itself as a novel diagnostic technique for cardiovascular disease. The constant improvements in temporal and spatial resolution of computed tomography systems permit increasingly stable imaging of the rapidly moving heart, and as a result of these improvements the number of clinical indications for cardiac computed tomography is increasing. Indications have expanded from prevention (where coronary calcium imaging is complemented by advanced analysis of plaque morphology and composition) to modern interventional treatment of cardiac disease; for example, detailed computed tomographic imaging is one of the major contributors to the success of transcatheter aortic valve implantation (TAVI). Based on the tremendous developments that we have witnessed in recent years, it can be expected that computed tomography will continue to expand its role in the work-up and management of cardiovascular disease, and everyone involved in the diagnosis and treatment of heart disease should take advantage of these new imaging capabilities. Cardiac computed tomography requires specialist knowledge. Cardiologists need to familiarize themselves with computed tomography technology, image interpretation tools, typical findings and artifacts, while radiologists need deeper insight in cardiac anatomy, function, and pathophysiology than ever before. The second edition of Cardiac CT Made Easy is therefore published just at the right time. Along with the basic information everyone should know, and new and recent techniques, the applications of cardiac computed tomography are thoroughly explained and put in a clinical context. With a clear structure, well-written text, and a large number of impressive illustrations, this book will be a very useful resource for all those new to the field, and a trustworthy reference for those who have been involved for a while but would like to update their knowledge or are looking for a resource to turn to for very specific questions.

ix

x Foreword

The second edition of Cardiac CT Made Easy will certainly help to optimize the utilization of cardiac computed tomography and to improve the care of patients with known or suspected heart disease. I would like to thank the editors and authors for creating a very comprehensive book that will certainly be appreciated by a wide range of readers worldwide. Stephan Achenbach, MD, FACC, FESC, FSCCT Professor of Medicine University of Erlangen Germany

Contributors

Paul Schoenhagen MD Imaging Institute and Heart & Vascular Institute Cleveland Clinic Cleveland, Ohio

Stephan Achenbach MD University of Erlangen Erlangen, Germany Dominik Fleischmann MD Department of Radiology Stanford University Stanford, California

Carl J Schultz MD Department of Cardiology Erasmus MC Rotterdam, Netherlands and Royal Perth Hospital and School of Medicine and Pharmacology University of Western Australia Perth, Western Australia

Sandra S Halliburton PhD Imaging Institute and Heart and Vascular Institute Cleveland Clinic Cleveland, Ohio Kheng-Thye Ho MD Heart Consultants Pte Ltd Mount Alvernia Hospital Singapore

Zhaoqi Zhang MD Department of Radiology Beijing Anzhen Hospital Capital Medical University Beijing, China

Xiaohai Ma MD, PhD Department of Radiology Beijing Anzhen Hospital Capital Medical University Beijing, China

xi

Part 1 Basics of Multidetector Computed Tomography (MDCT)

Chapter 1

Introduction to cardiovascular MDCT imaging

The diagnostic use of computed tomography (CT) is based on seminal developments in the field of physics during the 1970s.1–3 Since then CT has matured into an established diagnostic modality in the evaluation of cardiovascular disease. The diagnostic spectrum includes routine indications such as the assessment of aortic, pulmonary, and coronary vascular disease, as well as novel applications, for example the evaluation in the context of minimally invasive cardiothoracic surgery and transcatheter interventions.4–6 Based on the Atlas and Manual of Cardiovascular Multidetector Computed Tomography (2005), the first edition of this “Made Easy” book was published in 2006, and was updated in an electronic version in 2008. Since the first publication, cardiovascular CT imaging has witnessed an exponential increase in use.7,8 This revised and updated edition of Cardiac CT Made Easy captures these advances in CT scanner technology and clinical experience. Combining the experience of leading cardiovascular imaging groups in North America, Europe, and Asia, this edition focuses on appropriate use and impact on clinical outcome. The book maintains its character as an easy, understandable introduction to cardiovascular CT imaging. It describes the principles of multidetector computed tomography (MDCT) for cardiovascular applications, practical aspects of scan acquisition and interpretation, clinical indications and imaging protocols, and clinical findings of common cardiovascular disease conditions. The comparison with other imaging modalities such as conventional angiography, intravascular ultrasound, magnetic resonance imaging, and echocardiography allows understanding of the strength and limitations of CT in the assessment of specific clinical questions. The text is illustrated by a large number of selected images, highlighting key findings. These images have been extensively revised and expanded, reflecting the transition to “post-64” slice scanners and advanced software.9,10

3

4

Cardiac CT Made Easy

Cardiovascular CT imaging is complementary to standard X-ray-based planar imaging. Planar imaging modalities, including the chest X-ray and conventional angiographic techniques, project three-dimensional structures onto a two-dimensional image plane. The image reflects the X-ray attenuation of all the structures between the X-ray tube and detector, limiting the differentiation of individual structures and understanding of the three-dimensional relationship. In contrast, the basic concept of CT is the reconstruction of a thin image slice from multiple projections obtained by rotating an X-ray source and detector system around the patient. In the resulting tomographic image individual structures are differentiated by different image intensities. The acquired slices from the entire covered scan range (z-coverage) are combined into a three-dimensional volume, which can be reconstructed along unlimited oblique planes following the data acquisition using a dedicated workstation (Figure 1.1). The advantages of tomographic CT imaging are partially offset by the lower temporal resolution or longer time required to obtain data (Figure  1.2). The temporal resolution is less relevant for the imaging of large static organs (e.g. the liver or kidney) and organs where motion can temporarily be suspended (e.g. lungs).

Figure 1.1  Planar versus tomographic imaging The center panel of this figure shows a 3-D volume-rendered CT image of the chest. The panels on the left and right show planar and tomographic images, respectively. The standard chest X-ray (upper left panel) is a planar projection of the cardiac chambers. The intra-arterial injection of contrast material during coronary angiography selectively enhances the coronary arteries (lower left panel). However, similar to the chest X-ray, the angiogram is a planar image, projecting the silhouette of the contrast-filled coronary artery lumen. The tomographic CT images of the cardiac chambers (right upper panel) and of a coronary artery (right lower panel) allow the visualization of details not seen with planar imaging.



Introduction to cardiovascular MDCT imaging 5

Figure 1.2  Image acquisition time, acquisition window As demonstrated by the vertical bars in the upper part of the figure, cine-angiography acquires multiple image frames in one cardiac cycle. The time needed to acquire an individual planar image frame during cine-angiography is about 10 ms, allowing real-time imaging. In contrast, as shown in the lower part of the figure, the acquisition time for CT images is longer and is timed during late diastole of consecutive cardiac cycles. Minimal temporal resolution with multi-detector scanners is 135 ms (single source) and 75 ms (dual source).

However, because of the rapid, constant motion of the heart during the cardiac cycle, long acquisition times increase cardiac motion artifact (image blurring). The development of dedicated cardiovascular CT systems therefore required optimized acquisition times and synchronization of imaging acquisition with the cardiac cycle. Initial cardiovascular CT systems used electron-beam computed technology (EBCT). A rapidly oscillating X-ray beam was reflected onto a stationary tungsten target ring, encircling the patient. By eliminating the need to rotate the X-ray source mechanically around the patient, EBCT scanners were characterized by high temporal resolution.11 However, these scanners have been almost completely replaced by multi-detector systems (MDCT). In MDCT systems, the gantry (X-ray tube and detector) rotates rapidly around the patient. Initial single-detector CT systems, introduced in 1972 for body imaging, were limited by very slow rotation and long acquisition time. Fast gantry rotation, thin collimated detector rows, ECG-synchronized imaging, and acquisition of multiple slices per gantry rotation have since allowed the development of modern cardiovascular systems.12–14 Multi-slice scanners with 8, 16, 64, 256, and 320 slice acquisitions per rotation were introduced over the last decade.15–26

6

Cardiac CT Made Easy

Figure 1.3  Multi-detector CT technology (MDCT) This figure shows a second-generation dual-source scanner, photographed from the “control room.” Modern systems acquire up to 320 slices per rotation, with a minimum slice thickness below 0.75 mm, and spatial resolution about 0.5 mm.

Dual-source scanners, with two X-ray tubes/detector systems, were introduced in 2008, and allowed a 50% reduction in temporal resolution.27,28 Today, high-end scanners permit rotation times as low as 270 ms, with resulting temporal resolution of 135 ms (single source) and 75 ms (dual source). Modern systems acquire data with a minimum collimated detector row width of 0.5 or 0.625 mm, resulting in isotropic spatial resolution of around 0.5 × 0.5 × 0.5 mm (Figure 1.3). The following chapters describe technical aspects of CT scan acquisition and evaluation, normal anatomy, and pathologic findings with MDCT in a variety of clinical conditions.

Chapter 2

CT perspective of normal cardiovascular anatomy

Because of the oblique orientation of the cardiovascular structures in the chest, cardiovascular imaging depends on reconstructions of defined image planes ­ oblique to the body axes (z-axis), well known from echocardiography.29 With two-­ dimensional imaging modalities (e.g. standard echocardiography, most magnetic resonance sequences, and standard angiography), these image planes are obtained at the time of image acquisition. For 3-D modalities (computed tomography, 3-D echocardiography, 3-D MRI sequences, and rotational angiography) a 3-D data volume is acquired and oblique planes are reconstructed at the time of image analysis. The following paragraphs and the accompanying images introduce the most common reconstructed planes used to visualize cardiac structures.

2.1  Cardiac Chambers

The left and right cardiac chambers are typically visualized in two-chamber, threechamber, four-chamber, and short-axis views (Figure 2.1). • The two-chamber view of the left ventricle (LV) is comparable to the right anterior oblique (RAO) ventriculogram performed during angiography (Figure 2.2). In contrast to angiography, computed tomography (CT) (also magnetic resonance imaging and echocardiography) visualizes both the contrast-filled ventricular cavity and the myocardial wall. • The three-chamber view includes the left atrium (LA), left ventricle, and aortic root. It visualizes the relationship between the LV, mitral valve, and  left ventricular outflow tract (LVOT). It is also the basis to reconstruct additional images of the aortic root (Figure 2.3).

7

8

Cardiac CT Made Easy

Figure 2.1  Standard views of the cardiac chambers Standard planes for visualization of the cardiac chamber are two-chamber (left upper panel), three-chamber (right lower panel), four-chamber (left lower panel), and short-axis (right upper panel) views. (Video 2.1)

• The four-chamber view allows simultaneous assessment of the left and right ventricles (LV and RV), the atria (LA and RA), and the atrioventricular valves (mitral and tricuspid valves) (Figures 2.4 and 2.5). • Quantification of left and right ventricular function is possible if data are acquired throughout the entire cardiac cycle (retrospective gating) and reconstructed at end-diastole and end-systole (Figures 2.6 and 2.7).30–33

2.2  Central Venous and Pulmonary Venous Return

• Venous return from the upper and lower part of the body drains via the superior (SVC) and inferior (IVC) vena cava into the right atrium (RA) (Figure  2.8). The SVC and IVC extend in a cranial-caudal orientation.



CT perspective of normal cardiovascular anatomy 9

Figure 2.2  Two-chamber view The two-chamber view is comparable to the left ventriculogram in the RAO projection, p­ erformed during angiography. The CT two-chamber view of the left ventricle (lower panel) visualizes both the contrast-filled ventricular cavity and the myocardial wall.

Therefore, simple review of the axial images provides near cross-sectional images, frequently without need for additional 3-D reconstructions. • In addition, the coronary venous blood flow drains via the coronary sinus into the right atrium (Figure 2.9). It originates at the inferior-medial aspect of the right atrium, and bifurcates into branches extending parallel to the coronary arteries. The largest branch lies inferior to the left atrium, and then extends as the great cardiac vein along the left AV groove (along the left circumflex (LCX)) to the anterior interventricular groove (parallel to the left anterior descending (LAD)). • Venous return from the lungs drains via the pulmonary veins into the left atrium. The veins are oriented horizontally. Each lung lobe has separate drainage, which merge centrally. Therefore there are typically two left (the left lingua/middle lobe is a branch of the left superior vein and not infrequently there is a common antrum or stem of the left veins) and two right (the right middle lobe vein is typically a branch of the right superior vein or drains separately into the LA) veins entering the left atrium. Initial review in axial and sagittal images provides a good overview. If necessary, dedicated reconstructions along individual veins can be obtained and also visualized with volume-rendered images (VRIs) (Figures 2.10 and 2.11).

10 Cardiac CT Made Easy

Figure 2.3  Three-chamber view This figure shows a typical three-chamber view in the left upper panel and a two-chamber view in the right lower panel. The cross-sectional images (short-axis view) show the mitral valve in diastole (right upper panel) and systole (left lower panel). The three-chamber view shows the normal relationship of the LV, LA, mitral annulus, mitral valve, LVOT, and aortic valve. The three-chamber view is the basis to reconstruct additional images of the aortic root.

2.3  Pulmonary artery

The right ventricle connects via the right ventricular outflow tract (RVOT) with the pulmonary artery (PA). The pulmonary valve lies at the transition between the RVOT and PA. The normal pulmonary valve is typically not well seen due to the thin, mobile leaflets. The central pulmonary artery bifurcates into the right and left main vessels before further branching in the lungs (Figures 2.12 and 2.13). Depending on the timing of the contrast bolus, the vascular tree with smaller segmental and subsegmental branches is visualized.



CT perspective of normal cardiovascular anatomy 11

Figure 2.4  Four-chamber view The four-chamber view (center panels) allows simultaneous assessment of left and right ventricles, atria, and atrioventricular valves (mitral and tricuspid valves). If the CT images are acquired in different phases of the cardiac cycle (retrospective gating), data reconstruction allows display of systolic and diastolic images for functional analysis. Systolic (upper panels) and diastolic (lower panels) reconstructions of the LV are shown. The two-chamber view is shown on the left, the fourchamber view in the middle, and the short-axis view on the right. The LV cavity is automatically segmented and highlighted in color. The middle panel on the left shows the LV endocardial and epicardial borders. Combining several reconstructions along the cardiac cycle, functional cineloops can be created.

2.4 Aorta 2.4.1 Aortic root

The aortic root is a transition zone between the left ventricular outflow tract (LVOT) and tubular ascending aorta (Figures 2.14–2.19). • The anatomic transition between the LVOT (Figure 2.14) and root is the crown-shaped insertion of the aortic valve leaflets. By imaging, the aortic annulus is defined by the lowest insertion point of the aortic valve leaflets (Figures 2.15 and 2.16). Precise measurement of the minimal and maximal diameter, circumference, and area is critically important for the evaluation in the context of transcatheter aortic valve replacement (TAVR).

12 Cardiac CT Made Easy

Figure 2.5  LV volume rendering The LV including systolic and diastolic frames can also be displayed in advanced 3-D images, fusing representations of the LV cavity and myocardium with tomographic images (systolic and diastolic frames are shown in the upper and lower panels).

Figure 2.6  Assessment of LV function Semi-automated planimetry allows calculation of ejection fraction, LV volumes, and myocardial mass, as demonstrated in this figure. The results are summarized in table format for subsequent reporting. (Video 2.6)



CT perspective of normal cardiovascular anatomy 13

Figure 2.7  Assessment of RV function Similarly, RV function can be evaluated. Because of the more complex shape of the RV and depending on contrast enhancement, volumetric assessment is more challenging.

Figure 2.8  Central venous return—SVC and IVC The superior and inferior vena cava drain into the right atrium. Because the SVC and IVC extend in a cranial-caudal orientation, review of the axial images provides near cross-sectional images, frequently without need for additional 3-D reconstructions. This figure shows axial images at several levels in the SVC and IVC and the location in a sagittal image.

14 Cardiac CT Made Easy

Figure 2.9  Coronary sinus The coronary sinus (#) drains the coronary flow into the right atrium. This figure shows the close relationship to the left atrium.

Figure 2.10  Pulmonary veins Venous return from the lungs drains via the pulmonary veins into the left atrium. The upper left and upper middle panels show axial and sagittal images with the cross-hair centered on the left superior vein. In the upper right panel, the planes are tilted through the left upper and lower veins, resulting in an oblique axial image showing both veins (lower middle panel). The lower right panel shows a volume-rendered image of the pulmonary veins.



CT perspective of normal cardiovascular anatomy 15

Figure 2.11  Pulmonary veins This figure shows the right pulmonary veins in a curved MPR (upper panel) and volume-rendered images (lower panel). In the right lower image, the contrast volume is subtracted, giving a view inside the left atrium.

Figure 2.12  Pulmonary artery The pulmonary valve lies at the transition between the RVOT and PA. The central p­ ulmonary artery bifurcates into the right and left main vessels before further branching in the lungs. This figure shows axial (upper left and upper middle) and sagittal (upper right) images of the ­central pulmonary artery. In the lower panels, oblique images are reconstructed at the level of the ­pulmonary valve.

16 Cardiac CT Made Easy

Figure 2.13  Pulmonary artery Depending on the timing of the contrast bolus, the vascular tree with smaller segmental and subsegmental branches can be visualized. This is shown in the volume-rendered images (lower panels).

Figure 2.14  Aortic root, LVOT As shown in this figure, the base of the anterior mitral valve leaflet is continuous with the left ventricular outflow tract (LVOT) and aortic root. The cross-hair in the right panel demonstrates the location of the cross-sectional reconstruction (left panel).



CT perspective of normal cardiovascular anatomy 17

Figure 2.15  Aortic root, aortic annulus The transition between the LVOT and root is the aortic annulus. The annulus anatomically has the shape of a crown. By imaging, the annular plane is defined by the lowest insertion point of the aortic valves.

• At the aortic valve, the left, right, and non-coronary cusp can be differentiated. In retrospective gated studies, images can be reconstructed with the valve open (systole) and closed (diastole) and opening area can be assessed (Figure 2.17). • Beyond the aortic valve level, there is mild physiologic bulging in the area of the sinuses of Valsalva (Figure 2.18). The sinuses correspond to the three aortic valve cusps including the non-coronary cusp (the cusp ­originating between left and right atria), and the right and left coronary cusps with the origin of the corresponding coronary arteries (Figure 2.19). • The segment between the sinuses of Valsalva and ascending aorta is called the sinotubular junction (STJ) and typically causes a mild waist.

18 Cardiac CT Made Easy

Figure 2.16  Aortic annulus Precise measurement of the aortic annulus with minimal and maximal diameters, circumference, and area is critically important for the evaluation in the context of TAVR.

2.4.2 Aorta

The anatomy of the tubular aorta is reconstructed along the centerline of the vessel, with longitudinal and cross-sectional images. This can be done by manual reconstruction or semi-automated centerline reconstructions (Figures  2.20 and 2.21). The aorta is divided into several segments. Beyond the aortic root, these segments include: • The ascending aorta • The aortic arch with the ostia of the arch branch vessels (Figure 2.20) • The descending aorta



CT perspective of normal cardiovascular anatomy 19

Figure 2.17  Aortic root, aortic valve This figure shows reconstructions of the aortic root at the aortic valve level. Cross-sectional images are reconstructed in systole (right upper panel) and diastole (left lower panel). The crosshairs in the left upper and right lower panels demonstrate the location of the cross-sectional reconstruction. (Videos 2.17-i, 2.17-ii)

• The juxtarenal aorta with the origin of the arch branch vessels • The infrarenal aorta and the iliac arteries

2.5  Coronary Arteries

The standard display of coronary anatomy with conventional angiography includes views described by the position of the X-ray tube in relation to the patient. Standard views are, for example right anterior oblique (RAO 20), left anterior oblique (LAO 60),

20 Cardiac CT Made Easy

Figure 2.18  Aortic root, diameter measurement at the sinuses of Valsalva This figure shows diameter measurements of the aortic root at the level of the sinuses of Valsalva.

cranial, caudal, etc. Volume-rendered images allow visualization of the course of the coronary arteries in relation to the underlying cardiac chambers corresponding to the angiographic planes (Figure 2.22). These images allow initial orientation and can also be visualized in virtual angiographic appearance (Figure 2.23). Further evaluation is performed along individual segments or entire arteries using multi-planar reformation (MPR) and maximum intensity projection (MIP). This can be achieved with manual reconstruction and semi-automated centerline reconstructions (Figures 2.24 and 2.25).

2.6 Extracardiac Structures: Lungs and Mediastinum

The extracardiac structures are part of the CT acquisition volume, and in c­ ontrast to echocardiography and angiography, the acquired images are diagnostic.



CT perspective of normal cardiovascular anatomy 21

Figure 2.19  Aortic root, coronary ostia Reconstruction of the aortic root also allows identifying the origin of the coronary arteries relative to the cusps of the aortic root.

Figure 2.20  Aorta The anatomy of the tubular aorta is reconstructed along the centerline of the vessel, with longitudinal and cross-sectional images. This can be done by manual reconstruction (left panels) or semi-­automated centerline reconstructions (right panels). The origin of the arch branch vessels is identified. (Video 2.20)

22 Cardiac CT Made Easy

Figure 2.21  Aorta, cross-sectional and distance measurements The reconstructed cross-sectional images allow manual or semi-automated diameter and area measurements. Additional length measurements can be performed.



CT perspective of normal cardiovascular anatomy 23

Figure 2.22  Coronary arteries, volume-rendered images (VRIs) of coronary arteries This figure shows volume-rendered images (VRIs) of the heart corresponding to a LAO 60 view (right panel). Left main coronary artery (green), left anterior descending coronary artery (red), left circumflex coronary artery (blue), and right coronary artery (yellow). (Video 2.22)

Figure 2.23  VRI, virtual angiographic images Volume-rendered images allow visualization of the course of the coronary arteries in relation to the underlying cardiac chambers corresponding to the angiographic planes. These images allow initial orientation and can also be visualized in virtual angiographic appearance, as shown in this figure.

24 Cardiac CT Made Easy

Figure 2.24  Segmental coronary visualization with CT While volume-rendered images allow showing the course of the coronary arteries in relation to the underlying cardiac chambers corresponding to the angiographic planes, they do not allow detailed assessment of the complex coronary anatomy. This is achieved with dedicated coronary reconstruction along individual segments of the coronary arteries in multiple MPR and MIP images, as shown in this figure.

Therefore careful review is part of CT analysis and reporting. While a discussion of these structures is beyond the focus of this book, examples of lung images are shown (Figures  2.26–2.28) Modern software increasingly allows semi-­ automated, computer-aided analysis, e.g. quantifying emphysematous lung tissue (Figure 2.28).



CT perspective of normal cardiovascular anatomy 25

Figure 2.25  LAD This figure shows a dedicated coronary reconstruction of the LAD with manual (left panels), semi-automated, and centerline-based (middle panel) reconstructions, and volume-rendered images (right panel).

Figure 2.26  Extracardiac findings The extracardiac structures are part of the CT acquisition volume, and in contrast to echocardiography and angiography, the images are typically diagnostic. This figure shows a cross-sectional image with a soft tissue window (left upper panel) and lung window. The lower panels show volume-rendered images.

26 Cardiac CT Made Easy

Figure 2.27  Extracardiac findings: lungs This figure shows additional semi-automated images’ analysis of the lung window (lower panel). The left and right lung are segmented and the arterial tree highlighted in red.



CT perspective of normal cardiovascular anatomy 27

Figure 2.28  Extracardiac findings: lung parenchyma This figure shows further analysis of the lung tissue. Specifically, emphysematous tissue is highlighted in blue and quantified.

Chapter 3

Technical aspects of multi-detector row computed tomography

3.1 Data Acquisition 3.1.1  Current CT systems

As described previously, technical advances over the past decade have allowed the development of CT systems suitable for cardiovascular imaging. However, important limitations remain, which are related to the following requirements of cardiovascular imaging: 1. High temporal resolution to avoid cardiac motion artifacts 2. High, isotropic (identical in-plane and through-plane) spatial resolution to visualize small anatomy detail even on oblique reformats 3. Fast volume coverage during one breath-hold period to avoid respiratory motion artifacts 4. ECG synchronization of data acquisition or reconstruction to avoid cardiac motion artifacts Scanners capable of ECG-synchronized scanning and 64 or more slices/rotation are recommended for cardiovascular imaging.34 Temporal resolution depends on the gantry rotation time (270–350 ms) and the number of X-ray sources (1 or 2). It ranges from 75 to 175 ms for scanners with 64 or more slices. These systems achieve an isotropic spatial resolution of 0.5 × 0.5 × 0.5 mm9 (Figure 3.1). The number of detector rows determines the volume covered in a single rotation. Most scanners cover between 20 and 80 mm per rotation. Coverage of the entire heart in one rotation is only possible with one scanner type, a 320-slice scanner that permits 160 mm of coverage per rotation.

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Figure 3.1  Current scanner systems Modern CT systems with high spatial and temporal resolution allow imaging of the coronary arteries, which is particularly challenging because of their small size, rapid motion, and tortuosity. This figure shows images of the coronary arteries acquired with a dual-source scanner with a temporal resolution of 75 ms. The volume-rendered images show the left and right coronary arteries. The curved MPR shows the left anterior descending (LAD).

3.1.2 ECG referencing

The rapid, constant motion of the heart causes significant image artifact. Cardiac motion varies throughout the cardiac cycle, with minimal motion in diastole (about 75% RR interval). A second window with limited motion is found in end-systole (about 35% RR interval). If motion-free images of the heart, aortic root, and ­ascending aorta are required, it is important to synchronize data acquisition or reconstruction to the cardiac cycle. Synchronization of data is also a prerequisite to combine data acquired from consecutive gantry rotations in volumetric data sets, without “­misalignment ­artifact” (Figures 3.16 and 3.17). Synchronization is based on observation of the ECG signal. The time between two consecutive heartbeats is described by the RR interval (the interval between consecutive R waves of the ECG, which is 1000 ms for a heart rate of 60 beats per minute (bpm)).



Technical aspects of multi-detector row computed tomography 31

The ECG signal is used to either prospectively trigger data ­acquisition or retrospectively gate data reconstruction to a certain phase of the cardiac cycle. The starting position of the data acquisition or reconstruction ­window is chosen in relation to the R wave of the ECG signal, typically using a ­relative delay value, which is defined as a given percentage of the RR interval. For morphologic evaluation, data are usually selected from the diastolic phase of the cardiac cycle where heart motion is minimal, using a relative delay of 75% of the RR interval. However, the precise phase with minimal motion is patient, scanner, and heart rate dependent, and should be optimized to ensure maximum image quality.35,36 In addition, several reconstructions may be necessary, because different structures may reach minimal motion in slightly different phases of the cardiac cycle (e.g. left versus right coronary artery (RCA)). Importantly, data can also be chosen from multiple phases throughout the cardiac cycle for functional evaluation. 3.1.3 Acquisition mode 3.1.3.1  Sequential (axial) mode

Early mechanical CT systems required the gantry to return to its initial position after each image slice acquisition. Individual transaxial image slices were acquired, followed by incremental advancement of the patient table and repeated image acquisition at the next level (the “step and shoot” mode). Modern multi-detector computed tomography (MDCT) scanners can be operated in this sequential mode, but with continuous gantry rotation and acquisition of multiple slices per table position. For these cardiovascular sequential protocols, data acquisition is prospectively triggered by the ECG signal, typically in late diastole. The main advantage of the sequential mode is lower radiation dose, because X-ray exposure occurs only during the prospectively triggered cardiac phase rather than throughout the entire cardiac cycle (X-ray source is turned on and off). Because image reconstruction is restricted to a single or a few phases of the cardiac cycle, this acquisition allows only limited correction in case of motion artifact. For these reasons, the prospective ECG-triggered sequential mode is reserved for patients with regular and low heart rates (typically 50% stenosis. In addition patency of the native left internal mammary artery was demonstrated (lower panel).



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Figure 8.56  Coronary assessment in patient with relative contraindication for cardiac catheterization, aortic dissection A patient presented with a type A aortic dissection and a recent stroke. Because of the type A ­dissection conventional cardiac catheterization was deemed high risk and a CT angiogram was performed. This figure shows the dissection flap in the aortic root. The maximum diameter of the mid ascending thoracic aorta was 5.1 cm. The coronary arteries originate from the true lumen.

Figure 8.57  Coronary assessment in patient with contraindication for cardiac catheterization, aortic dissection The coronary arteries originate from the true lumen. There is partially calcified atherosclerotic plaque of all three coronary arteries, which is likely associated with at least moderate stenosis.

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Figure 8.58  Coronary ectasia This figure shows angiographic and CT images of a patient with a history of CAD and previous myocardial infarction. Both angiogram and CTA show ectasia of the proximal LAD consistent with mild aneurysm formation. There is calcification of the arterial wall.

8.2.6.3  Differentiating fixed from reversible defects

In order to determine whether a perfusion defect that is detected during stress is reversible or fixed (Figure 8.75), it is necessary to compare its MBF to the flow in healthy myocardium at rest. If the defect is also present at rest, i.e. its MBF is less than that of normal tissue at rest, it is considered a fixed defect. If the defect resolves at rest, i.e. has the same MBF as normal tissue, it is considered reversible. 8.3  Coronary Veins and Coronary Sinus

Because of the peripheral intravenous rather than selective arterial contrast injection, the coronary sinus and coronary veins are typically slightly contrast enhanced on CT images.312–314 Segments of the coronary veins are parallel to the course of the coronary arteries and can therefore be mistaken for coronary arteries. If the venous structures are



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Figure 8.59  Coronary ectasia The images in this figure show a diffuse pattern of coronary ectasia, most notably involving the distal left main. The left main artery gives rise to a mildly ectatic left anterior descending coronary artery and a diminutive circumflex coronary artery. There is ectasia of the right coronary artery. No definite evidence of atherosclerotic changes of the coronary arteries is noted.

Figure 8.60  Coronary ectasia The MPR image shows the ectatic left main coronary artery (left panel) with the origins of the ectatic LAD (right upper panel) and diminutive LCX (right lower panel).

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Figure 8.61  Left anterior descending coronary aneurysm This figure shows a focal aneurysm of the proximal LAD with extensive calcification of the aneurysm wall.

Figure 8.62  Left anterior descending coronary aneurysm MPR image showing the calcified wall of the aneurysm and the small amount of adherent wall thrombus inside the aneurysm.



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Figure 8.63  Left circumflex coronary aneurysm An example of a focal aneurysm of the left circumflex (LCX) coronary artery is shown in these four axial images (cranial to caudal). There is calcification of the LCX proximal to the aneurysm and a moderate amount of adherent wall thrombus inside the aneurysm.

the primary focus of the examination, slightly different contrast timing or multi-phasic imaging is often performed (Figures 8.76–8.78). An emerging clinical question is assessment of the coronary sinus anatomy for the placement of biventricular pacer leads. 8.3.1 Other applications

• Issues of cost-effectiveness have recently been examined.315–317 • Guidelines for interpreting and reporting have been described.318 Coronary fistulas can be visualized with CT.292,293 Coronary anomalies are described in Chapter 13, Section 13.4. The potential value of CT in assessing perfusion defects associated with severe luminal stenosis is discussed in the following paragraphs.294–311

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Figure 8.64  Left main coronary aneurysm Non-atherosclerotic aneurysmal disease is also seen with inflammatory diseases. This figure shows a large left main coronary artery aneurysm in a patient with a history of Kawasaki disease. (Video 8.64)



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Figure 8.65  LAD aneurysm, angiogram Images of a patient with a suspected inflammatory coronary aneurysm are shown. The patient presented with an acute coronary syndrome. Cardiac catheterization demonstrated a contrast-filled structure in the distal LAD distribution, measuring about 3 cm. There appears to be a small communication with the right ventricle, with a small amount of contrast seen as it is ejected through the right ventricle (RV) and RV outflow tract in the cine-angiogram.

Figure 8.66  LAD aneurysm, MRI An MRI was performed for further characterization of the pseudoaneurysms of the LAD and LCX (left panel). Delayed contrast enhanced imaging showed no evidence of myocardial scar (right panel).

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Figure 8.67  LAD aneurysm, CT A cardiac CTA clearly demonstrated the aneurysms of the LAD and LCX. A rim of thrombus is seen in the LAD aneurysm. CT defined the entry and exit points of the LAD and LCX into the aneurysm. (Video 8.67)

Figure 8.68  LAD aneurysm, CT The cardiac CTA also demonstrated a small communication with the right ventricle was identified, which is also seen on the angiogram.



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Figure 8.69  LAD aneurysm, CT The patient underwent stenting of the LAD and LCX, with exclusion of the aneurysms.

Figure 8.70  LAD aneurysm, CT The patient underwent stenting of the LAD and LCX, with exclusion of the aneurysms. This figure shows corresponding CT images before (left panel) and after (right panel) PCI.

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Figure 8.71  Dynamic CT MPI TACS and snapshot images The graph shows typical time-attenuation curves (TACs) acquired with dynamic computed tomography (CT) myocardial perfusion imaging (MPI), and two snapshot images of the same mid ventricular slice, corresponding to different time points of the CT MPI scan. The yellow curve (I) in the graph represents the TAC in normal tissue, and the gray curve (II) that of infarcted area. The red curve (III) is the TAC of the ascending aorta. Image (A) was taken at the time point indicated by line (a) in the graph. Image (B) was taken 6 seconds later, as indicated by line (b). The variation between the images emphasizes the difficulty of timing a static scan to robustly assess the extent of a perfusion defect. HU = Hounsfield unit.



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Figure 8.72  Display of CT myocardial perfusion images Display of CT myocardial perfusion images in the short-axis and vertical and horizontal long-axis views. In each view, the stress image is in the upper row and the rest image below. The corresponding nuclear perfusion image is displayed side by side.

Figure 8.73  Reversible myocardial perfusion defect Nuclear myocardial perfusion imaging (middle panels) demonstrates a large reversible defect involving the left anterior descending (LAD) coronary artery territory in the mid ventricle. CT myocardial perfusion imaging (left panels) shows the same findings: during stress, the defect (SD), involving the anterior wall and septum, has a myocardial blood flow (MBF) or 0.57 cc/cc/minute (blue), whereas the normal tissue (SN), i.e. the inferior and lateral walls, has an MBF of 1.09 cc/cc/ minute (red). At rest, the defect (RD) resolves and has an MBF similar to that of the normal myocardium at rest (RN): 0.82 and 0.81 cc/cc/minute (yellow-green). These findings are compatible with the angiographic findings (right panel) of a severe proximal LAD stenosis (top row, white arrow).

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Figure 8.74  Fixed myocardial perfusion defect Demonstration of a fixed defect involving the anterior wall and septum on CT myocardial perfusion imaging and nuclear myocardial perfusion imaging and the corresponding occluded proximal left anterior descending artery in the invasive angiography study. The infarcted area shows a severely reduced myocardial blood flow (MBF) of similar magnitude in both the rest and stress images (0.54 and 0.56 cc/cc/minute, respectively, displayed in blue).



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Figure 8.75  Resolution of perfusion defect after PCI CT angiogram of the mid RCA showing 95% stenosis (top row, before stent, arrowheads), with correlation of invasive angiography, and the presence of a reversible defect (green) of the inferolateral wall (arrows) shown on stress (top) and rest (bottom) CT MPI. After stent (bottom row), the CT angiogram of mid RCA shows the patent stent (arrowheads), with correlation of invasive angiography. There is resolution of the reversible defect of the inferolateral wall on stress (top), compared with the initial rest scan (bottom) as a reference.

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Figure 8.76  Normal coronary vein anatomy (64-slice scanner) In this figure, normal vein anatomy is shown. The great cardiac vein runs parallel to the proximal LAD (lower panel), then follows the LCX into the atrioventricular groove (right upper panel), and drains into the right atrium as the coronary sinus (left upper panel).



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Figure 8.77  Coronary sinus In this figure the right atrium (yellow) and coronary sinus (red) are illustrated. The coronary sinus has several branches. The branch shown in this image continues along the left AV groove to the anterior interventricular groove.

Figure 8.78  Biventricular pacemaker lead in coronary sinus Assessment of the coronary venous anatomy is performed prior to placement of biventricular pacer leads. In this figure pacer leads of a biventricular pacing lead are visible in the right ventricle and coronary sinus.

Chapter 9

Pulmonary circulation

9.1  Pulmonary Artery

Compared with ventilation-perfusion (VQ) scans, contrast-enhanced computed tomography (CT) has a high sensitivity and specificity for the diagnosis of ­pulmonary embolism (PE) (main through segmental arteries)319–323 (Figures 9.1 and 10.30d). The advantages of CT are the speed and the wide availability in emergency ­departments. The CT scan allows direct visualization of the thrombus, and simultaneous ­assessment of the lung parenchyma and size of the cardiac chambers (e.g. right ­ventricular enlargement). On the other hand, CT does not provide an assessment of lung ventilation or perfusion (VQ scan) or right ventricular function (echocardiography, MRI). Pulmonary CT angiography can occasionally show other fi ­ ndings, including PA pseudoaneurysms (Figure  9.2). While most scans are ­ performed with non-gated protocols, more recently ECG-synchronized protocols have been described.323 Programs for computer-aided PE detection have been described.324

9.2  Pulmonary Veins

Historically, pulmonary vein anatomy was mainly relevant in the assessment of abnormal venous return as part of congenital syndromes (see Chapter 13).325 This changed after percutaneous ablation procedures at or close to the pulmonary vein ostia became a standard treatment for chronic atrial fibrillation. Imaging of the ­pulmonary veins before the procedure for three-dimensional guidance and after the procedure for diagnosis and surveillance of pulmonary vein stenosis is now ­commonly performed.326–331 In addition, the left atrium and left atrial appendage can be assessed for thrombus (Figure 9.3). Post-interventional complications include wall thickening and luminal stenosis (Figures 9.3 and 9.4). CT is sensitive in identifying and grading stenosis, but limited in differentiating subtotal and total venous occlusion (Figures 9.5 and 9.6).

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Figure 9.1  Pulmonary embolism This figure shows images of a large left central pulmonary embolus.

Figure 9.2  Pulmonary artery pseudoaneurysm This figure shows images of a patient with a suspected pseudoaneurysm following the placement of a pulmonary artery catheter. There are moderate bilateral pleural effusions with consolidation and atelectasis of the lower lobes. There is a pseudoaneurysm arising from the right middle lobe pulmonary artery, which measures approximately 4.0 × 3.3 cm.



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Figure 9.3  Pulmonary vein stenosis Images after pulmonary vein isolation (PVI). The left atrium and left atrial appendage show no evidence of thrombus (right upper panel). There is thickening of the vessel wall at the right inferior pulmonary vein ostium, with about 40% luminal stenosis (right lower panel).

Other imaging modalities including echocardiography and MRI can ­reliably  image the pulmonary veins.332–335 An important advantage of CT is the ­ability to visualize inflammatory changes associated with the development of vein s­tenosis, including wall thickening at the vein ostia and mediastinal lymph node ­enlargement (Figures 9.7 and 9.8). If severe pulmonary vein stenosis requires angioplasty and stenting, pre-procedural planning and post-procedural ­assessment of stent  ­position  and patency can reliably be performed with CT (Figures 9.9 and 9.10).

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Figure 9.4  Pulmonary vein stenosis More severe narrowing of the left superior vein ostium after pulmonary vein ablation. Note the location of the left atrial appendage anterior to the proximal left superior vein ostium.



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Figure 9.5  Pulmonary vein occlusion Images of two CT scans obtained 6 months apart. The scan 1 month after ablation showed 60% stenosis of the right superior vein ostium (upper panels). The follow-up scan 6 months later showed total occlusion of the right superior vein (lower panels).

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Figure 9.6  Pulmonary vein occlusion (subtotal/total) In this figure CT images 3 months (upper panels) and 6 months (lower panels) after vein ablation are shown. There is an increase in stenosis of the pulmonary vein ostia with total/subtotal occlusion of the left superior vein ostium. However, CT is limited in differentiating subtotal and total occlusion, which can be assessed with pulmonary angiography.

Figure 9.7  Pulmonary vein stenosis with surrounding soft tissue Severe pulmonary vein stenosis of all four veins, with increased soft tissue in the mediastinum.



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Figure 9.8  Fibrosing mediastinitis with pulmonary vein occlusion This figure shows images of a patient with fibrosing mediastinitis. There is partially calcified soft tissue in the mediastinum surrounding the left atrium. Only the right superior vein is patent. The other veins are occluded.

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Figure 9.9  Pulmonary vein stent This figure shows a patent stent in the left inferior pulmonary vein ostium.

Figure 9.10  Pulmonary vein stent This figure shows patent stents of the right superior, left superior, and left inferior veins. Both leftsided stents demonstrate small amounts of soft tissue lining the stent lumen. However, assessment of in-stent thrombosis or neointimal tissue inside the stents is limited with CT.

Chapter 10

Aortic disease

Computed tomography (CT) imaging of the aorta is the diagnostic standard for a wide range of clinical indications, including acute aortic syndromes (aortic dissection and its variants, penetrating atherosclerotic ulcers, leaking or unstable aneurysms, and trauma), as well as elective imaging for surgical or ­endovascular treatment planning, surveillance, and follow-up of aortic aneurysms, chronic d ­ issections, and other pathologies, such as infectious or noninfectious aortitis.336–338b Contrast enhancement is crucial for most indications to differentiate the lumen and the vessel wall. Diagnostic alternatives are magnetic resonance imaging (MRI)  and  ­echocardiography (in particular transesophageal echocardiogram (TEE)). Modern multi-detector scanners allow scanning of the entire thoracic and abdominal aorta in one breath-hold with or without ECG synchronization of the thoracic segments. ECG synchronization is achieved with standard retrospectivegated or prospective-triggered acquisition techniques, and is crucial for indications focused on the ascending aorta in order to reduce cardiac motion artifacts transmitted to the aortic root 339–342 (Figures 10.1 and 10.2). In contrast, non-gated acquisitions of the chest, abdomen, and pelvis provide continuous data sets with good enhancement of visceral branch vessels and are better suited for indications focused on the descending thoracoabdominal aorta including endovascular stent planning.

10.1 Acute aortic syndromes 10.1.1 Definition

CT imaging plays a critical role in the diagnosis and management of acute aortic syndromes (AASs).338a Acute aortic syndrome is a clinical term describing an acute aortic pain syndrome associated with acute, life-threatening aortic diseases (in analogy

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Figure 10.1  Motion artifact aortic root Because of the rapid motion of the heart and the relatively long acquisition window of CT, blurring of the image occurs, in particular if the acquisition window is not synchronized to the cardiac cycle. In this image of a non-gated CT scan, image artifact at the aortic root is seen (left panel), which could be mistaken for a dissection flap. However, the symmetry with linear structure on both sides of the aortic root is more typical for motion artifact.

Figure 10.2  Motion artifact aortic root In this figure images of the aortic root are compared in a gated (left panel) and non-gated (right panel) acquisition. The motion artifact seen in the non-gated images is eliminated by the cardiac gating.

to the term acute coronary syndrome), and encompasses several different entities.342a Classic aortic dissection describes a splitting or separation of the aortic wall within the media layer of the aorta. The pathological substrate that predisposes the aorta for dissection is an abnormal media layer, which is traditionally (although not perfectly accurately) described as “cystic medianecrosis.”342b Cystic medianecrosis can be caused



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by several unrelated entities, including congenital and genetic disorders (Marfan syndrome, Ehlers-Danlos type IV, aortitis), but is most commonly associated with severe, long-standing hypertension. 10.1.2 Morphologic classification

It is important to understand the spectrum of anatomic manifestations of acute aortic dissection, which are classified in distinct morphologic classes, as described in the most recent guidelines for the diagnosis and management of patients with thoracic aortic disease336: • Class I: Classic aortic dissection. Characterized by a primary intimal tear, separation in the media with a true and false lumen divided by a “flap,” and an exit or reentry tear (Figures 10.3, 10.4a and b, and 10.7). • Class II: Intramural hematoma (IMH). Describes a variant of aortic dissection where the space within the diseased aortic media layer is filled with clotted blood rather than a flow channel (false lumen) (Figure 10.10). Highquality CT scans occasionally allow identification of intimal tears, which are more frequently found during surgery or autopsy.342c,d • Class III: Also called limited dissection or subtle intimal tears. Describe localized confined intimal tears without extensive undermining of the

Figure 10.3  Type A aortic dissection—class I The figure shows a type A dissection. The dissection flap originates in the aortic root (upper ­panels) and extends throughout the ascending thoracic aorta and aortic arch (lower panel). In the dilated mid ascending aorta (lower left panel) the smaller true lumen is surrounded by the larger false lumen.

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Figure 10.4a  Type A aortic dissection—class I The corresponding saggital reconstructions show the extent of the dissection in the ascending aorta and aortic arch.

intima or flap formation.343–345 These are often seen with Marfan syndrome and can rupture or cause tamponade. The typical appearance is of a small outpouching of the aortic wall (Figures 10.11, 10.12a, 10.12b, and 10.12c). • Class IV: Penetrating atherosclerotic ulcers with localized dissections or wall hematomas. Often with calcium at the base of a mushroom-shaped area of extraluminal contrast. Penetrating atherosclerotic ulcers (PAUs) are pathologically defined by penetration of an atherosclerotic ulcer through the internal elastic lamina into the aortic media (Figure 10.13). PAUs are a manifestation of severe, advanced atherosclerosis, and typically affect older individuals with more cardiovascular comorbidities than patients with classic aortic dissection. In the acute setting (patients typically present with aortic pain) this may be associated with a local intramural hematoma surrounding the PAU. Large ulcers often have undermined edges that may have a similar appearance on cross-sectional imaging as dissection flaps. The plane of dissection is often between the media and adventitia, and PAUs can penetrate



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Figure 10.4b  Type A aortic dissection—class I This figure shows a volume-rendered image (left panel) and MPR image (right panel) of a patient with acute type A aortic dissection. The right panel defines the origin of the left main (LM) from the true lumen and shows the proximal entry tear just above the LM ostium. It also shows a reentry tear in the proximal descending segment.

all through the aortic wall resulting in periaortic and mediastinal hematoma, hemothorax, or aortic rupture. • Class V: Iatrogenic or posttraumatic dissection (Figures 10.12b, 10.12c, and 10.14). 10.1.3 Location and extent

The anatomic extent and location of the dissection process has critical implications on treatment decisions. The traditional anatomic classifications for aortic dissection are the 1965 DeBakey classification and the 1970 Stanford classification.345a,b ,346 The DeBakey system is based on the location of the primary intimal tear (ascending or descending), and the extent of the dissection within the aorta. Of note, the DeBakey system does not classify dissections with tears in the arch. The original Stanford system is exclusively based on the extent of the dissection (irrespective of the site of the primary intimal tear), and classifies aortic dissections into type A (involvement of the ascending aorta) or type B dissections, which do not involve the ascending aorta. Involvement of the aortic arch without involvement of the ascending aorta is therefore considered type B. This is clinically meaningful, because arch involvement without ascending involvement does not mandate surgical repair. The terms type A and type B are also used to describe the location of aortic intramural hematoma

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Figure 10.4c  Type A aortic dissection—class I This figure shows a volume-rendered image (left panel) and MPR images (right panels) of another patient with acute type A aortic dissection. The right upper panel defines the origin of the right coronary artery (RCA) from the true lumen. The right middle panel shows a tear in the mid ascending aorta.

or penetrating ulcers. Another clinical classification classifies dissection based on involvement proximal or distal to the left subclavian artery (proximal and distal dissection). 10.1.4 Diagnostic consideration

Multi-detector computed tomography (MDCT) is highly diagnostic for the identification of acute aortic syndromes and allows identification of the above-described morphologic criteria, location and extent.344 In the diagnostic assessment of acute aortic disorders, reliable assessment of the aortic root and ascending aorta is critical for management decisions. However, the cardiac pulsation is transmitted to the aortic root and ascending aorta, and often causes significant motion artifact (Figures 10.1 and 10.2). ECG-synchronized acquisition protocols substantially reduce



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Figure 10.5  Type A aortic dissection with hemopericardium The images in this figure show an acute type A aortic dissection beginning at the sinotubular junction and extending into the arch. The false channel is partially thrombosed. There is a hemorrhagic pericardial effusion, which compresses the right pulmonary artery.

motion artifact and should be used if detailed assessment of the aortic root and ascending aorta is required. While class I dissections with visible dissection flap are seldom missed, knowledge about the appearance of intramural hematoma (IMH) is critical for its identification (Figures 10.10 and 10.15).351–357 In the acute phase, the blood products in the wall have high Hounsfield units (range of 60–70), which is higher than unenhanced blood in the aortic lumen. Therefore an IMH is easily identified on a non-contrast-enhanced scan as a rim of high signal. In the sub-acute phase, the HU decreases (Figures 10.16– 10.18). An interesting aspect of IMH is its temporal change. Patterns of regression, evolution in class I dissection, development of ulcer-like projections, and intramural blood pools are described (Figures 10.19–10.22).357a,b It is important to differentiate blood product in the aortic wall (IMH) from structures adjacent to the aortic wall, including pericardial fluid in the folds adjacent to the ascending aorta, atelectasis adjacent to the descending aorta, and lung masses (Figures 10.23–10.26). Acute penetrating ulcerations with localized dissections or wall hematomas can be identified with CT358 (Figures 10.13 and 10.27). Similarly, in patients presenting with painful or leaking degenerative aneurysms, CT is critical in determining the presence of the location of the aneurysm and whether the presenting pain is from compression of surrounding tissue, or from leakage (Figures 10.28–10.30b).

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Figure 10.6  Type A aortic dissection with hemopericardium This figure shows the hemopericardium at the superior aspect of the left ventricle, causing compression of the pulmonary artery.

Figure 10.7  Type B aortic dissection and rupture This figure shows images of a patient with a type B aortic dissection beginning just beyond the origin of the left subclavian artery. There are luminal irregularities in the aortic isthmus, which may represent the site of tear. The mediastinum is notable for a large amount of blood products surrounding the descending thoracic aorta extending to the level of the diaphragm. This is associated with partial compression of the left atrium and pulmonary veins. There are bilateral pleural effusions with increased density consistent with complex and hemorrhagic effusions.

10.1.5 Differential diagnosis (triple rule-out)

CT scans performed for the assessment of the aorta in a patient with suspected acute aortic syndrome allow assessment for other conditions considered in the differential diagnosis, including acute pulmonary embolism or acute coronary syndromes (Figures 10.30d and 10.30e). It has been suggested that CT protocols for patients presenting with acute chest pain could be modified to allow simultaneous



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Figure 10.8  Aneurysm of the aortic isthmus with contained rupture This figure shows images of a patient with an aneurysm of the aortic isthmus and proximal descending aorta with evidence of contained rupture. The aneurysmal dilatation beyond the left subclavian artery is surrounded by blood products. The patient presented with acute symptoms and underwent emergent surgery.

assessment of these entities (triple rule-out).358a,b However, these protocols are not widely used.358c 10.1.6 Therapeutic implications

Patients with aortic dissection (class I to class V) and documented involvement of the ascending aorta are typically operated on immediately (Figures 10.3 and 10.4).345 However, in certain patient populations, successful initial medical management of class II IMH of the ascending aorta has been described, but remains controversial.357c–e The identification of acute complications, in particular hemopericardium and mediastinal hematoma, is critical in the management of these patients (Figures 10.5, 10.6, and 10.7). For patients without involvement of the ascending aorta, initial treatment is typically conservative, with aggressive blood pressure control.344,345 However, distal complications including visceral branch vessel compression/ischemia, aortic rupture, intractable pain, and uncontrollable hypertension can require immediate surgical or endovascular treatment (Figures 10.7–10.9). Distal class IV and V tears may require either open or endovascular surgical intervention. In distal dissections that are subacute (2–6 weeks old), the Investigation of Stent Grafts in Patients with Type B Aortic Dissection (INSTEAD)347 study documented no benefit of prophylactic stenting. There is no proof that stenting is beneficial if the aortic dissection is chronic, i.e. more than 6 weeks old.348–350

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Figure 10.9  Type B aortic dissection with visceral branch vessel compression—aortic dissection class IV This figure shows images from a patient with recent aortic valve replacement and acute post-­ operative clinical deterioration with loss of peripheral pulses. The CT scan shows evidence of a type B aortic dissection beginning in the mid descending thoracic aorta and extending into the infrarenal abdominal aorta. There is almost complete compression of the anteriorly located true lumen in the lower descending thoracic and abdominal aorta compressing the origins of the celiac artery, superior mesenteric artery, and right renal artery, which originate from the true lumen. The left renal artery originates from the false lumen. There is severe hypoperfusion of both kidneys, which is uniform on the right and patchy on the left. There is no evidence of pneumatosis or bowel wall thickening to suggest mesenteric ischemia. The patient underwent emergent endovascular repair with placement of two sequential stent grafts in the proximal and mid descending thoracic aorta.



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Figure 10.10  Intramural hematoma—aortic dissection class II This figure shows an intramural hematoma of the descending thoracic aorta. There is wall ­thickening of the isthmus and descending thoracic aorta (right upper panel). The cross-sectional image shows the crescentic shape of the intramural hematoma in the mid descending aorta (right lower panel).

10.2 Aortic aneurysmal disease

CT is routinely performed for the identification and characterization of thoracic and abdominal aortic aneurysmal (AAA) disease.336 CT is used for screening of aortic aneurysms,359–361 and for surveillance of aneurysms deemed too small to warrant surgical repair. CT protocols with 1–3 mm slice reconstruction allow precise assessment of the aorta and arch branch, visceral branch vessels, and iliac arteries. Modern workstations allow semi-automated centerline reconstructions (Figure  2.20). In contrast to conventional angiographic techniques, CTA shows luminal dimensions and the vessel wall. In aortic aneurysm, luminal dimensions and adherent wall thrombus and calcification of the aneurysm sac can be assessed. Dimensions of the aneurysm are described by measuring the outer dimensions of the aneurysm sac. The size of the aneurysm (including the aneurysm sac) has prognostic and therapeutic implications. Reconstruction of images perpendicular to the vessel axis for each segment of the aorta allows precise assessment and measurement of aneurysms of the sinuses of Valsalva (Figures 10.31 and 10.32a), ectasia of the aortic root and ascending aorta (Figures 10.33 and 10.34), atherosclerotic aneurysms of the descending thoracic aorta (Figure 10.35a), and aneurysms of the abdominal aorta. Post-traumatic aneurysms are typically seen in the proximal descending aortic segment. The initial features are those of a focal dissection/transection (Figure 10.14). In later stages, there is often focal aneurysmal dilatation with wall calcification (Figure 10.36a).

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Figure 10.11  Acute penetrating ulceration/focal dissection—aortic dissection class II In contrast, this figure shows a focal penetrating ulceration in the proximal ascending aorta, associated with the clinical presentation of an acute aortic syndrome. Careful review of the axial images demonstrated evidence of mediastinal blood products, consistent with aortic leakage.

Occasionally aneurysms typical of the abdominal aorta are surrounded by a rim of inflammatory tissue. These aneurysms are described as inflammatory aneurysms (Figure 10.36b).361a There is overlap with retroperitonal fibrosis. Connective tissue diseases including Marfan syndrome are associated with aortic aneurysms and dissection, and skeletal abnormalities (Figures  10.37–10.42). While CT is typically preferred for diagnosis in symptomatic patients and for treatment planning, because of its lack of radiation exposure, MRI of the aorta is the preferred modality in younger patients during follow-up.

10.3 Endovascular stent graft

CT imaging of the aorta is an integral part of endovascular stent graft therapy of aortic aneurysms.362–377 CT is critical for procedural planning, with detailed three-­ dimensional reconstructions used for precise quantitative assessment for custommade stent grafts378 (Figures 10.43–10.48a). It is also an integral part of post-procedural surveillance (Figures 10.49–10.51).



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Figure 10.12a  Acute penetrating ulceration/focal dissection—aortic dissection class II The patient underwent urgent replacement of the ascending thoracic aorta with a composite graft. The mechanical aortic valve prosthesis and the grafts of the ascending aorta are seen in the postoperative images (lower panels).

Figure 10.12b  Focal type A ascending aortic dissection with partial compression of the central pulmonary artery This and the next figure show images of a young patient, without history of aortic disease, who presented 24 hours after minor blunt trauma to the chest, with now sudden onset of severe chest pain. The axial CT images identify a dilated ascending thoracic aorta with a focal dissection of the proximal ascending segment. This is associated with a focal outpouching just above the left main coronary artery ostium and evidence of aortic rupture/leakage with mediastinal blood products. The mediastinal blood products cause partial obstruction of the central pulmonary artery. There are additional blood products tracking along the ascending aorta and aortic arch, likely hemorrhagic pericardial and pleural effusions.

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Figure 10.12c  Focal type A ascending aortic dissection with partial compression of the central pulmonary artery The frontal plane CT images better demonstrate the focal outpouching and the mediastinal blood products causing partial obstruction of the central pulmonary artery.

Figure 10.13  Penetrating ulceration Penetrating ulcerations can be found in the context of acute and chronic aortic conditions. Penetrating atherosclerotic ulcers with localized dissections or wall hematomas are classified as class IV dissection processes. This figure shows a focal, relatively large penetrating ulceration in the diffusely diseased retrocardiac descending thoracic aorta. The maximum diameter of the aorta at the level of the ulceration is 3.0 × 5.6 cm. The inhomogeneous Hounsfield units of the wall may be consistent with wall hematoma.

10.4 Aortic surgery

Pre- and post-operative CT scans are useful for surgical planning and in the assessment of surgical results (Figures  10.37–10.41, 10.52–10.58) and early and late complications. In the early post­operative phase, complications at the repair site or in the operative field, including mediastinal hematoma or infection (Figures  10.59 and 10.60), pericardial or pleural effusion, and pneumothorax, can be identified. Late complications include prosthetic valve graft infections, postoperative pseudoaneurysms, and fistulas after surgery (Figures 10.61–10.71).



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Figure 10.14  Traumatic type B aortic dissection This figure shows images of a patient after recent motor vehicle accident. The left panels show axial (left upper panel) and sagittal (left lower panel) images of the descending aorta with a focal dissection. There are blood products in the adjacent mediastinum and layering of blood in the pleural effusion. The right panels show the corresponding images after treatment with an endovascular stent graft.

10.5 Non-aortic pre-operative imaging

An important application of CT is perioperative imaging of the aorta in patients undergoing cardiothoracic surgery.379,380 In patients undergoing open-heart surgery, the local extent of calcified atherosclerotic plaque of the ascending aorta determines the cannulation site during cardiopulmonary bypass. If extensive plaque and calcification preclude cannulation of the ascending aorta, a temporarily placed bypass conduit to the axillary or subclavian artery is a frequently used alternative.381 To assess for calcification, a non­contrast-enhanced CT scan is sufficient, but does not allow to assessment of non-calcified atherosclerotic changes (Figure 10.71). Contrast-enhanced

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Figure 10.15 Intramural hematoma of the descending thoracic aorta and aneurysm of the abdominal aorta This figure shows an intramural hematoma of the descending thoracic aorta with enlargement of the involved aortic segments (upper panels). The maximum diameter in the retrocardiac descending aorta is 6.3 cm. There is a large area of communication breakdown between the lumen and the hematoma in the proximal descending aorta. The intramural hematoma ends in the supra-renal aorta. There is an additional infrarenal abdominal aortic aneurysm with a maximum diameter of 5.1 cm (lower panels). The differences in Hounsfield units help to differentiate the two entities.

scans show the amount of calcified and non-calcified atherosclerotic plaque, which is related to postoperative stroke incidence and outcome382–384 (Figure 10.72).

10.6 Other conditions

Morphologic changes associated with aortitis in the context of connective tissue diseases can be assessed with CT.385 Typical findings are wall thickening and extensive



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Figure 10.16  Intramural hematoma—increased Hounsfield units of the wall This figure demonstrates the characteristic increased density (Hounsfield unit) of the aortic wall secondary to an acute intramural hematoma. The panels demonstrate areas of increased Hounsfield unit of the thickened aortic wall consistent with an acute intramural hematoma. The increase in the density of the wall is often more obvious in the non-contrast-enhanced images (right panel). For comparison, the contrast-enhanced images are shown in the left panel.

Figure 10.17  Intramural hematoma—increased Hounsfield units of the wall This figure demonstrates the increased HU of an acute IMH (left upper panel). After 1 week the HU has decreased (left lower panel).

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Figure 10.18  Endovascular stenting, Hounsfield units of thrombosed aneurysm sac In contrast to the characteristic increased density (Hounsfield unit) of the aortic wall in patients with acute intramural hematoma, this figure shows images of a patient after endovascular stenting of a thoracic aortic aneurysm. The upper and lower panels show images before and after stenting, respectively. The left and right panels show images before and after contrast administration, respectively. The pre-stenting images show the lumen of the aneurysm and the layer of adherent, chronic wall thrombus (upper panels). After stenting, there is fresh thrombus filling the space between the stent struts and the chronic wall thrombus. The low HU of the thrombus and the higher HU of the fresh thrombus are shown (lower panels).

calcification in later stages (Figure 10.73a and 10.73b). The potential role of positron emission tomography (PET)/CT scanners for the assessment of disease activity is currently being evaluated (Figure 10.74); however, it is not an approved or reimbursed application.386 An incidental finding of an intra-aortic balloon pump in the aorta is shown in Figure 10.75. Aortic coarctation is further described in the section on congenital disease in Chapter 13 (Figure 10.76).



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Figure 10.19  Resolving intramural hematoma This figure shows a chronic intramural hematoma with evidence of partial resolution. The upper (saggital) and lower (axial) panels show the massive wall thickening at baseline (left panel) and the significant resolution over the next 6 months (3 months, middle panel; 6 months, right panel). However, there is development of a focal pseudoaneurysm/ulcer-like projection at the aortic isthmus (middle panels), which was subsequently treated with an endovascular stent graft.

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Figure 10.20  Resolved intramural hematoma of the ascending thoracic aorta This figure shows images of a patient who presented initially with an intramural hematoma/ dissection process beginning in the ascending aorta (type A). The upper row images show the crescentic wall thickening of the posterior aspect of the ascending aorta (4–8 o’clock position of the two left upper images). Wall thickening extends into the aortic arch and arch branch vessels. The intramural hematoma is continuous with a communicating dissection process of the arch and descending thoracic aorta (right upper images). A repeat CT scan 1 year later (lower row of images) demonstrates spontaneous resolution of the wall thickening in the ascending aorta and arch. However, the residual dissection process of the descending thoracic aorta (type B) is associated with aneurysmal dilatation and increased diameter.

Figure 10.21  Intramural hematoma—ulcer-like projection This figure shows a chronic intramural hematoma of the descending thoracic aorta. Wall ­thickening of the isthmus and upper descending thoracic aorta is consistent with residuals of an intramural hematoma. In the descending thoracic aorta there is an area of intimal disruption a­ ssociated with mild bulging of the aorta (3.9 cm). The appearance is that of a penetrating ulceration.



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Figure 10.22  Intramural hematoma—intramural blood pool This figure shows two intramural blood pools in the medial aspect of the descending thoracic aorta. They are related to intercostal arteries.

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Figure 10.23  Intramural hematoma, differential diagnosis This figure shows an IMH in a type A distribution. There is a small amount of pericardial fluid in the pericardial fold adjacent to the IMH of the ascending aorta.

Figure 10.24  Intramural hematoma, differential diagnosis This figure shows a small rim of atelectasis of the lung adjacent to the descending thoracic aorta, which mimics the crescentic appearance of an intramural hematoma. The upper panels show different axial slices at the level around the bifurcation of the pulmonary arteries. The lower panels show images during early and late injection of the contrast bolus.



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Figure 10.25  Intramural hematoma, differential diagnosis This figure shows images of a patient with bilateral small- to moderate-sized pleural effusions. In the descending thoracic aorta, the fluid lies adjacent to the aorta, and on some images has an appearance similar to an aneurysm or intramural hematoma (upper panel). However, close observation demonstrates that aortic wall and fluid are separate (lower panels).

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Figure 10.26  Intramural hematoma, differential diagnosis This figure shows images of a patient who presented with chest pain. The CT shows changes in the area of the aortic arch with an appearance reminding of blood products. The panels show images from the arterial phase (upper panels) and delayed venous phase (lower panels). Careful review, in particular of the delayed phase images, demonstrates that the lesion is separated from the aortic wall, more consistent with a lung tumor, developing adjacent to the aorta. Supporting a diagnosis of a malignant process, there was evidence of a left ventricular thrombus, and evidence of likely metastatic lesions of the liver (right panels).

Figure 10.27  Ruptured PAU Patient with rupture penetrating atherosclerotic ulceration (PAU) at the distal arch. There are blood products surrounding the aorta and a moderate pericardial effusion.



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Figure 10.28  Suspected unstable aneurysm Occasionally, aneurysms demonstrate morphologic features that could indicate instability. An example is shown in this image, which shows cross sections of an infrarenal aneurysm at two different levels, less than 10 mm apart. The left panel shows mild wall enhancement (12 o’clock position) and a small area of breakdown (4 o’clock) position. The patient presented with abdominal pain. Further evaluation demonstrated evidence of acute cholecystitis, with a rim of fluid around the gallbladder.

Figure 10.29  Leaking abdominal aneurysm This figure shows an axial image of an infrarenal aortic aneurysm. The ill-defined luminal border and contrast enhancement surrounding the aneurysm are consistent with chronic leakage.

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Figure 10.30a  Leaking abdominal aneurysm Patient with AAA prior renal stent. Blood products surrounding the AAA.



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Figure 10.30b  Leaking abdominal aneurysm, active contrast extravasation Images of a patient presenting to the ED with abdominal pain and hypotension. An emergently performed CT scan demonstrated an abdominal aortic aneurysm with evidence of rupture with active contrast extravasation and a large amount of retroperitoneal blood products. The patient was immediately prepared for emergent surgical repair, which was successful.

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Figure 10.30c  Leaking abdominal aneurysm, active contrast extravasation Images of a patient with a ruptured abdominal aortic aneurysm with evidence of rupture, active contrast extravasation, and left hemothorax (right panels). The patient underwent successful surgical repair with replacement of the descending thoracic and supra-renal abdominal aorta and side grafts to the iliac arteries (left panel).



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Figure 10.30d  Acute aortic syndromes, differential diagnosis CT scans performed for the assessment of the aorta in a patient with suspected acute aortic syndrome allow assessment for other conditions considered in the differential diagnosis, including acute pulmonary embolism, as shown in this figure. There is an embolus straddling the bifurcation of the proximal left pulmonary artery.

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Figure 10.30e  Acute aortic syndromes, differential diagnosis Another occasional finding is an acute coronary syndrome. It has been suggested that CT protocols for patients presenting with acute chest pain could be modified to allow simultaneous assessment of these entities (triple rule-out). However, these protocols are not widely used.



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Figure 10.31  Sinus of Valsalva aneurysm This figure shows images of a sinus of Valsalva aneurysm. There is a 1.4 × 2.4 × 1.9 cm saccular outpouching of the right coronary sinus limited to its lower portion immediately above the trileaflet aortic valve. The RCA arises from the more superior portion of the otherwise normalappearing right coronary sinus of Valsalva. (Videos 10.31-i, 10.31-ii)

Figure 10.32a  Sinus of Valsalva aneurysm Another example of a sinus of Valsalva aneurysm is shown in this figure. It originates from the non-coronary cusp and measures 2.5 × 2.1 cm. It is in close relation to the atria aspect of the sepal leaflet of the tricuspid valve. The aneurysm is partially thrombosed but well perfused in the ­central portion. No communication is evident. (Videos 10.32a-i, 10.32a-ii)

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Figure 10.32b  Ruptured sinus of Valsalva aneurysm Ruptured sinus of Valsalva aneurysm.

Figure 10.33  Dilated aortic root (annuloaortic ectasia) This figure shows images of a patient with Marfan syndrome. The aortic valve is trileaflet. There is a dilated aortic root with moderate to severe effacement of sinotubular junction. Beyond the dilated root, the aorta has normal dimensions. The pattern of dilatation is consistent with annuloaortic ectasia.



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Figure 10.34  Annuloaortic ectasia Another example of annuloaortic ectasia with prominence of aortic root and proximal ascending aorta (maximum diameter 5.2 cm) is shown. There is associated moderate effacement of the sinotubular junction.

Figure 10.35a  Descending aortic aneurysm This figure shows an aortic aneurysm of the descending thoracic aorta with a moderate to severe amount of adherent wall thrombus. There is also dilatation of the ascending aorta, with minimal effacement of the sinotubular junction.

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Figure 10.35b   Celiac artery aneurysm A patient presented with acute abdominal pain and an ultrasound showed a large lesion in the upper abdomen. The CT scan showed a large aneurysm of the celiac artery. There was evidence of rupture (right lower panel).

Figure 10.36a  Post-traumatic aneurysm This figure shows images of a patient with a remote history of a motor vehicle accident. There is a focal aneurysm in the area of the isthmus and proximal descending thoracic aorta with eccentric expansion and calcification of its anterolateral surface. The maximum diameter is 4.8 cm. Proximal and distal to the aneurysm, the aorta has normal dimensions and minimal atherosclerotic changes.



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Figure 10.36b  Inflammatory aneurysm This figure shows images of a patient with suspected inflammatory aneurysms, with an extensive a rim of inflammatory tissue.

Figure 10.37  Ascending aortic aneurysm, Marfan syndrome Images from a patient with Marfan syndrome and associated massive dilatation of the aortic root with a maximum diameter of 8 cm. This figure shows axial images of the aneurysm of the aortic root and ascending aorta. The aortic valve is trileaflet. There is dilatation of the annulus and massive dilatation of the aortic root, measuring 8 cm in diameter.

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Figure 10.38  Ascending aortic aneurysm, Marfan syndrome These oblique reconstructions demonstate the dilated annulus with effacement of the sinotubular junction and the massive aneurysm of the ascending aorta.

Figure 10.39  Pre- and post-operative imaging, aortic root replacement This figure shows pre- and post-operative images of the aneurysmally dilated ascending aorta. There is massive dilatation of the aortic root with a maximum diameter of 8 cm (left panel). The post-operative CT (right panel) demonstrates replacement of the aortic valve, and sequential grafts covering the aortic root, ascending aorta, and parts of the aortic arch. (Videos 10.39-i, 10.39-ii)



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Figure 10.40  Pre- and post-operative imaging, aortic root replacement These images show the aortic valve, aortic root, and ascending aorta before (upper panels) and after (lower panels) the surgery. A mechanical aortic valve prosthesis is placed inside a graft of the root and ascending aorta (composite graft). The coronary arteries are reimplanted into the graft.

Figure 10.41  Pre- and post-operative imaging, aortic root replacement The origin of the coronary arteries from the dilated root pre-operatively (upper panels) and reimplanted coronary arteries from the graft after the surgery (lower panels) are shown.

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Figure 10.42  Extracardiac findings with Marfan syndrome This patient with history of Marfan syndrome had undergone prior aortic surgery. The surgical grafts are shown in the left upper panel in a volume-rendered image (VRI). The right upper panel demonstrates pectus deformity of the chest. The left and right lower panels show dural ectasia with a Tarlov cyst.



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Figure 10.43  Endovascular stent graft This figure shows images of a patient with a focal pseudoaneurysm of the descending thoracic aorta (left upper and lower panels). The aorta at the level of the pseudoaneurysm measures 6.9 × 5.0 cm. The patient was treated with an endovascular stent graft (middle and right panels). The endovascular stent graft series extends from the proximal descending thoracic aorta to the level just above the celiac artery. The stent successfully excludes the aneurysm sac of the retrocardiac descending thoracic aorta. There is no endoleak.

Figure 10.44  Endovascular stent graft This figure shows images of a patient with a focal aneurysm of the descending thoracic aorta, which was treated with an endovascular stent graft. The left panel shows the position of the graft. The right panel shows a cross section at the level of the retrocardiac aorta. The stent struts and the excluded and thrombosed aneurysm sac are seen. There is no evidence of endoleak.

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Figure 10.45  Persistent flow, endovascular stent graft This figure shows images of a patient who was treated with a repeat endovascular stent procedure because of endoleak. The lower images show the areas of endoleak after the initial procedure (left lower, arterial phase; right lower, venous phase). After repeat stenting no leak is seen in the same area (upper panels).

Figure 10.46  Endovascular stent graft, ruptured aneurysm These images show a ruptured aneurysm at the level of the retrocardiac descending thoracic aorta (left upper panels). There is contrast extravasation in the anterior aspect of the aneurysm and evidence of a hemorrhagic left pleural effusion. The patient was treated emergently with a thoracoabdominal endovascular stent graft (left lower panels and right panel).



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Figure 10.47a  Endovascular stent, hybrid procedure The “elephant trunk procedure” describes a two-stage surgical technique for patients with extensive aneurysmal disease of the thoracic aorta. This figure shows a patient that underwent a combined open surgical (first-stage) and endovascular (second-stage) approach. The left panels show the extensive aneurysm of the thoracic aorta before surgery. In the first stage (via median sternotomy), the patient underwent surgical replacement of ascending aorta and aortic arch. The surgical graft is hanging freely in the dilated descending aorta (second panel from left). The second stage was performed via an endovascular approach. The stent grafts, excluding the dilated descending aorta, are seen in the right panels.

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Figure 10.47b  Endovascular stent, hybrid procedure This figure shows a large aneurysm of the distal aortic arch and isthmus with a moderate amount of adherent wall thrombus. (Video 10.47b)



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Figure 10.47c  Endovascular stent, hybrid procedure This figure shows images after surgical repair. There is evidence of placement of an endovascular stent excluding the aneurysm. The left subclavian and carotid artery ostia were occluded. The distal vessels fill via patent axilloaxillary graft with a side limb to the left carotid artery. (Video 10.47c)

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Figure 10.47d  Endovascular stent, hybrid procedure This figure shows images of a patient with a type A dissection (upper panels). The patient underwent surgical grafting of the ascending aorta, and a stent of the descending aorta (lower panels).

Figure 10.47e  Endovascular stent, hybrid procedure This figure shows images of another patient with a type A dissection (upper panels). The patient underwent aortic valve replacement, surgical grafting of the ascending aorta, and a stent of the descending aorta (lower panels).



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Figure 10.47f  Endovascular stent, complex hybrid procedure This figure shows images of a patient with complex hybrid repair of the thoracoabdominal aorta. There is a composite graft of the ascending aorta and aortic arch with reimplantation of the arch branch vessels. The graft extended in the descending aorta as an elephant trunk graft. Subsequently an endovascular stent was placed in the proximal descending aorta. The distal descending aorta and supra-renal abdominal aorta were replaced with a surgical graft with reimplantation of the visceral branch vessels and renal arteries and graft to both iliac arteries.

Figure 10.47g  Endovascular stent, complex hybrid procedure This figure shows pre-operative images of a patient with an aortic root aneurysm (left panel) and a type B aortic dissection.

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Figure 10.47h  Endovascular stent, complex hybrid procedure In a first-stage operation, the patient underwent replacement of the aortic root and ascending aorta with a composite graft (left panel).

Figure 10.47i  Endovascular stent, complex hybrid procedure In a second-stage procedure, the patient underwent placement of an endovascular stent graft in the true lument of the dissected descending aorta. There is residual flow in the false lumen (right panel).

Figure 10.48  Endoleak These images show a large endoleak, status post-fenestrated, and bifurcated endovascular stent graft placement in the thoracoabdominal aorta.



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Figure 10.49  Endovascular stent graft, stent separation, endoleak Images of a patient with prior endovascular stent grafting of the abdominal aorta. The upper images show baseline images; the lower images are obtained at the time of presentation with abdominal pain. There is evidence of separation of stent components with an associated large endoleak.

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Figure 10.50  Endovascular stent graft, stent separation, endoleak This figure shows the volume-rendered image (VRI) baseline (upper panels) and follow-up (lower panels).



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Figure 10.51  Pre-operative assessment of thoracoabdominal aortic aneurysm Pre-operative CT can help in deciding about the surgical access site in patients with thoracoabdominal aneurysms. This is demonstrated in this figure. There is evidence of a supra-coronary graft of the ascending thoracic aorta. There is an additional graft of the proximal and mid descending aorta. Beyond the graft, there is a thoracoabdominal aneurysm with a maximum diameter of 7.4 × 6.0 cm in the retrocardiac descending thoracic aorta. There is a moderate amount of adherent wall thrombus (right lower panel). The VRIs show the ribs and the aneurysm and allow planning of the surgical access site.

Figure 10.52  Pre-operative assessment of sternal anatomy The patient has a history of type A aortic dissection, which was in the past repaired with a short supra-coronary graft of the ascending aorta. The left panel shows pre-operative images of the level of the mid ascending aorta, where the residual dissection is seen. There was a history of sternal wound infection with non-union of the sternum. The anterior aspect of the false lumen of the ascending aorta had expanded through the space between the sternal fragments into the subcutaneous tissue. This information was critical in planning the approach for the planned redo median sternotomy and aortic cannulation. The right panel shows the same level after redo open heart surgery. A new graft of the ascending aorta is surrounded by post-operative blood products and small amounts of air.

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Figure 10.53  Aortic root repair This figure shows images of a patient with aortic root repair. Only the non- and right coronary sinuses of Valsalva were replaced with a surgical graft. The native left sinus of Valsalva was maintained. Therefore only the right coronary artery was reimplanted. The native aortic valve was resuspended in a modified David procedure. The origin of the native left main coronary artery of the left sinus of Valsalva is shown in the upper panels. The upper right panel shows highdensity surgical material adjacent to the replaced non- and right sinuses of Valsalva. The lower panels show the reimplanted right coronary artery, with surgical material at the coronary button. (Videos 10.53-i, 10.53-ii)



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Figure 10.54  Surgical grafts, post-operative This figure shows images of a surgical graft of the upper descending thoracic aorta. The graft is intact and the proximal and distal anastomoses are seen.

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Figure 10.55  Surgical graft, elephant trunk procedure The elephant trunk procedure describes a two-stage surgical technique for patients with extensive aneurysmal disease of the thoracic aorta. In the first stage (via median sternotomy), the ascending aorta and aortic root are replaced with a surgical graft. An additional surgical graft is anastomosed at the isthmus and left hanging freely in the dilated descending aorta. In a second stage of the procedure, the free distal end of the graft is anastomosed to the descending aorta (via a left thoracotomy), excluding the dilated descending aorta. This figure shows post-operative images of a patient after the first (upper panels) and second (lower panels) stages of an elephant trunk procedure. The upper images show surgical grafts of most of the ascending aorta and continuation of the graft, freely hanging into the proximal descending aorta. There are metallic markers at the distal end of the graft, which are also seen in the cross-sectional image (right upper panel). The graft inside the dilated proximal descending thoracic aorta can be confused with a dissection if the surgical history is not known. In the second stage of the elephant trunk procedure, the free end of the graft was connected to the mid descending aorta, with excision of the dilated proximal descending aorta.



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Figure 10.56  Surgical graft, elephant trunk procedure This figure shows pre- and post-operative images of a patient after the first stage of an elephant trunk procedure. The pre-operativew images (upper panels) show the massive dilatation of most of the thoracic aorta. The post-operative images (lower panels) show surgical grafts of most of the ascending aorta and continuation of the graft, freely hanging into the proximal descending aorta. There is partial thrombosis of the lumen of the native, massively dilated isthmus and descending aorta, surrounding the elephant trunk graft. The metallic markers at the end of the graft are seen.

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Figure 10.57  Surgical graft, elephant trunk procedure This figure shows a post-operative axial image at the level of the aortic isthmus. There is evidence of median sternotomy. The complex appearance of the aorta is consistent with the surgical graft freely hanging into the proximal descending aorta. There is partial thrombosis of the lumen of the native, massively dilated isthmus and descending aorta. Without knowledge of the operative procedure, understanding this complex anatomy is very difficult and can be mistaken as an acute dissection process.



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Figure 10.58  Post-operative empyema This figure shows images of a patient with remote history of aortic valve replacement and recent bacterial endocarditis. Ten days before the CT scan the patient underwent replacement of the aortic valve and ascending thoracic aorta using a composite graft. The patient remained febrile and demonstrated an elevated white blood count. The CT scan shows evidence of aortic valve replacement and replacement of the ascending thoracic aorta with a composite graft. The graft is surrounded by the expected post-operative blood products. There is a small-sized right-sided and a moderate-sized left-sided pleural effusion with adjacent atelectasis. There is a large air/fluid collection measuring 13 × 7 cm in the left upper pleural space, most consistent with an abscess. There are small mediastinal lymph nodes and prominent axillary lymph nodes.

Figure 10.59  Infected abdominal, surgical graft This figure shows images of a patient several days after placement of an infrarenal aortobifemoral graft. There is a large perigraft fluid collection consistent with graft infection. The more superior fluid collection with a prominent air/fluid level suggests the possibility of an aortoenteric fistula as the source of the infection.

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Figure 10.60  Endocarditis and ascending aortic graft infection A patient with a remote history of aortic dissection and surgical grafting of the ascending aorta. The patient was evaluated for suspected endocarditis. The CT scan shows a moderate-sized right pleural effusion. The aortic root is dilated, measuring 5.6 cm. There has been replacement of the proximal ascending aorta with a supra-coronary graft. There is fluid surrounding the graft, which compresses the superior vena cava. The appearance is suspicious for graft infection. Beyond the distal anatomy of the graft, there is dilatation of the aortic arch (maximum diameter is 7.5 cm, consistent with pseudoaneurysm) and residual dissection. Findings during subsequent surgery were consistent with endocarditis of the native aortic valve caused by Staphylococcus aureus. The graft of the ascending aorta was surrounded by pus. There was a false aneurysm beyond the distal anastomosis of the graft.



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Figure 10.61  Post-operative pseudoaneurysm This figure shows images of a patient with remote aortic valve replacement for endocarditis and pericardial patch repair of a subcoronary abscess cavity. The patch had partially dehisced, generating a supra-annular/sub-coronary pseudoaneurysm. The CT demonstrates a largely thrombosed pseudoaneurysm of the aortic root at the right sinus of Valsalva. The right coronary artery (RCA) is draped over the pseudoaneurysm (right lower panel).

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Figure 10.62  Root abscess This figure shows images of a patient who presented with fever months after aortic valve replacement with a mechanical valve. The small contrast-filled cavities at the aortic root are consistent with sequelae of a root abscess.



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Figure 10.63  Root abscess The small cavities are better appreciated in these cross-sectional images of the aortic root.

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Figure 10.64  Post-operative pseudoaneurysm This figure shows images of a patient with remote placement of a supra-coronary graft of the aorta for type A aortic dissection repair. There is a prominent native aortic root measuring 4.2 cm and a supra-coronary graft of the ascending aorta. There is a small saccular outpouching at the proximal anastomosis adjacent to the non-coronary sinus of Valsalva consistent with a pseudoaneurysm (upper panels). Suture material at the proximal anastomosis of the supra-coronary graft of the ascending aorta is demonstrated (right lower panel).



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Figure 10.65  Post-operative pseudoaneurysm This figure shows images of a patient with a history of aortic valve endocarditis and subsequent homograft replacement of the aortic root with reimplantation of the coronary arteries. The CT images show a pseudoaneurysm originating primarily from the posterior aspect of the left coronary cusp. The cavity measures 2.3 × 0.8 cm. The pseudoaneurysm extends superiorly as well as inferiorly into the area of the fibrous confluence of the anterior mitral leaflet and the posterior wall of the aorta.

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Figure 10.66  Post-operative pseudoaneurysm Axial images at the aortic root demonstrate the origin of the pseudoaneurysm from the posterior aspect of the left coronary cusp, straddling the commissure between the left and non-coronary cusps (left lower panel). During subsequent open-heart surgery, an autologous pericardial patch repair of the opening to the subvalvular space was performed. Additionally, an aortic valve replacement with a Carpentier-Edwards valve was performed.



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Figure 10.67  Post-operative pseudoaneurysm This figure shows images of a patient with a history of orthotopic heart transplantation. There is a large pseudoaneurysm of the ascending aorta at the anastomosis site with a maximum size of 6.2 cm. The typical anastomosis site of the native and transplanted left atrium is seen.

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Figure 10.68  Mycotic pseudoaneurysm of the ascending aorta This figure shows images of a patient who developed a mycotic pseudoaneurysm after mitral valve repair. Residuals of retained epicardial pacer wires are seen in the subcutaneous tissue of the ­anterior chest wall (right lower panel). There is a small amount of subcutaneous fluid surrounding the wire. There is a presumably mycotic pseudoaneurysm arising from the mid ascending aorta, in a retrosternal location. The saccular outpouching measures 3.6 × 4.7 × 4.7 cm and is partially thrombus filled (upper panels).



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Figure 10.69  Paravalvular leak with small fistula of the aortic valve This figure shows images of a patient with a remote history of aortic valve replacement with a composite graft (aortic valve and graft of the ascending aorta) with reimplantation of the coronary arteries. During a cardiac catheterization, a paravalvular tract was observed (left upper panel and middle panels). The CT images show evidence of aortic valve replacement with a composite graft (lower right panel). There is paravalvular leakage beginning adjacent to the origin of the right coronary artery and draining into the left ventricular outflow tract as a fistula. There is mild dilatation of the left ventricle.

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Figure 10.70  Post-operative pseudoaneurysm of left ventricle originating at mitral annulus This figure shows images of a patient with a remote history of aortic and mitral valve replacement, with mechanical valves. Originating from the inferolateral and lateral aspects of the mitral annulus is a contrast-filled space measuring 6.5 × 4.8 cm. It extends along the lateral wall of the left atrium and basal segments of the left ventricle. Its borders are partially calcified. It communicates at the level of the mitral valve prosthesis with the left ventricle. In addition, there is a small outpouching originating from the inferior aspect of the mitral annulus, which is thrombosed and has calcification of the wall. It measures 1.0 × 1.9 cm.

Figure 10.71  Calcified aorta In patients undergoing reoperative open-heart surgery, the local extent of calcified atherosclerotic plaque can determine the cannulation site for cardiopulmonary bypass. To assess the amount of calcification, a non-contrast-enhanced CT scan is performed. In this figure, volume-rendered images from a patient with severe calcification of the aorta and aortic valve are shown. The soft tissues are faded, allowing a three-dimensional image of the calcification.



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Figure 10.72  Aortic arch thrombus and atheroma Contrast-enhanced scans can assess the amount of calcified and non-calcified atherosclerotic plaque, which appears to have a relation to post-operative stroke incidence. This figure shows a protruding soft tissue in the aortic arch, consistent with thrombus. There is underlying calcified atherosclerotic plaque.

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Figure 10.73a  Calcified aorta in a patient with a history of aortitis This figure shows images of a severely calcified aorta in a patient with a remote history of Takayasu’s aortitis. The patient presented with left main coronary artery stenosis. The CT images show severe circumferential calcification of the thoracic aorta with an area of narrowing in the descending thoracic aorta. The calcified right coronary artery (RCA) and left anterior descending (LAD) coronary artery are seen. Because of the severe aortic calcification, the patient was not considered to be a candidate for open heart surgery and subsequently underwent left main percutaneous coronary intervention (PCI).



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Figure 10.73b  Patient with history of aortitis and aortic stenosis This figure shows images of a patient with Takayaso arteritis. There is diffuse disease of the descending thoracic aorta with several areas of stenosis and extensive collaterals. Specifically, there is collateral between the internal thoracic arteries and the iliac arteries. (Video 10.73b)

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Figure 10.74  Aortitis, positron emission tomography (PET)/CT This figure shows MDCT and PET images of a patient with aortitis. The CT (left panels) demonstrates smooth wall thickening of the aorta compatible with aortitis. There is prominent wall thickening in the mid-lower descending thoracic aorta with a maximum thickness of 1.2 cm. There is also prominent wall thickening of the aorta at the renal artery level, which is indistinguishable from a large amount of para-aortic soft tissue. The metabolic PET images (right panels) demonstrate regions of moderately intense fluorodeoxyglucose (FDG) uptake associated with the descending thoracic aorta and segments of the abdominal aorta. These findings are consistent with hypermetabolic inflammatory changes involving the aorta. Fusion images (middle panels) combine the anatomic and functional information.



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Figure 10.75  Intra-aortic balloon pump This figure shows images of a patient with a pericardial effusion. In the descending aorta an intra-aortic balloon pump is seen. In the late diastolic images, the inflated balloon is seen in crosssectional (left panel) and longitudinal (right panel) images. Additional image reconstruction in systole (during balloon deflation) allows better visualization of the aortic wall.

Figure 10.76  Aortic coarctation This figure shows evidence of aortic coarctation with severe stensosis just beyond the left subclavian artery. Coarctation is associated with a bicuspid aortic valve (right lower panel).

Chapter 11

Peripheral artery disease

Because of their relatively large size, lack of motion, and straight course, assessment of peripheral arteries, including the identification and quantification of luminal stenosis, can be performed with computed tomography (CT) angiography (Figure 11.1).387,388 Vessel wall calcification remains a major limitation, in particular in smaller vessels. Multi-detector computed tomography (MDCT) protocols typically use a spiral examination mode with thin, overlapping images and rapid contrast bolus injection.389 CT angiography has developed into an alternative imaging modality in several vascular regions. The experience in lower-extremity peripheral artery disease (PAD) imaging is described below. The assessment of subclavian artery access in the context of transcatheter aortic valve replacement (TAVR) is discussed in Chapter 7. In neuroradiology, modern systems allow simultaneous imaging of the carotid arteries, intracranial vessel, brain morphology, and brain perfusion.390 CT angiography is increasingly being used as a “road map” for subsequent angioplasty.391–400 Disadvantages of CT in comparison with ultrasound and MRI are the associated radiation exposure and the lack of flow information.

11.1 Lower-extremity CT angiography

CT angiography (CTA) of the entire lower-extremity arterial system, which includes supra-inguinal inflow vessels and infrainguinal runoff, has only become possible with the introduction of multi-detector-row CT and has virtually replaced diagnostic intra-arterial angiography.400a,b The most important indication for lower-extremity CTA is treatment planning in patients with PAD.400c,d Other indications include acute ischemia, trauma, and anatomic imaging, such as before free-flap harvesting, or in athletes suspected of functional or anatomic popliteal entrapment syndrome, or iliac endofibrosis.400b The role of lower-extremity CTA in the setting of PAD is not necessarily to establish the diagnosis, which is typically based on symptoms, clinical exam, and non-invasive testing such as ankle-brachial index.400e The strength of

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Figure 11.1  Iliac arteries This figure shows centerline reconstructions of the left and right iliac arteries.

lower- extremity CTA is to map the disease process within this large territory, which is critical for treatment planning. The two main categories of PAD warranting intervention are patients with lifestyle-limiting intermittent claudication (Fontain IIb) (Figure 11.2), and patients with critical limb ischemia (rest pain and/or tissue loss; Fontain III and IV) (Figure 11.3). In the claudication group, treatment aims at symptom relief, and is typically restricted to lesions above the knee. In patients with critical limb ischemia, revascularization aims at prevention of tissue loss and amputation, which requires more aggressive endovascular and/or surgical treatment of above- and below-knee arteries.400f The anatomic coverage for a lower-extremity CT angiogram typically extends from T12 (if supra-renal aorta is to be included) down to the toes, with a relatively small field of view (SOV), in order to maintain adequate in-plane resolution.400b Through-plane resolution (in the z-axis) is typically 0.7–1.25 mm. While lowerextremity CTA data acquisition is relatively straightforward with state-of-the-art equipment, synchronization with contrast medium delivery requires particular attention to the fact that bolus propagation in a diseased lower-extremity arterial tree may be substantially delayed.400g A simple strategy is to deliberately acquire the CT data in a relatively long scan time of 40 seconds, and preprogramming an optional second pass from above the knees down through the toes.400g Technically the most challenging component of lower-extremity CTA is visualization and post-processing of the typically 1000–2000 axial CT images: viewing axial source images is tedious, and inadequate for communicating findings to the



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Figure 11.2  Lower-leg CT angiography Maximum intensity projection (MIP) image (left panel) and multi-path curved planar reformation (right panel) of a lower-extremity CTA obtained in a 55-year-old man with a 10-year history of claudication and an ankle-brachial index of 0.5 on the right and 0.8 on the left. Moderate atherosclerotic calcification in the MIP image (left) precludes assessment of supra-inguinal vessels. Multi-path curved planar reformation (mpCPR) (right) clearly shows a 6 cm occlusion of the right external iliac artery. Collateral vessels (via an obturator artery) are shown in the MIP image (left). Both the MIP image (left) and the mpCPR show a well-collateralized 9 cm distal superficial femoral artery occlusion. On the left, there are approximately 50% focal stenoses at the external iliac arteries, and more than 50% stenoses of the superficial femoral artery at the level of the adductor hiatus. Crural arteries are patent.

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Figure 11.3  Lower-leg CTA Maximum intensity projection (MIP) image (left) and multi-path curved planar reformation (mpCPR) of a lower-extremity CT angiogram obtained in a 69-year-old woman with right lowerextremity ischemia and gangrenous toes. Extensive atherosclerotic calcification of the aortoiliac vasculature in the MIP (left) image obscures a short complete occlusion of the right common iliac artery, and extensive stenosis of the bilateral supra-inguinal system, as shown in the mpCPR (right). The right superficial femoral artery is diffusely diseased and occluded, and reconstitutes in the distal thigh. The anterior tibial artery below the knee is moderately diseased and patent. There is a congenitally absent posterior tibial artery with compensatory enlargement of a patent, proximally diseased peroneal artery. Multiple stenoses are also seen in the left superficial femoral artery. The left anterior tibial artery is completely occluded.



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treating physician. The classic 3-D techniques for displaying cardiovascular CT data, such as maximum intensity projection (MIP) and volume-rendered (VR) images, are often limited in patients with PAD, because approximately half of these patients have significant vessel wall calcifications or stents in place. Both preclude visualization of the diagnostically and therapeutically relevant flow channels.400h Analysis of the vessel lumen is best achieved with so-called curved planar reformations (CPRs), either through each arterial branch separately or as so-called multi-path CPRs (Figures 11.2 and 11.3).400i Processing of lower-extremity CTA may be time-consuming, and large programs might benefit from dedicated technologists or a 3-D laboratory to generate standardized images of the lower-extremity arterial tree. Lower-extremity CTA is an accurate imaging modality in patients with intermittent claudication, with a sensitivity of 95% (95% CI, 92–97%) and a specificity of 96% (95% CI, 93–97%) for detecting more than 50% stenoses or occlusions reported in a recent meta-analysis.400j CTA is more accurate than Doppler ultrasound, and performs equal to or better than MRA.400k The accuracy of lower-extremity CTA decreases in below-knee vessels, with the main limiting factor being the presence of arterial calcifications. Since below-knee arteries are not a treatment target in patients with intermittent claudication, this is not a significant drawback in this population.400l However, in patients with critical limb ischemia, who may also be diabetic, and may have significant arterial calcification, this is a greater concern. Recent data suggest, however, that CTA provides accurate recommendations for the management of patients with critical limb ischemia as well.400m Very recently, dual-energy CT technology has become available on commercial CT systems. In principle, basic material decomposition of CT projection data acquired at two different X-ray energy levels (e.g. 140 and 80 kVp) allows differentiation of iodine from calcium.400n While successfully applicable to the identification of densely opacified vessels (containing iodine), and to dense calcifications (large plaque or cortical bone), as in large proximal vessels, dual-energy CT has not been shown to reliably separate calcium from iodine in small, below-knee peripheral vessels, where this would be particularly desirable.400o,p This may be explained by the low signal provided by low-attenuation contrast medium (due to partial volume artifacts) in small arteries, and low-attenuation vessel wall calcium (mostly due to partial volume artifacts related to the limited spatial resolution of current CT systems) in the presence of noise. Continued evolution of CT technology with improving spatial resolution, better separation of energy spectra, and novel iterative reconstruction and other postprocessing techniques may ultimately overcome the few remaining technical limitations of this powerful technology.

Chapter 12

Cardiac masses

Computed tomography (CT) is not the imaging modality of choice for a­ ssessment of cardiac masses, which are typically initially imaged with echocardiography, MRI, and positron emission tomography (PET)/single-photon emission computed tomography (SPECT).401,402 However, CT provides valuable anatomic information in selected patients. It is for example superior in defining the r­ elationship of lung masses to the pericardium and heart,403 and may allow definition of the blood supply of ­cardiac masses. If dedicated CT imaging is planned, the protocol should be modified for the specific clinical question.404 In other ­situations, CT may occasionally identify incidental cardiac masses. The anatomic criteria ­seldom allow a definitive histologic diagnosis, but rather d ­ ifferentiate between likely benign versus malignant lesions, with implications for further management. Cardiac masses are described with regard to size, location, and spatial relationship to adjacent structures. It is important to evaluate the border of the mass (capsulated, well defined, irregular, infiltrative), the density (HU) of the mass, its homogeneity, and contrast enhancement before and after contrast administration. A dedicated ­protocol similar to a coronary acquisition may also define details of blood supply (Figures 12.13 and 12.16). Similar to MRI, which allows superior tissue characterization, ­classification of masses according to these criteria allows association of ­certain patterns with corresponding masses.405–410 As described above, an important ­clinical question is the differentiation between likely benign and malignant ­processes. Imaging can provide important clues, but the definitive diagnosis requires ­surgical sampling and pathology. From the wide variety of primary benign and m ­ alignant cardiac tumors and cardiac metastases, the following examples of benign and ­malignant tumors demonstrate basic imaging criteria. Common benign tumors are atrial myxomas. Myxomas often originate from the left atrium or mitral annulus with a stalk, and may demonstrate tumor calcification (Figures 12.1 and 12.2). However, definitive characterization is often not possible with CT imaging alone (Figures 12.3–12.6).411,412 An example of a left atrial paraganglioma is shown in Figures 12.9 and 12.10. Benign masses of the left ventricle have 283

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Figure 12.1  Atrial myxoma This figure shows an atrial tumor, consistent with a myxoma. The mass appears to be broadly attached in the area of the posterior mitral annulus and measures 2.8 × 2.8 × 3.7 cm. It is noncalcified and homogeneous and shows no evidence of enhancement.

Figure 12.2  Atrial myxoma This figure shows multiple reconstructions of the mass at different phases of the cardiac cycle. The images demonstrate that the mobile tumor passes through the valve plane during diastole. (Videos 12.2-i, 12.2-ii)



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Figure 12.3  Suspected atrial myxoma This figure shows a large tumor in the left atrium, attached with a broad base to the intra-atrial septum. The tumor is partially calcified. The findings are suggestive of atrial myxoma.

Figure 12.4  Suspected atrial myxoma This figure shows a tumor contiguous with the roof of the left atrial body near the origin of the atrial appendage. The tissue is slightly heterogeneous with internal calcification and mild enhancement, measuring 2.0 × 1.6 × 1.7 cm. Originating from the proximal circumflex artery is an atrial branch that extends into the region of the mass of the left atrium. Although these finding are most consistent with atrial myxoma with atypical location, definitive characterization is not possible.

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Figure 12.5  Calcified right atrial thrombus This figure shows images of a patient with a history of Hodgkin’s disease. Image acquisition was delayed in relation to the contrast injection to avoid contrast streak artifacts in the right atrium. At the inferior wall of the right atrium close to the junction with the inferior vena cava is a small tissue mound, which extends over a distance of 2 cm and has a thickness of 0.8 cm. There is calcification of the tissue. The appearance suggests a benign process, most likely a calcified thrombus, secondary to trauma from a central line.

similar characteristics. Additional MRI is often utilized for further characterization (Figures 12.7 and 12.8). Signs of malignancy, which can be assessed with CT, include infiltration of adjacent structures and the presence of tumor vessels. Examples are shown (Figures 12.11–12.18).



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Figure 12.6  Right atrial thrombus This figure shows images of a low-density mass extending from the inferior vena cava (IVC) near the confluence of the hepatic veins to the level of the tricuspid valve. The mass does not appear to occlude the IVC or the right-sided atrioventricular inflow. Its low attenuation suggests thrombus. The cardiac chambers are otherwise unremarkable. The kidneys are intact and there is not evidence of renal malignancy. The patient underwent excision of the mass. Pathology was consistent with an organizing thrombus.

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Figure 12.7  Suspected left ventricular fibroma A relatively large mass of the lateral left ventricular wall is shown. The CT (upper panels) shows inhomogeneity and a small calcification. The MRI images (lower panels) are shown in comparison. The images in the right lower panel demonstrate contrast enhancement after gadolinium administration. Based on these findings a fibroma of the left ventricle was suspected.



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Figure 12.8  Suspected left ventricular fibroma Another example of a suspected left ventricular fibroma is shown in this figure. CT images (upper panels) and MRI images (lower panels) are shown in comparison. Within the anteroapical region of the left ventricle is a mass measuring 4 × 4.7 × 5.8 cm. The lesion is well circumscribed without evidence of surrounding edema or neovascularity. The findings suggest dense fibrotic tissue with focal areas of calcification. The patient subsequently underwent surgery with excision of the mass. Pathology confirmed the diagnosis of a cardiac fibroma.

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Figure 12.9  Left atrial paraganglioma This and the next figure show pre- and post-operative images of a tumor at the roof of the left atrium. The patient underwent surgery and an intraoperative biopsy was consistent with an intrapericardial paraganglioma situated on the roof of the left atrium. The tumor was subsequently removed.



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Figure 12.10  Left atrial paraganglioma Images at follow-up did not show evidence of residual or recurrent tumor. Surgical clips are seen in the operative field.

Figure 12.11  Fibrous tumor versus sarcoidosis This and the next figure show images from a patient presenting with ventricular arrhythmia. The imaging studies demonstrate a fibrous mass of the inferior wall of the left ventricle. Infiltration of the basal inferior wall of the left ventricle is demonstrated with delayed contrast-enhanced MRI (right panel). The same area shows faint hypoenhancement on the multi-detector computed tomography (MDCT) image (left panel). (Video 12.11)

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Figure 12.12  Fibrous tumor versus sarcoidosis The short-axis view demonstrated the location of the tumor of the left ventricle, extending into the right ventricle (MRI right panel, CT left panel). Further work-up of the patient demonstrated active sarcoidosis. His clinical symptoms and imaging findings improved during immunosuppressive therapy.

Figure 12.13  Right atrial spindle cell sarcoma The figure shows a tumor of the right atrium. Several small tumor vessels are seen extending into the lesion. The patient underwent surgery with removal of the tumor. Pathology was consistent with a high-grade spindle cell sarcoma.



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Figure 12.14  Cardiac lymphoma This figure shows images of a patient with lymphoma. There is a large mediastinal tumor with predominantly intrapericardial location. It involves the intra-atrial septum and the posterior and superior walls of the left and right atria. The tumor encases the pulmonary veins, with partial compression of the right superior vein ostium. In addition, the tumor encases the superior vena cava, left main coronary artery, proximal left anterior descending artery, and proximal left circumflex artery without causing significant compression. Pathology was consistent with a diffuse primary mediastinal diffuse large B cell lymphoma.

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Figure 12.15  Mesothelioma These images show a soft tissue mass that encases the aorta and central pulmonary arteries. The ­narrowing of the central pulmonary arteries is shown in the magnetic resonance angiography (MRA) (left upper panel). There is additional encasement and narrowing of the left superior pulmonary vein. The tumor also involves the right atrial wall and the inflow portion of the right ventricle with suspected myocardial invasion. It extends through the pericardium in the area of the right atrioventricular groove, with complete encasement of the dominant right coronary artery (RCA). Pathology was consistent with a malignant spindle cell neoplasm consistent with sarcomatoid mesothelioma.



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Figure 12.16  Pericardial sarcoma The identification of tumor vessels, as a sign of malignancy, is often possible secondary to the high spatial resolution of MDCT. This figure shows images of a large pericardial synovial sarcoma at the inferior aspect of the heart. The CT demonstrated tumor vessels extending from the apical left anterior descending (LAD) into the tumor.

Figure 12.17  Pulmonary artery intimal sarcoma This figure shows images of a patient with pulmonary artery intimal sarcoma. The initial presentation was shortness of breath, secondary to occlusion of pulmonary artery branches (left panel). The CT scan demonstrates extension into the mediastinum and left atrium, which was confirmed at autopsy.

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Figure 12.18  Suspected neoplastic involvement of pulmonary artery This figure shows images from a patient with chest discomfort and worsening shortness of breath. The pulmonary valve demonstrates a nodular appearance. There are mobile nodular lesions of the main pulmonary arteries. The walls of the pulmonary arteries are markedly thickened confluent with the abnormal increase of tissue of the mediastinum. Additional lung lesions were observed. A malignant process was suspected. (Videos 12.18-i, 12.18-ii)

Chapter 13

Adult congenital heart disease

Multi-detector computed tomography (MDCT) is used in pediatric patients as a ­second-line imaging modality after echocardiography and MRI, if anatomic findings are unclear or confirmation is required.413–416 Because of its short acquisition time, CT can frequently be performed with mild sedation. However, because of the radiation exposure, a particularly careful evaluation of the risks and benefits is necessary in the pediatric patient population.417–422 Consistent with the overall focus of the book, this section mainly describes ­congenital abnormalities that are seen in adult populations.423–427

13.1  Cardiac Chambers and Myocardium

Atrial septal defects (ASDs) are common congenital heart defects. The different types of defects (ostium secundum defect, ostium primum defect, sinus venosus defect, coronary sinus defect, and patent foramen ovale (PFO)) are related to the embryonal development of the intra-atrial septum. Unrepaired defects are occasionally identified in asymptomatic or symptomatic adults. Symptoms can include right heart failure or neurologic symptoms secondary to paradoxical embolization. Because the central intra-atrial septum is a very thin structure, anatomic assessment with non-invasive imaging modalities is limited. Identification of these defects typically relies on the assessment of flow by echocardiography and MRI. Anatomic assessment with CT can define the relationship of the defect to other anatomic structures, such as the ­coronary sinus (Figure 13.1) or the sinus venosus (Figure 13.2). Surgical or ­percutaneous closure of ASD is considered, depending on anatomic characteristics, shunt volume (Qp/Qs), and clinical symptoms. CT is increasingly used for pre- and post-interventional imaging in the setting of percutaneous ASD closure (Figure 13.3).428 More recently several papers describe “septal pouch” as a blind ending tubular remnant at the interatrial septum.429,430

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Figure 13.1  Coronary sinus atrial septal defect (ASD) This figure shows images of a coronary sinus ASD. There is an unroofed coronary sinus, with a resulting ASD measuring 1.6 × 1 cm. There is mild right atrial and right ventricular enlargement.

Figure 13.2  Sinus venosus atrial septal defect (ASD) This figure shows images of a sinus venosus type atrial septal defect. The defect is located at the roof of the intra-atrial septum. There is partial anomalous venous return involving the superior right pulmonary vein, which empties into the superior vena cava (mid upper panel).



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Figure 13.3  Percutaneous atrial septal defect (ASD) closure CT is used for pre- and post-interventional imaging in the setting of percutaneous closure. This figure shows post-interventional images after PFO closure with a #33 Cardio-Seal device. The cardiac structures are faded in this VRI. The high-density metal struts are clearly seen in relation to the surrounding structures. (Video 13.3)

Ventricular septal defects (VSDs) are common in childhood, but either close s­ pontaneously or are closed surgically at an early age. Therefore, in adult p­ opulations, mainly surgical changes are identified. The different types of VSD (­perimembranous VSD, muscular or apical VSD, inlet of atrioventricular canal VSD, supracristal or subaortic VSD) are related to the embryonal development of the interventricular ­septum. CT can identify the defect and describe the ­relationship to surrounding structures (Figures 13.4–13.7). Echocardiography, MRI, and cardiac catheterization with evaluation of oxygen saturation, flow, shunt volume (Qp/Qs), and pressure measurements are important for functional assessment. Arrhythmogenic right ventricular dysplasia (ARVD), LV non-compaction, and hypertrophic obstructive cardiomyopathy (HOCM) are described in Chapter 4.

13.2  Pericardial Disease

Images of patients with absence of the pericardium (Figures 5.3–5.6) are shown in Chapter 5.

13.3  Valvular Heart Disease

Images of patients with bicuspid and quatrocuspid aortic valves (Figures  6.1–6.7), sub-aortic membrane (Figure  6.10), and Ebstein’s anomaly of the tricuspid valve (Figure 6.16) are included in Chapter 6.

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Figure 13.4  Ventricular septal defect This image shows a small left ventricular septal defect in the inferior aspect of the basal septum.

Figure 13.5  Suspected spontaneous closure of VSD This figure shows images of a patient with suspected, spontaneous closure of a VSD. Below the right coronary sinus is a saccular outpouching of the left ventricular outflow tract, extending to the right atrioventricular groove. There is no communication to the right atrium or right ventricle. The findings are consistent with an aneurysm of the membranous septum, likely secondary to remote closure of a VSD with redundant tissue of the tricuspid valve.



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Figure 13.6  Aneurysm of membranous interventricular septum This figure shows another example of an aneurysm of the membranous interventricular septum (wind sock aneurysm). Below the right leaflet of the aortic valve, there is a small saccular outpouching of the membranous interventricular septum, extending to the right ventricle. The left three images in the upper row show VRIs of the aortic root with the aneurysm visible inferior to the right coronary cups. In the lower row, the left panel shows the aneurysm anterior to the left ventricular outflow tract in a three-chamber view. The second panel from the left shows a short-axis view of the aortic root at the level of the aneurysm. The aneurysm leads to eccentric outpouching (7 o’clock). Additional short-axis views at higher levels show a densely calcified bicuspid aortic valve.

13.4  Coronary Arteries

The assessment of coronary anomalies is a strength of MDCT, in particular because of the ability of three-dimensional reconstruction.431,432 Image reconstruction allows definition of the origin and course of anomalous arteries. There are multiple different types of anomalies with different clinical ­significances.433,434 Variants without clinical significance include a right c­oronary artery (RCA) origin of the non-coronary instead of the right coronary cusp (Figure 13.8). More significant is the origin of the right or left coronary system from the contralateral cusp or artery (Figures 13.9–13.21). The course of the anomalous artery relative to the aorta and pulmonary artery determines the clinical significance. A course of the anomalous artery posterior to the aortic root, between the aortic root and the left atrium (Figure 13.11), is considered a benign course, because

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Figure 13.7  Surgically repaired VSD in tetralogy of Fallot This figure shows images of a patient with repaired tetralogy of Fallot. There is dilatation of both ventricles. The patient has undergone reconstruction of the pulmonary outflow tract and closure of the ventricular septal defect with a patch.

the left atrium is a low-pressure chamber. In contrast, a course of the anomalous artery anterior to the aortic root, between the aorta and the pulmonary artery, can be associated with intermittent compression between the two high-pressure vessels. For this interarterial course, two variants are described: (1) A low course, crossing between the aortic root and pulmonary outflow, extending into the interventricular septum, is described as intracristal (Figures 13.12 and 3.13). Some investigators describe the risk of compression with significant clinical complications for this variant as being lower. (2) In contrast, a high course, crossing between the aorta and pulmonary artery, has a higher risk of systolic compression between the two structures (Figures 13.14–13.18). The demonstration of an anomalous course between the aorta



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Figure 13.8  Anomalous coronary origin An established indication for coronary CTA is the assessment of anomalous coronary arteries. Image reconstruction allows to define the origin of the arteries. In this figure the left main (LM) coronary artery originates from the non-coronary (7 o’clock) instead of the left coronary cusp.

Figure 13.9  Anomalous origin of RCA from LM This figure shows images of a 15-year-old patient, symptomatic with exertional chest pain. The right coronary artery originates from the left main coronary artery. The RCA takes a course between the right ventricular outflow tract and the aorta and continues in the right a­ trioventricular groove. (Video 13.9)

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Figure 13.10  Anomalous RCA ostium of left coronary cusp This figure shows images of an anomalous RCA. The RCA has a separate ostium from the left cusp, originating toward the raphe between the left and right coronary cusps. The RCA takes a course between the pulmonary outflow tract/pulmonary artery (at the level of the pulmonary valve) and aorta into the right atrioventricular groove.

and the pulmonary artery may therefore define an indication of surgical correction. However, recent papers demonstrate that clinical symptoms and documentation of myocardial ­ischemia are most critical in the decision about management in these patients.435 An advantage of CT is description of the relationship of the anomalous coronary artery to other cardiovascular structures. This becomes obvious in cases of coronary fistulas (Figures 13.22–13.26) and in the evaluation of an intramyocardial course of a coronary muscle bridge (Figures 13.23–13.28).436 The large branches of the coronary arteries are located in the epicardial fat. However, individual segments occasionally have an intramyocardial location (myocardial bridges). MDCT permits the evaluation of these segments. CT is likely very sensitive in the identification of bridges but does not provide information about the hemodynamic significance of bridges. In contrast, conventional angiography, which defines bridges by their systolic compression, is likely more specific for significant myocardial bridges.

13.5  Coronary Veins and Coronary Sinus

Images of a patient with a coronary sinus aneurysm are shown in Figures  13.29 and 13.30.



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Figure 13.11  Anomalous coronary origin In this figure the left and right coronary arteries originate with a common coronary ostium from the right coronary cusp. The left coronary artery then takes a course posterior to the aortic root, between the aortic root and the left atrium. Because the left atrium is a low-pressure system, this anomaly has low risk of complication.

13.6  Pulmonary Veins

Partial anomalous return of the pulmonary veins is seen as an isolated finding or as part of other abnormalities (Figures 13.2, 13.31, 13.32). 13.7 Aortic Disease

CT can demonstrate the anatomy of unrepaired aortic coarctation189 (Figures 13.33 and 13.34), and results after percutanous endovascular (Figures 13.35 and 13.36) and surgical (Figures 13.37–13.39) repair. The known association with bicuspid aortic valve should be considered (Figure 13.33).

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Figure 13.12  Anomalous coronary artery, intramyocardial course Anomalous origin of the left main coronary artery from the right coronary cusp, with a common ostium together with the right coronary artery. The left main takes an inferior, intramyocardial course below the level of the pulmonic valve in the interventricular septum between the left and right ventricular outflow tracts. The vessel resurfaces on the anterior aspect of the left ventricle and trifurcates into the left anterior descending (LAD), a Ramus intermedius, and the left circumflex. This anatomy is thought to be associated with a lower risk of systolic compression and clinical complications.

Figure 13.13  Anomalous coronary artery, intramyocardial course Another patient with an anomalous origin of the left main coronary artery with a common ostium from the right coronary cusp is shown in these images. The volume-rendered images show the low course of the anomalous left main with the typical hammock appearance. The maximum intensity projection (MIP) image (left upper panel) shows the associated position of the left main in the interventricular septum. The vessel resurfaces on the anterior aspect of the left ventricle.



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Figure 13.14  Anomalous coronary artery, course between aorta and pulmonary artery Similar to the previous figure, the LAD originates from the right coronary cusp and takes a course anterior to the aortic root. However, the LAD crosses above the level of the pulmonary artery, between the aorta and pulmonary artery. This anatomy is associated with a higher risk of systolic compression and clinical complications.

Figure 13.15  Anomalous coronary artery, course between aorta and pulmonary artery This and the following two figures show images of a symptomatic patient with an anomalous RCA and coronary artery disease (CAD). The RCA originates from the left coronary cusp, next to the left main ostium, and takes an initial course between the pulmonary artery and aorta (center panel). There is slit-like compression of the artery at the ostium and the proximal interarterial course (right panels). More distally, the RCA has a normal diameter (left upper panel), but shows eccentric, partially calcified atherosclerotic plaque accumulation (center and left lower panels).

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Figure 13.16  Anomalous coronary artery, course between aorta and pulmonary artery This figure is a copy of Figure 13.13 but illustrates the findings with arrows.

Figure 13.17  Anomalous RCA and CAD of the LAD In the same patient, there is eccentric non-calcified plaque of the proximal LAD with likely significant luminal stenosis. This was confirmed during invasive angiography. The images demonstrate that in adults with anomalous coronary arteries, clinical symptoms of angina may be related to superimposed CAD rather than compression of the anomalous artery. Careful clinical evaluation and correlation of anatomic and functional results is necessary in these patients.



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Figure 13.18  Anomalous RCA and CAD of the LAD This figure is a copy of Figure 13.15 but illustrates the findings with arrows.

Figure 13.19  Anomalous coronary artery, angiography The following are images of a patient with suspected anomaly of the left coronary system. The  angiogram shows the origin of the LAD and RCA from a common ostium in the right ­coronary cusp.

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Figure 13.20  Anomalous coronary artery, comparison of angiography and CT This figure compares angiographic and CT images. The CT demonstrates the origin of the left coronary system from the right coronary sinus of Valsalva. There is a common ostium shared by the left coronary system and the right coronary artery (RCA). The anomalous left main (LM) coronary artery takes a course between the aortic root and the outflow tract of the right ventricle within the musculature of the crista of the upper interventricular septum.

Figure 13.21  Anomalous coronary artery, CT Additional images show the origin and proximal course of the anomalous left coronary artery. In addition, the more distal course and bifurcation into the left anterior descending (LAD) and left circumflex (LCX) coronary arteries are shown.



Adult congenital heart disease 311

Figure 13.22  Complex coronary fistula The following figures show images of a patient with a complex coronary fistula. The fistula originates in the right coronary sinus. It gives rise to the RCA and then continues into a bellshaped structure, which eventually connects to the left atrium. In this figure, the comparison between angiographic and CT images provides a three-dimensional understanding of the fistula. (Video 13.22)

Figure 13.23  Coronary fistula, angiogram Different images from the conventional angiogram are shown in this figure. An enlarged fistula originates from the right coronary cusp and leads into a bell-shaped structure. There is filling of the left atrium, likely secondary to communication between the fistula and LA.

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Figure 13.24  Coronary fistula, CT Corresponding CT images are shown in this figure. The origin of the fistula of the right coronary cusp is seen (left upper panel). The other panels show cut-planes at different levels. The origin of the right coronary artery (RCA) and the connection of the fistula to the bell-shaped structure are demonstrated.

Figure 13.25 Coronary arteriovenous malformation (AVM) with connection to pulmonary artery This figure shows an arteriovenous malformation with contributions from the conus branch of the right coronary artery as well as left main and left anterior descending coronary arteries. There appears to be an additional supply from a branch of the left internal mammary artery, although this is incompletely imaged. The malformation appears to drain into the pulmonary artery just above the pulmonary valve. There is coronary artery atherosclerosis involving the coronary arteries.



Adult congenital heart disease 313

Figure 13.26 Coronary arteriovenous malformation (AVM) with connection to pulmonary artery This figure demonstrates the vessel tangle located between the proximal left anterior descending coronary artery and pulmonary artery.

Figure 13.27  Myocardial bridge CT is very sensitive in the identification of bridges but does not provide information about the hemodynamic significance of bridges. An example is shown in this figure. The proximal LAD has a brief intramyocardial course consistent with a myocardial bridge. There are calcified atherosclerotic changes in the proximal LAD. Typically, the intramyocardial segment is spared.

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Figure 13.28  Myocardial bridge Another example is shown in this figure. The mid LAD has a shallow intramyocardial course consistent with a myocardial bridge.

Figure 13.29  Coronary sinus venosus aneurysm Abnormal coronary sinus anatomy including coronary sinus aneurysms can be visualized. The images in this figure show a coronary sinus with normal proximal dimensions. Shortly after the ostium, there is aneurysmal dilatation with a maximum dimension of 2.5 × 1.7 cm at the base of the interventricular septum.



Adult congenital heart disease 315

Figure 13.30  Coronary sinus fistula This figure shows a fistula connecting the coronary sinus and left atrium.

Figure 13.31  Partial anomalous return of pulmonary veins (Scimitar syndrome) Partial anomalous return of the pulmonary veins is seen as an isolated finding or as part of other abnormalities. In this patient, there is anomalous pulmonary venous return of the right pulmonary veins to the inferior vena cava above the diaphragm. Together with hypoplasia of the right lung lobe, that finding is consistent with the Scimitar syndrome. There is normal central venous return. The cardiac chambers are notable for moderate to severe right atrial and right ventricular enlargement. There is severe dilatation of the central pulmonary artery, measuring 4.6 cm before the bifurcation (right lower panel).

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Figure 13.32  Partial anomalous return of the left superior pulmonary vein This figure shows images of a left superior pulmonary vein, draining into the left subclavian vein.

Figure 13.33  Aortic coarctation This figure shows images of a patient with a remote history of coronary bypass surgery. The CT scan demonstrates aortic coarctation. There is hypoplasia of the arch with discrete juxtaductal narrowing of the isthmus. There are prominent collaterals including the internal mammary arteries. The known association with the bicuspid aortic valve should be considered (right lower panel).



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Figure 13.34  Coarctation of the aorta This figure shows images of a pediatric patient with aortic coarctation. Because of the young age of the patient, the scan was performed with the patient breathing and without ECG gating. Despite  the resulting decrease in image quality, the images are diagnostic. However, radiation exposure in pediatric patients requires careful consideration of indication and alternative imaging modalities.

Marfan syndrome, a multisystem connective tissue disorder associated with a mutation in the fibrillin (FBN1) gene, Ehlers-Danlos syndrome, and Loeye-Dietz syndrome are examples (see Chapter 10, Figures 10.37–10.42).437–441

13.8 Arteriovenous Shunt Defects

The ductus arteriosus is a communication between the proximal descending aorta and main pulmonary artery. In the fetus it physiologically bypasses the pulmonary circulation. A patent ductus can be found in asymptomatic adults, in particular if the size is small (Figures 13.40 and 13.41). The fibrotic and often calcified remnant is called the ligamentum arteriosum.

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Figure 13.35  Coarctation and stent This figure shows images of a patient with a history of aortic coarctation and percutaneous repair with a stent. There is replacement of the aortic valve with a low-profile mechanical prosthesis (right upper panel). There is fusiform dilatation of the mid ascending aorta with a maximum diameter of 5.3 cm. Beyond the origin of the left subclavian artery, there is rapid tapering of the isthmus to approximately 1.5 cm. An intact stent covering the area of the coarctation is seen.

Figure 13.36  Coarctation of the aorta/stent This figure shows images of a patient with a history of aortic coarctation, status post-remote surgical repair, with a subclavian flap and subsequent stent placement for residual stenosis. The aortic valve appears bicuspid (left lower panel), with fusion of the left and right coronary cusps. The aortic root has normal dimensions. There is a stent in the area of the proximal descending aorta. The minimal stent diameter in the proximal segment is 1.5 cm. At the distal end, the stent is not completely apposed to the aortic wall. In this segment, the native aorta measures 2.5 cm.



Adult congenital heart disease 319

Figure 13.37  Coarctation and surgical repair This figure shows images of a patient with a history of surgical repair of aortic coarctation and aortic valve repair. There is evidence of end-to-end anastomosis of the aorta.

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Figure 13.38  Coarctation and surgical repair This figure shows images of a patient with a history of surgical repair of aortic coarctation. There is a shunt graft extending from the ascending to the descending thoracic aorta. The narrowed area of the proximal descending aorta is seen.

Figure 13.39  Grafted interrupted arch This figure shows images of a patient with a history of surgical repair for an interrupted aortic arch. There is an intact but calcified graft of the aortic arch, which measures 1.2 cm in diameter.



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Figure 13.40  Patent ductus arteriosus (PDA) The patent ductus arteriosus (PDA) is a communication between the descending aorta (beyond left subclavian) and main pulmonary artery (near bifurcation) and physiologically bypasses the pulmonary circulation in the fetus. A patent ductus can be found in asymptomatic adults, in particular if the size is small.

Figure 13.41  Spontaneous closure of ductus arteriosus: ligamentum arteriosum Physiologically, the ductus arteriosus closes after birth. The fibrotic remnant of the ductus ­arteriosus is called ligamentum arteriosum.

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354  References 400h. Ouwendijk R, Kock MC, van Dijk LC, van Sambeek MR, Stijnen T, Hunink MG. Vessel wall calcifications at multi-detector row CT angiography in patients with peripheral arterial disease: effect on clinical utility and clinical predictors. Radiology 2006; 241:603–8. 400i. Roos JE, Fleischmann D, Koechl A, Rakshe T, Straka M, Napoli A, et al. Multipath curved planar reformation of the peripheral arterial tree in CT angiography. Radiology 2007; 244:281–90. 400j. Met R, Bipat S, Legemate DA, Reekers JA, Koelemay MJ. Diagnostic performance of computed tomography angiography in peripheral arterial disease: a systematic review and meta-analysis. JAMA 2009; 301:415–24. 400k. Ouwendijk R, de Vries M, Pattynama PM, van Sambeek MR, de Haan MW, Stijnen T, et al. Imaging peripheral arterial disease: a randomized controlled trial comparing contrast-enhanced MR angiography and multi-detector row CT angiography. Radiology 2005; 236:1094–103. 400l. Schernthaner R, Fleischmann D, Lomoschitz F, Stadler A, Lammer J, Loewe C. Effect of MDCT angiographic findings on the management of intermittent claudication. AJR Am J Roentgenol 2007; 189:1215–22. 400m. Schernthaner R, Fleischmann D, Stadler A, Schernthaner M, Lammer J, Loewe C. Value of MDCT angiography in developing treatment strategies for critical limb ischemia. AJR Am J Roentgenol 2009; 192:1416–24. 400n. Alvarez RE, Macovski A. Energy-selective reconstructions in x-ray computerized tomography. Phys Med Biol 1976; 21:733–44. 400o. Tran DN, Straka M, Roos JE, Napel S, Fleischmann D. Dual-energy CT discrimination of iodine and calcium: experimental results and implications for lower extremity CT angiography. Acad Radiol 2009; 16:160–71. 400p. Kau T, Eicher W, Reiterer C, Niedermayer M, Rabitsch E, Senft B, et al. Dual-energy CT angiography in peripheral arterial occlusive disease—accuracy of maximum intensity projections in clinical routine and subgroup analysis. Eur Radiol 2011; 21:1677–86. 401. Schwartzman PR, White RD. Imaging of cardiac and paracardiac masses. J Thorac Imaging 2000; 15:265–73. 402. Araoz PA, Mulvagh SL, Tazelaar HD, Julsrud PR, Breen JF. CT and MR imaging of benign primary cardiac neoplasms with echocardiographic correlation. Radiographics 2000; 20:1303–19. 403. Prakash P, Kalra MK, Stone JR, Shepard JA, Digumarthy SR. Imaging findings of pericardial metastasis on chest computed tomography. J Comput Assist Tomogr 2010; 34(4):554–58. 404. Buckley O, Madan R, Kwong R, Rybicki FJ, Hunsaker A. Cardiac masses. Part 1. Imaging strategies and technical considerations. AJR Am J Roentgenol 2011; 197(5):W837–41. 405. Buckley O, Madan R, Kwong R, Rybicki FJ, Hunsaker A. Cardiac masses. Part 2. Key imaging features for diagnosis and surgical planning. AJR Am J Roentgenol 2011; 197(5):W842–51. 406. Chu LC, Johnson PT, Halushka MK, Fishman EK. Multidetector CT of the heart: spectrum of benign and malignant cardiac masses. Emerg Radiol 2012; 19(5):415–28. 407. Kim EY, Choe YH, Sung K, Park SW, Kim JH, Ko YH. Multidetector CT and MR imaging of cardiac tumors. Korean J Radiol 2009; 10(2):164–75. 408. Hoey E, Ganeshan A, Nader K, Randhawa K, Watkin R. Cardiac neoplasms and pseudotumors: imaging findings on multidetector CT angiography. Diagn Interv Radiol 2012; 18(1):67–77. 409. Rajiah P, Kanne JP, Kalahasti V, Schoenhagen P. Computed tomography of cardiac and pericardiac masses. J Cardiovasc Comput Tomogr 2011; 5(1):16–29. 410. Anavekar NS, Bonnichsen CR, Foley TA, Morris MF, Martinez MW, Williamson EE, Glockner JF, Miller DV, Breen JF, Araoz PA. Computed tomography of cardiac pseudotumors and neoplasms. Radiol Clin North Am 2010; 48(4):799–816.

References 355 411. Scheffel H, Baumueller S, Stolzmann P, Leschka S, Plass A, Alkadhi H, Schertler T. Atrial myxomas and thrombi: comparison of imaging features on CT. AJR Am J Roentgenol 2009; 192(3):639–45. 412. Gheysens O, Cornillie J, Voigt JU, Bogaert J, Westhovens R. Left atrial myxoma on ­FDG-PET/CT. Clin Nucl Med 2013 Mar 18 [Epub ahead of print]. 413. Goo HW, Park IS, Ko JK, Kim YH, Seo DM, Yun TJ, Park JJ, Yoon CH. CT of congenital heart disease: normal anatomy and typical pathologic conditions. Radiographics 2003; 23:S147–65. 414. Boxt LM. Magnetic resonance and computed tomographic evaluation of congenital heart disease. J Magn Reson Imaging 2004; 19:827–47. 415. Achenbach S, Barkhausen J, Beer M, Beerbaum P, Dill T, Eichhorn J, Fratz S, Gutberlet M, Hoffmann M, Huber A, Hunold P, Klein C, Krombach G, Kreitner KF, Kühne T, Lotz J, Maintz D, Mahrholdt H, Merkle N, Messroghli D, Miller S, Paetsch I, Radke P, Steen H, Thiele H, Sarikouch S, Fischbach R. [Consensus recommendations of the German Radiology Society (DRG), the German Cardiac Society (DGK) and the German Society for Pediatric Cardiology (DGPK) on the use of ­cardiac imaging with  computed tomography and magnetic resonance imaging]. Rofo 2012; 184(4):345–68. 416. Jelnin V, Co J, Muneer B, Swaminathan B, Toska S, Ruiz CE. Three dimensional CT angiography for patients with congenital heart disease: scanning protocol for pediatric patients. Catheter Cardiovasc Interv 2006; 67(1):120–26. 417. Goske MJ, Applegate KE, Bulas D, Butler PF, Callahan MJ, Coley BD, Don S, Frush DP, Hernanz-Schulman M, Kaste SC, Morrison G, Sidhu M, Strauss KJ, Treves ST; Alliance for Radiation Safety in Pediatric Imaging. Image gently: progress and challenges in CT education and advocacy. Pediatr Radiol 2011; 41(Suppl 2):461–66. 418. Goske MJ. Getting it right: are regulation and registries for CT radiation dose in children the answer? Pediatr Radiol 2011; 41(Suppl 2):567–70. 419. Mahesh M. Advances in CT technology and application to pediatric imaging. Pediatr Radiol 2011; 41(Suppl 2):493–97. 420. Strauss KJ, Goske MJ. Estimated pediatric radiation dose during CT. Pediatr Radiol 2011; 41(Suppl 2):472–82. 421. Yu L, Bruesewitz MR, Thomas KB, Fletcher JG, Kofler JM, McCollough CH. Optimal tube potential for radiation dose reduction in pediatric CT: principles, clinical implementations, and pitfalls. Radiographics 2011; 31(3):835–48. 422. Ou P, Iserin L, Raisky O, Vouhe P, Brunelle F, Sidi D, Bonnet D. Post-operative cardiac lesions after cardiac surgery in childhood. Pediatr Radiol 2010; 40(6):885–94. 423. Baron MG, Book WM. Congenital heart disease in the adult: 2004. Radiol Clin North Am 2004; 42:675–90. 424. Kilner PJ. Imaging congenital heart disease in adults. Br J Radiol 2011; 84(3):S258–68. 425. Hughes D Jr, Siegel MJ. Computed tomography of adult congenital heart disease. Radiol Clin North Am 2010; 48(4):817–35. 426. Kilner PJ, Geva T, Kaemmerer H, Trindade PT, Schwitter J, Webb GD. Recommendations for cardiovascular magnetic resonance in adults with congenital heart disease from the respective working groups of the European Society of Cardiology. Eur Heart J 2010; 31(7):794–805. 427. Wiant A, Nyberg E, Gilkeson RC. CT evaluation of congenital heart disease in adults. AJR Am J Roentgenol 2009; 193(2):388–96. 428. Bartel T, Müller S. Contemporary echocardiographic guiding tools for device closure of interatrial communications. Cardiovasc Diagn Ther 2013; 3(1):38–46. 429. Gurudevan SV, Shah H, Tolstrup K, Siegel R, Krishnan SC. Septal thrombus in the left atrium: is the left atrial septal pouch the culprit? JACC Cardiovasc Imaging 2010; 3(12):1284–86.

356  References 430. Tugcu A, Okajima K, Jin Z, Rundek T, Homma S, Sacco RL, Elkind MS, Di Tullio MR. Septal pouch in the left atrium and risk of ischemic stroke. JACC Cardiovasc Imaging 2010; 3(12):1276–83. 431. Ropers D, Moshage W, Daniel WG, Jessl J, Gottwik M, Achenbach S. Visualization of coronary artery anomalies and their anatomic course by contrast-enhanced electron beam tomography and three-dimensional reconstruction. Am J Cardiol 2001; 87:193–97. 432. Deibler AR, Kuzo RS, Vohringer M, Page EE, Safford RE, Patron JN, Lane GE, Morin RL, Gerber TC. Imaging of congenital coronary anomalies with multislice computed tomography. Mayo Clin Proc 2004; 79:1017–23. 433. Yamanaka O, Hobbs RE. Coronary artery anomalies in 126,595 patients undergoing coronary arteriography. Cathet Cardiovasc Diagn 1990; 21(1):28–40. 434. Angelini P, Velasco JA, Flamm S. Coronary anomalies: incidence, pathophysiology, and clinical relevance. Circulation 2002; 105(20):2449–54. 435. Krasuski RA, Magyar D, Hart S, Kalahasti V, Lorber R, Hobbs R, Pettersson G, Blackstone E. Long-term outcome and impact of surgery on adults with coronary arteries originating from the opposite coronary cusp. Circulation 2011; 123(2):154–62. 436. Hobbs RE, Millit HD, Raghavan PV, Moodie DS, Sheldon WC. Coronary artery fistulae: a 10-year review. Cleve Clin Q 1982; 49(4):191–97. 437. Robinson PN, Arteaga-Solis E, Baldock C, Collod-Béroud G, Booms P, De Paepe A, Dietz HC, Guo G, Handford PA, Judge DP, Kielty CM, Loeys B, Milewicz DM, Ney A, Ramirez F, Reinhardt DP, Tiedemann K, Whiteman P, Godfrey M. The molecular genetics of Marfan syndrome and related disorders. J Med Genet 2006; 43(10):769–87. 438. Cury M, Zeidan F, Lobato AC. Aortic disease in the young: genetic aneurysm syndromes, connective tissue disorders, and familial aortic aneurysms and dissections. Int J Vasc Med 2013; 2013:267215. 439. Barrett PM, Topol EJ. The fibrillin-1 gene: unlocking new therapeutic pathways in cardiovascular disease. Heart 2013; 99(2):83–90. 440. Beauchesne LM, Fulop J, Nizalik E, Gow R, Veinot JP. Fatal dissection in a non-dilated thoracoabdominal aorta in a patient with vascular type Ehlers-Danlos syndrome. Pathology 2011; 43(7):735–37. 441. Jamsheer A, Henggeler C, Wierzba J, Loeys B, De Paepe A, Stheneur Ch, Badziag N, Matuszewska K, Matyas G, Latos-Bielenska A. A new sporadic case of early-onset ­Loeys-Dietz syndrome due to the recurrent mutation p.R528C in the TGFBR2 gene ­substantiates interindividual clinical variability. J Appl Genet 2009; 50(4):405–10.

List of Videos

For users of the VitalSource® eBook: The accompanying video files as indicated by the throughout the text can be accessed via links in the eBook. Please see the front page of this text for login instructions. Alternately, you can use the URLs provided here. Figure # 2.1 2.6 2.17-i 2.17-ii 2.20 2.22 4.10a 4.10b-i 4.10b-ii 4.13-i 4.13-ii 4.18-i 4.18-ii 4.18-iii 4.19-i 4.19-ii 4.21 4.27-i 4.27-ii 5.1

Legend

URL

Standard views of the cardiac chambers Assessment of LV function Aortic root, aortic valve Aortic root, aortic valve Aorta Coronary arteries, volume-rendered images (VRIs) of coronary arteries HOCM HOCM HOCM Endocardial fibrosis, Loeffler’s endocarditis Endocardial fibrosis, Loeffler’s endocarditis Contained LV rupture and pseudoaneurysm Contained LV rupture and pseudoaneurysm Contained LV rupture and pseudoaneurysm LV pseudoaneurysm LV pseudoaneurysm Calcified left ventricular aneurysm, LAD territory Left ventricular apical diverticulum Left ventricular apical diverticulum Normal pericardium (64-slice scanner) 357

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358  List of Videos 5.18 6.1-i 6.1-ii 6.1-iii 6.1-iv 6.2-i 6.2-ii 6.2-iii 6.2-iv 6.3 6.6-i 6.6-ii 6.6-iii 6.6-iv 6.6-v 6.6-vi 6.7 6.8 6.9-i 6.9-ii 6.9-iii 6.9-iv 6.10 6.11-i 6.11-ii 6.11-iii 6.11-iv 6.11-v 6.12-i 6.12-ii 6.14-i 6.14-ii 6.15-i 6.15-ii 6.15-iii 6.19-i

Pericardial constriction Bicuspid aortic valve Bicuspid aoritc valve Bicuspid aoritc valve Bicuspid aoritc valve Bicuspid aortic valve with prominence of aortic root Bicuspid aortic valve with prominence of aortic root Bicuspid aortic valve with prominence of aortic root Bicuspid aortic valve with prominence of aortic root Bicuspid aortic valve Complex bicuspid aortic valve Complex bicuspid aortic valve Complex bicuspid aortic valve Complex bicuspid aortic valve Complex bicuspid aortic valve Complex bicuspid aortic valve Quatrocuspid aortic valve Aortic valve calcification, aortic stenosis Severe aortic stenosis with aortic valve calcification, status post-valvuloplasty Severe aortic stenosis with aortic valve calcification, status post-valvuloplasty Severe aortic stenosis with aortic valve calcification, status post-valvuloplasty Severe aortic stenosis with aortic valve calcification, status post-valvuloplasty Sub-aortic membrane (dual-source scanner) Severe aortic insufficiency with prolapse of the left coronary cusp Severe aortic insufficiency with prolapse of the left coronary cusp Severe aortic insufficiency with prolapse of the left coronary cusp Severe aortic insufficiency with prolapse of the left coronary cusp Severe aortic insufficiency with prolapse of the left coronary cusp Mitral valve calcification in mitral stenosis Mitral valve calcification in mitral stenosis Mitral valve prolapse Mitral valve prolapse Pulmonary valve, status post-valvuloplasty Pulmonary valve, status post-valvuloplasty Pulmonary valve, status post-valvuloplasty Aortic valve replacement, mechanical valve

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List of Videos  359 6.19-ii 6.19-iii 6.19-iv 6.19-v 6.22 6.24-i 6.24-ii 6.24-iii 6.28-i 6.28-ii 6.28-iii 6.28-iv 6.29 6.30-i 6.30-ii 6.30-iii 8.4-i 8.4-ii 8.4-iii 8.9 8.24-i 8.24-ii 8.24-iii 8.25-i 8.25-ii 8.25-iii 8.26 8.33 8.37 8.40-i 8.40-ii 8.49 8.64 8.67 10.31-i 10.31-ii 10.32a-i 10.32a-ii 10.39-i

Aortic valve replacement, mechanical valve Aortic valve replacement, mechanical valve Aortic valve replacement, mechanical valve Aortic valve replacement, mechanical valve Percutaneous aortic valve replacement, stent-valve Transapical aortic valve replacement, stent-valve Transapical aortic valve replacement, stent-valve Transapical aortic valve replacement, stent-valve Mitral valve and aortic valve replacement Mitral valve and aortic valve replacement Mitral valve and aortic valve replacement Mitral valve and aortic valve replacement Mitral valve aortic valve replacement with bioprosthesis and tricuspid valve ring Mitral valve (ball-in-cage) and aortic valve (tilting-disc) replacement Mitral valve (ball-in-cage) and aortic valve (tilting-disc) replacement Mitral valve (ball-in-cage) and aortic valve (tilting-disc) replacement Normal coronary anatomy Normal coronary anatomy Normal coronary anatomy Non-obstructive lesions with mild luminal stenosis Significant luminal stenosis, three-vessel disease Significant luminal stenosis, three-vessel disease Significant luminal stenosis, three-vessel disease Significant luminal stenosis, three-vessel disease Significant luminal stenosis, three-vessel disease Significant luminal stenosis, three-vessel disease Significant, ostial RCA lesion Stented bypass graft, stent location Bypass graft aneurysm, CT Location of bypass grafts Location of bypass grafts Left ventricular (LV) outflow tract pseudoaneurysm causing coronary compression Left main coronary aneurysm LAD aneurysm, CT Sinus of Valsalva aneurysm Sinus of Valsalva aneurysm Sinus of Valsalva aneurysm Sinus of Valsalva aneurysm Pre- and post-operative imaging, aortic root replacement

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360  List of Videos 10.39-ii 10.47b 10.47c 10.53-i 10.53-ii 10.73b 12.2-i 12.2-ii 12.11 12.18-i 12.18-ii 13.3 13.9 13.22

Pre- and post-operative imaging, aortic root replacement Endovascular stent, hybrid procedure Endovascular stent, hybrid procedure Aortic root repair Aortic root repair Patient with history of aortitis and aortic stenosis Atrial myxoma Atrial myxoma Fibrous tumor versus sarcoidosis Suspected neoplastic involvement of pulmonary artery Suspected neoplastic involvement of pulmonary artery Percutaneous atrial septal defect (ASD) closure Anomalous origin of RCA from LM Complex coronary fistula

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