Radcases Cardiac Imaging E-Book

Carlos S Restrepo

• Herausgeber: Thieme Medical Publishers
• Kategorie: Fachliteratur
• Sprache: Englisch

Veröffentlichungsjahr: 2011

Beschreibung

All the key Radiology cases for your rounds, rotations, and exams -- in print and online!

RadCases contains cases selected to simulate everything that you'll see on your rounds, rotations, and exams. RadCases also helps you identify the correct differential diagnosis for each case - including the most critical.

Visit RadCases.thieme.com for free sample cases and to experience this dynamic learning tool for yourself!

RadCases covers:

Cardiac Imaging, Interventional Radiology, Musculoskeletal Radiology, Neuro Imaging, Thoracic Imaging, Pediatric Imaging, Gastrointestinal Imaging, Breast Imaging, Nuclear Medicine, Ultrasound Imaging, Head and Neck Imaging, Genitourinary Imaging

Each RadCases title features 100 carefully selected, must-know cases documented with clear, high-quality radiographs. The organization provides maximum ease of use for self-assessment.

Each case begins with the clinical presentation on the right-hand page; simply turn the page for imaging findings, differential diagnoses, the definitive diagnosis, essential facts, and more.

Each RadCases title includes a scratch-off code that allows 12 months of access to a searchable online database of all 100 cases from the book plus an additional 150 cases in that book's specialty - 250 cases in total!

Learn your cases, diagnose with confidence and pass your exams. RadCases.

Cardiac Imaging will enable you to diagnose the full range of cardiovascular diseases.

Features of Cardiac Imaging:

• Numerous high-resolution color radiographs demonstrating key cardiac cases
• A variety of common and uncommon presentations covering everything from myocardial infarction to aortic stenosis
• Examples of cases that must be diagno

Leseprobe

To access the additional media content available with this e-book via Thieme MedOne, please use the code and follow the instructions provided at the back of the e-book.

Thieme Medical Publishers, Inc.333 Seventh Ave.New York, NY 10001

Executive Editor: Timothy HiscockEditorial Director: Michael WachingerEditorial Assistant: Adriana di GiorgioInternational Production Director: Andreas SchabertProduction Editor: Heidi Grauel, Maryland CompositionVice President, International Marketing and Sales: Cornelia SchulzeChief Financial Officer: James W. MitosPresident: Brian D. ScanlanCompositor: MPS Content ServicesPrinter: Everbest Printing Co.

Library of Congress Cataloging-in-Publication Data

Radcases cardiac imaging / edited by Carlos Santiago Restrepo, Dianna M.E. Bardo.

p. ; cm.

  Includes bibliographical references and index.

  ISBN 978-1-60406-185-7

  I. Heart–Imaging–Case studies. 2. Heart–Diseases–Diagnosis–Case studies. I. Restrepo, Carlos Santiago.

II. Bardo, Dianna M. E.

[DNLM: 1. Heart Diseases–diagnosis–Case Reports. 2. Diagnostic Imagin–methods–Case Reports. WG

141 R312 2010]

RC683.5.I42R33 2010

616.1'20754–dc22

2009031579

Copyright © 2010 by Thieme Medical Publishers, Inc. This book, including all parts thereof, is legally protected by copyright. Any use, exploitation, or commercialization outside the narrow limits set by copyright legislation without the publisher's consent is illegal and liable to prosecution. This applies in particular to photostat reproduction, copying, mimeographing or duplication of any kind, translating, preparation of microfilms, and electronic data processing and storage.

Important note: Medical knowledge is ever-changing. As new research and clinical experience broaden our knowledge, changes in treatment and drug therapy may be required. The authors and editors of the material herein have consulted sources believed to be reliable in their efforts to provide information that is complete and in accord with the standards accepted at the time of publication. However, in view of the possibility of human error by the authors, editors, or publisher of the work herein or changes in medical knowledge, neither the authors, editors, nor publisher, nor any other party who has been involved in the preparation of this work, warrants that the information contained herein is in every respect accurate or complete, and they are not responsible for any errors or omissions or for the results obtained from use of such information. Readers are encouraged to confirm the information contained herein with other sources. For example, readers are advised to check the product information sheet included in the package of each drug they plan to administer to be certain that the information contained in this publication is accurate and that changes have not been made in the recommended dose or in the contraindications for administration. This recommendation is of particular importance in connection with new or infrequently used drugs.

Some of the product names, patents, and registered designs referred to in this book are in fact registered trademarks or proprietary names even though specific reference to this fact is not always made in the text. Therefore, the appearance of a name without designation as proprietary is not to be construed as a representation by the publisher that it is in the public domain.

Printed in China

978-1-60406-185-7

Dedication

To my husband John, who makes it possible to work with passion and makes the rewards of that work worthwhile.

–Dianna M. E. Bardo

To my parents, Ovidio and Marielena, with all my love. And to my wife, Marta, and my children, Catalina, Juan, and Alejandro, the joy of my life.

–Carlos Santiago Restrepo

Series Preface

The ability to assimilate detailed information across the entire spectrum of radiology is the Holy Grail sought by those preparing for their trip to Louisville. As enthusiastic partners in the Thieme RadCases series who formerly took the examination, we understand the exhaustion and frustration shared by residents and the families of residents engaged in this quest. It has been our observation that despite ongoing efforts to improve Web-based interactive databases, residents still find themselves searching for material they can review while preparing for the radiology board examinations and remain frustrated by the fact that only a few printed guidebooks are available, which are limited in both format and image quality. Perhaps their greatest source of frustration is the inability to easily locate groups of cases across all subspecialties of radiology that are organized and tailored for their immediate study needs. Imagine being able to immediately access groups of high-quality cases to arrange study sessions, quickly extract and master information, and prepare for theme-based radiology conferences. Our goal in creating the RadCases series was to combine the popularity and portability of printed books with the adaptability, exceptional quality, and interactive features of an electronic case-based format.

The intent of the printed book is to encourage repeated priming in the use of critical information by providing a portable group of exceptional core cases that the resident can master. The best way to determine the format for these cases was to ask residents from around the country to weigh in. Overwhelmingly, the residents said that they would prefer a concise, point-by-point presentation of the Essential Facts of each case in an easy-to-read, bulleted format. Differentials are limited to a maximum of three, and the first is always the actual diagnosis. This approach is easy on exhausted eyes and provides a quick review of Pearls and Pitfalls as information is absorbed during repeated study sessions. We worked hard to choose cases that could be presented well in this format, recognizing the limitations inherent in reproducing high-quality images in print. Unlike other case-based radiology review books, we removed the guesswork by providing clear annotations and descriptions for all images. In our opinion, there is nothing worse than being unable to locate a subtle finding on a poorly reproduced image even after one knows the final diagnosis.

The electronic cases expand on the printed book and provide a comprehensive review of the entire subspecialty. Thousands of cases are strategically designed to increase the resident's knowledge by providing exposure to additional case examples—from basic to advanced—and by exploring “Aunt Minnie's,” unusual diagnoses, and variability within a single diagnosis. The search engine gives the resident a fighting chance to find the Holy Grail by creating individualized, daily study lists that are not limited by factors such as radiology subsection. For example, tailor today's study list to cases involving tuberculosis and include cases in every subspecialty and every system of the body. Or study only thoracic cases, including those with links to cardiology, nuclear medicine, and pediatrics. Or study only musculoskeletal cases. The choice is yours.

As enthusiastic partners in this project, we started small and, with the encouragement, talent, and guidance of Tim Hiscock at Thieme, we have continued to raise the bar in our effort to assist residents in tackling the daunting task of assimilating massive amounts of information. We are passionate about continuing this journey, planning to expand the cases in our electronic series, adapt cases based on direct feedback from residents, and increase the features intended for board review and self-assessment. As the National Board of Medical Examiners converts the American Board of Radiology examination from an oral to an electronic format, our series will be the one best suited to meet the needs of the next generation of overworked and exhausted residents in radiology.

Jonathan Lorenz, MDHector Ferral, MDChicago, IL

Preface

The opportunity to present a large group of cases to you in Cardiac Imaging, part of the RadCases series, is a real privilege for us. Working in academic medicine provides us the ability to teach and learn from residents and fellows as well as the chance to diagnose a broad range of common and uncommon cardiac diseases, and also further advance cardiac imaging modalities through research.

The high prevalence of cardiovascular diseases in the western world, as well as the amazing evolution of imaging technology available to us makes this book more relevant today than ever before. It is critical that radiologists are capable of diagnosing cardiovascular diseases.

The power of this cardiac case base is the presentation of strengths of both CT and MRI through 100 printed and an additional 150 electronic cases. The 250 cases we have prepared include not only common presentations, but uncommon presentations of common problems and examples of cases you must diagnosis immediately to avert potential disaster. The cases we have written prepare you for your opportunities to shine when confronted with cardiac cases whether that is on a board examination or in practice.

We hope this case base review series will be beneficial for you as you prepare for medical board examinations. This case base series and the learning experiences during your training are the foundation for a lifetime of learning you will experience throughout your career.

Dianna M.E. Bardo, MDCarlos Santiago Restrepo, MD

Acknowledgments

I wish to acknowledge my colleagues Craig S. Broberg, MD; Michael D. Shapiro, DO; and Thanjavur Bragadeesh, MB, ChB, who generously shared their cases for this text and who teach and inspire excellence in cardiac imaging.

Dianna M. E. Bardo, MD

I want to thank Santiago Martinez, MD (Duke University); Terry Bauch, MD (The University of Texas HSC, San Antonio); Jorge Carrillo, MD (Universidad Nacional, Bogota, Colombia); Ramon Reina, MD (Clinica de Marly, Bogota, Colombia); Julio Lemos, MD (University of Vermont); and Eric Kimura, MD (Instituto Nacional de Cardiologia Ignacio Chavez, Mexico), for their valuable contributions.

Carlos Santiago Restrepo, MD

Case 1

Clinical Presentation

The electrical system of the heart performs critical functions in synchronized depolarization, resulting in contraction of the atria and ventricles and ejection of blood into the pulmonary and systemic vascular beds. The important structures and events in cardiac electrical activity and the usual vascular supply to these structures are described.

Imaging Findings

Components of the electrical conduction system and coronary arteries have been drawn over four-chamber, short-axis, and two-chamber views of the heart.

(A) The sinoatrial (SA) node (green dot) is at the superior and posterior margin of the right atrium. Internodal pathways (dotted yellow arrows) span the SA and the atrioventricular (AV) nodes (red dot). The right (white arrow) and left (black arrow) bundle branches (orange lines) and Purkinje fibers (black circle) propagate depolarization through the ventricles. (B) The SA (green dot) and AV (red dot) nodes are supplied by the SA nodal (small white arrow) and AV nodal (black arrow) arteries; both are usually branches of the right coronary artery (open white arrow). Occasionally, the AV nodal branch arises from the lef t circumflex artery (white arrow). (C) The left anterior descending artery supplies septal branches that perforate the interventricular septum to supply the bundle branches (orange line). The P and T waves and the QRS complex of the electrocardiogram (ECG) trace are described below.

Differential Diagnosis

Normal cardiac conduction system: The myocardial muscle cells and tissue of a specialized conduction system allow conduction of electrical impulses. Specialized cells in the conductive tissue depolarize spontaneously.

Essential Facts

Components of the conduction system include the following: The SA node suppresses depolarization of other pacing cells and is therefore the dominant pacemaker of the heart. It excites the internodal pathways and the atrial myocardium.Anterior, middle, and posterior internodal tracts are activated by the SA node, propagating the electrical signal to the AV node, the His bundle, the bundle branches, the Purkinje network, and the ventricular myocardium.The AV node, located at the crux cordis, depolarizes to assist in propagating conduction of electrical activity to the His bundle.The His bundle and the right and left bundle branches are organized groups of cells that propagate electrical activity through the ventricles in an organized manner.Anterosuperior and posteroinferior divisions of the left bundle and the Purkinje network increase the speed of depolarization through the ventricles.The main components of the ECG trace are the following: P wave: The P wave represents the combination of right atrial activation and the slightly delayed activation of the left atrium; resulting in atrial systole.QRS complex: The electrical representation of ventricular muscle depolarization; resulting in ventricular systole.T wave: Recovery of the ventricular myocardium; ventricular diastole begins as the ventricles relax.

Other Imaging Findings

In patients with arrhythmia, look for thrombus in the left atrial appendage.

Pearls & Pitfalls

Myocardial infarction and ischemia can result in arrhythmia.

Variability of coronary artery dominance results in a minor inconsistency in the vascular supply of the conduction system.

Case 2

Clinical Presentation

Shortness of breath and chest pain in a 45-year-old man

Imaging Findings

(A) Axial T1-weighted and (B) gradient echo (GRE) images at the level of the heart demonstrate a large mass in the left atrium (white arrow, Fig. A) attached to the interatrial septum and protruding through the mitral valve into the upper left ventricle.

Differential Diagnosis

Atrial myxoma: A well-delineated, smooth, oval left atrial mass attached to the interatrial septum is characteristic of an atrial myxoma. When large enough, an atrial myxoma may protrude into the left ventricle through the mitral valve.Atrial thrombus: An atrial thrombus more commonly arises from the posterior or lateral wall of an enlarged left atrium.Sarcoma: An atrial sarcoma typically involves the right atrium and presents as an irregular infiltrative mass of soft-tissue density.

Essential Facts

Myxomas account for one half of all primary cardiac tumors and are the most common primary cardiac neoplasms.Women are aff ected more than men. The mean age at diagnosis is 50 years.Large left atrial myxomas commonly cause mitral valve obstruction (60%).Constitutional symptoms (fever, malaise, and weight loss), cardiac arrhythmias, and embolic manifestations are the most common clinical complaints.Myxomas are attached to the endocardium, and origin from the fossa ovalis of the interatrial septum is characteristic.Seventy-five percent of myxomas arise in the left atrium and 20% in the right atrium.On computed tomography, > 50% exhibit calcification.

Other Imaging Findings

On magnetic resonance imaging (MRI), atrial myxomas have heterogeneous signal intensity.On T1-weighted images, they have low signal intensity.On cine GRE images, atrial myxomas exhibit contrast enhancement after gadolinium injection.

Pearls & Pitfalls

The majority of atrial myxomas are sporadic, but 7% are associated with a familial predisposition or manifest as multicentric myxomas with skin pigmentation, endocrine disorders, and other tumors (Carney complex).

Atrial myxomas and thrombi can have a similar appearance on MRI. Contrast-enhanced MRI can help differentiate between these two conditions because myxomas exhibit enhancement and thrombi do not.

Case 3

Clinical Presentation

A 50-year-old woman presents with a stroke and a heart murmur on physical examination.

Imaging Findings

On cardiac-gated multidetector computed tomography angiography:

(A) Axial image at the level of the aortic valve. A well-defined, low-density polypoid lesion is appreciated on the inferior surface of the aortic valve leaflets. (B) Coronal image at the level of the aor tic valve. A well-defined, low-density polypoid lesion is appreciated on the inferior surface of the aortic valve leaflets.

Differential Diagnosis

Papillary fibroelastoma: Contrast-enhanced cardiac-gated computed tomography (CT) shows a soft-tissue-density polypoid mass arising from an aortic valve leaflet. The lesion exhibits smooth contour, consistent with the typical appearance and location of a papillary fibroelastoma.Endocarditis vegetation: Infective and noninfective endocarditis can present with a similar appearance as a result of an aortic valve vegetation. In cases of infective endocarditis, typically more significant damage and dysfunction of the involved valve are present, and the clinical history and presentation favor an infectious process.Other valvular tumors: In general, valvular tumors other than papillary fibroelastomas are rare. Myxomas, lipomas, and hematic cysts have been reported originating from cardiac valves.

Essential Facts

Despite being an uncommon tumor, papillary fibroelastoma is the most common valvular neoplasm. More than 90% are attached to valves. The most common location is in the aortic valve (45%), followed by the mitral valve (36%).Papillary fibroelastoma is the third most common benign cardiac tumor, after myxoma and lipoma.Papillary fibroelastomas are usually small (< 20 mm in diameter), mobile, single lesions.The mean age at the time of diagnosis is 60 years.Papillary fibroelastomas can be an incidental finding in asymptomatic patients evaluated for unrelated conditions, or they can be associated with a distal arterial embolization (e.g., stroke and transient ischemic attack) or valvular dysfunction.

Other Imaging Findings

On echocardiography, a papillary fibroelastoma appears as a small round or oval echogenic polypoid lesion < 2 cm in diameter with a homogeneous echotexture. It is usually mobile and has a small stalk attached to the commissure of a cardiac valve.

Pearls & Pitfalls

Papillary fibroelastomas are benign, rare gelatinous tumors derived from the endocardium, primarily of the left-sided cardiac valves, with the potential for embolization.

These small lesions can be easily overlooked in a nongated cross-sectional imaging examination.

Case 4

Clinical Presentation

A 57-year-old man presents with a history of recent myocardial infarction with ST wave elevation on electrocardiogram. The apex was not moving normally on echo, and the ejection fraction was measured at 17%.

Imaging Findings

(A) A left ventricular (LV) outflow tract view shows a rounded shape and apparent thickening of the LV apex (black arrow). (B) This four-chamber white blood image of the heart shows apparent thickening of the rounded apex (black arrow). (C,D) Following intravenous administration of gadolinium, delayed images in a four-chamber and a two-chamber view show rim enhancement of a mass in the apex (white arrows), a thrombus that has formed on the endocardial surface of the infarcted myocardium. The thrombus does not enhance (open white arrow).

Differential Diagnosis

LV apical infarction; aneurysm with thrombus formation: The LV apex is rounded and the wall thickness decreased. Linear enhancement of the subendocardial surface of the myocardium and no enhancement within the crescent-shaped thrombus are typical of this diagnosis.Hypertrophic cardiomyopathy: Although the apical myocardium appears thickened before gadolinium is given, the wall is clearly markedly thinned once the endocardium is defined. Localized hypertrophic cardiomyopathy usually aff ects the septal wall.Apical cardiac metastasis: The appearance of the apex prior to gadolinium administration could suggest an infiltrating metastatic lesion; however, the patient does not have a known malignancy.

Essential Facts

Most thrombi that form in the LV following myocardial infarction occur within the first 2 weeks, but as early as 48 hours.Inflammatory cells infiltrate necrotic myocardium following infarction, inducing platelet and fibrin deposition on the endocardial surface of the myocardium, encouraging thrombus formation.Inflammatory markers such as C-reactive protein may help to predict in which patients thrombi are more likely to form.Potential embolic complications from LV thrombi portend a poor prognosis.

Other Imaging Findings

Look for areas of wall motion abnormality, akinesis, marked hypokinesis, or aneurysm as a site of thrombus formation.Calcium within or on the surface of the LV thrombus is a sign of chronicity.Calcium may be missed on magnetic resonance imaging but should be obvious on computed tomography (CT).

Pearls & Pitfalls

Describe wall motion abnormalities in a systematic manner:

If the face of a clock is used for reference, 12:00 is the anterior wall, 3:00 the lateral wall, 6:00 the inferior wall, and 9:00 the septal wall.Between these are regions called the anteroseptal, inferolateral, inferoseptal, and anteroseptal segments.

On CT, the mixing of contrast with non–contrast-enhanced blood is an unusual finding in the LV, but it may be seen in the right side of the heart.

Case 5

Clinical Presentation

A 29-year-old man presents with a murmur. What is the high-signal structure adjacent to the spine, parallel to the aorta? Explain how this structure and the abnormal morphology of the heart (Fig. B) are related.

Imaging Findings

(A) In the axial plane, a defect in the septal wall is seen adjacent to the aortic valve (black arrow). In (B) systolic and (C) diastolic images, the defect in the interventricular septum at the base of the heart (black arrows) is seen in a left ventricular (LV) outflow tract view. The more densely enhanced blood in the left side of the heart flows from the left to the right; a jet of contrast-enhanced blood is seen in the right ventricle (white arrows).

Differential Diagnosis

Membranous VSD: An obvious defect is seen in the interventricular septum, just below the aortic valve, which allows the flow of contrast (blood) from left to right.Muscular VSD: The muscular interventricular septum is intact and is normal thickness.Aneurysm of the interventricular septum: An inter-ventricular aneurysm is thought to form during the process of spontaneous closure of membranous defects. Such an aneurysm looks like a windsock, and when completely closed, it does not allow shunting of blood.

Essential Facts

VSD is the most common congenital heart defect.It is one feature of numerous types of congenital heart disease.It is the most common symptomatic congenital heart defect in neonates.The ventricular septum has four segments: inlet, trabecular, outlet, and membranous.Defects of the interventricular septum are classified in different ways: Muscular—entirely surrounded by septal muscle (inlet, outlet, or trabecular)Membranous—lies just below the aortic valve; bordered partially by fibrous tissue inferior to the aortic valve and medial to the mitral valve. The defect may extend to the crista, adjacent to the septal leaflet of the tricuspid valve.Doubly committed, subarterial (combined)—in the outlet septum and bordered partially by fibrous tissue between the aortic and pulmonary valvesInlet—near the mitral valveOut—letbelow the aortic valveSupracristal—below the pulmonary valve

Pearls & Pitfalls

Qp:Qs is a ratio that indicates the degree of shunting, where Qp is the pulmonary resistance and Qs is the systemic resistance.

Restrictive VSD: Qp:Qs < 1.5/1.0 A high-pressure defect exists between the left and right ventricles; the shunt is small, and most children are asymptomatic. A high-frequency holosystolic murmur is noted.

Moderately restrictive VSD: Qp:Qs 1.5/1.0 to 2.5/1.0 This degree of shunting results in a hemodynamic load on the LV. Children present with failure to thrive and congestive heart failure. Holosystolic murmur and apical diastolic rumble are noted.

Nonrestrictive VSD: Qp:Qs > 2.5/1.0 Right ventricle volume overload is seen early, and progressive pulmonary artery overload becomes symptomatic in early life. Holosystolic murmur and apical diastolic rumble are noted.

VSD with Qp:Qs > 2.0/1.0 should be closed before pulmonary hypertension becomes irreversible.

Progressive aortic regurgitation may develop with a restrictive VSD.

View the heart in anatomically correct planes to accurately classify and measure the VSD.

Electrocardiogram-gated computed tomography (CT) or magnetic resonance imaging (MRI) will show the contrast flow or flow void, respectively, through a VSD.

Quantification of the Qp:Qs is possible with MRI and echocardiography but is currently not possible with CT.

Case 6

Clinical Presentation

A 68-year-old man with history of left internal mammary artery (LIMA) coronary artery bypass graft (CABG) to the left anterior descending (LAD) coronary artery after diagnosis of severe proximal LAD stenosis. He now presents with new angina.

Imaging Findings

(A) In a two-dimensional (2D) planar view, the LIMA bypass graft (small white arrow) courses from its origin on the left subclavian artery (not shown) to an end-to-side anastomosis with the mid LAD (large white arrow). The proximal LAD is patent (black arrows), likely opacified by retrograde flow. The hyperattenuating foci along the course of the LIMA are surgical clips (white circle), which are used to close branches of the LIMA.

(B) A three-dimensional surface-rendered view of the heart and the LIMA graft shows the patent anastomosis with the LAD. (C) Using a diff erent windowing technique, the surgical clips (white circle) are seen. Clips at or near the anastomosis may make it impossible to make a confident diagnosis of patency.

Differential Diagnosis

Patent LIMA–LAD CABG: The anastomosis of the LIMA with the LAD is patent, best seen in the 2D view. Retrograde flow into the proximal LAD is a common finding when the stenotic or occlusive lesion is very proximal.Re-established antegrade flow in the LAD: If a CABG is performed to an epicardial coronary artery that does not have a severe stenosis or occlusion (i.e., the distal myocardium is not ischemic), the CABG will close because blood flow in the native artery is maintained.Saphenous vein–LAD CABG: Saphenous and other venous grafts are sewn to the ascending aorta, forming an anastomosis with the LAD and other epicardial coronary arteries similar to that shown between the LIMA and LAD.

Essential Facts

64 MDCT has been shown to have a sensitivity, specificity, and diagnostic accuracy of 100% for the diagnosis of occlusion of CABG.Studies show a slight variation in the sensitivity (100–80%) but agreement in the excellent specificity (91%) and diagnostic accuracy (87%) for determination of flow-limiting stenosis within a graft vessel.MDCT allows sensitive and specific determination of CABG patency and stenosis without the risks of an invasive procedure.Serial evaluation of CABG patency is essential, especially in patients with multiple grafts, as they may be asymptomatic if only one graft is stenosed or occluded.Venous grafts may develop atherosclerotic disease, aneurysms, or pseudoaneurysms.

Other Imaging Findings

Because of their cephalocaudal course, lesser motion artifacts, and larger luminal caliber, arterial and venous bypass grafts easier to image and follow on multidetector CT imaging than are the native epicardial arteries.The metal surgical clips used to close branches of bypass grafts can be beneficial in marking the course of the graft but detrimental if streak artifact obscures the graft–native vessel anastomosis.Evaluate native epicardial coronary arteries and myocardium for progressive stenosis and evidence of prior infarction, aneurysm, and thrombus.

Pearls & Pitfalls

Heart rate control with beta-blockers is recommended to achieve a heart rate between 60 and 65 beats/min.

Use retrospective electrocardiogram (ECG) gating to calculate left and right ventricle function.

Use prospective ECG gating to conserve radiation dose.

Evaluation of CABG vessels may be limited by slowed flow through a graft if there is stenosis and potentially by streak/blooming artifacts from surgical clips and calcium.

Case 7

Clinical Presentation

Dyspnea on exertion in a 55-year-old man

Imaging Findings

(A–C) Contrast-enhanced computed tomography of the thorax, with axial images at three diff erent levels. An abnormal vessel is seen arising from the trunk of the pulmonary artery and continuing into the position of the left anterior descending coronary artery (LAD).

Differential Diagnosis

Anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA): The origin of the left coronary artery from the pulmonary artery, also known as Bland–White–Garland syndrome, is a rare congenital anomaly that induces ischemia and hypoperfused myocardium resulting from “steal” phenomenon, in which blood flow is diverted from the heart to the pulmonary artery.Coronary artery fistula: A coronary artery fistula may present as an abnormal-caliber vessel in close relation to the main pulmonary artery.

Essential Facts

ALCAPA is a rare condition seen in 1 in 300,000 live births and accounts for ~0.25% of all cases of congenital heart disease. The flow in the aff ected coronary artery is reversed and is toward the pulmonary artery.This is one of the most common causes of myocardial ischemia and infarction in children, and if not treated, the mortality rate during the first year of life is ~90%.Occasionally, untreated patients with a lesser degree of ischemia survive until adulthood, and their condition is diagnosed later in life.In the majority of cases, this is an isolated defect, but an association with other anomalies (e.g., atrial and ventricular septal defects and aortic coarctation) has been reported.The goal of surgical correction is to restore two coronary artery systems from the aorta.

Other Imaging Findings

Untreated patients who survive usually exhibit significant intercoronary collateral circulation with prominent tortuous vessels. The right coronary artery is usually dilated and tortuous as well.

Pearls & Pitfalls

The landmark case reported by Drs. Bland, White, and Garland (Massachusetts General Hospital) in 1933 was a 3-month-old child with ALCAPA, the son of the prestigious thoracic radiologist Dr. A. O. Hampton.

Other diseases that can present with dilatation of the coronary arteries are vasculitis (Kawasaki disease, poly-arteritis nodosa), scleroderma, Ehlers–Danlos syndrome, and fistulas.

Case 8

Clinical Presentation

A 74-year-old woman presents with a possible right coronary artery (RCA) anomaly on echocardiogram (ECG).

Imaging Findings

(A) The RCA origin is from the main pulmonary artery (MPA: white arrow). The RCA and the left anterior descending (LAD) artery (black arrows) are extremely tortuous, but along with their branches, they follow a normal course on the epicardial surface of the heart. (B) An oblique view of the main pulmonary artery shows contrast-enhanced blood flowing into the MPA (arrows) from the RCA. This MPA steal occurs because of the lower pressure in the MPA than in the RCA. (C) Nuclear myocardial perfusion images reveal less blood flow to the inferior wall of the left ventricle (purple) than to the anterior and lateral walls (red and yellow, respectively) in the vascular distribution of the RCA. The defect is larger in diastole than it is in systole.

Differential Diagnosis

Anomalous origin of the right coronary artery from the pulmonary artery (ARCAPA): The RCA origin arises from the MPA. An RCA origin is not seen arising from the expected location on the aorta.Coronary vein drainage to the MPA: Although the abnormal vessel drains into the MPA, its branches are clearly typical of the RCA anatomy. Normal coronary veins drain to the coronary sinus or to the cardiac chambers.Venous coronary artery bypass graft: Bypass grafts never originate from the pulmonary arteries. There are no other postoperative changes in the chest.

Essential Facts

ARCAPA is a very rare anomaly, with only 72 cases reported in the literature.Embryologically, the truncus arteriosus is the structure from which the ascending aorta and the MPA are formed. Theoretically, the coronary artery origins are displaced from their normal site by abnormal division of the truncus arteriosus. Therefore, the coronary artery may arise from the pulmonary artery instead of the aorta.Patients with origin of the RCA from the pulmonary artery may be asymptomatic.If the left coronary artery arises from the pulmonary artery, patients present with ischemia in infancy.

Other Imaging Findings

Nuclear myocardial perfusion imaging as in this patient shows regional deficits.Tortuosity of the coronary arteries occurs presumably because of increased flow.In the LAD artery, blood flow is antegrade, with a greater volume of blood supplied to the myocardium. Septal and epicardial branches of the left coronary arteries are of large caliber.Blood flow in the RCA is retrograde, stealing blood from the myocardium and delivering it to the lower-pressure pulmonary artery.Normal coronary blood flow from the epicardial coronary arteries is antegrade during diastole.The pulmonic and aortic valves are closed during diastole.Myocardial perfusion imaging shows a larger perfusion defect during diastole than in systole because of the steal eff ect of the ARCAPA.

Pearls & Pitfalls

Inspect each aortic valve cusp for origins of the coronary arteries.

If the coronary artery origin is not found on the aorta, look elsewhere.

Anomalous coronary artery origins may be from any of the sinuses of Valsalva of the aortic valve, the ascending aorta, or the MPA.

ECG gating is necessary to view the details of the coronary artery anatomy.

The right side of the heart should be nearly empty of contrast-enhanced blood so that the blood flow from the coronary artery into the pulmonary artery can be seen.

Case 9

Clinical Presentation

Progressive shortness of breath, abdominal swelling, and orthopnea

Imaging Findings

(A,B) Contrast-enhanced computed tomography (CT) of the thorax demonstrates extensive pericardial thickening and calcification (black arrows), more prominent on the atrioventricular groove. There is abnormal dilatation of the right atrium and coronary sinus, indicating constrictive physiology.

Differential Diagnosis

Constrictive pericarditis: Fibrous or calcified thickening of the pericardium that prevents normal diastolic ventricular filling is characteristic of restrictive pericarditis.Pericarditis without constriction: Pericardial thickening from diverse acute and chronic inflammatory causes may occur in the absence of a constrictive physiology.Myocardial calcification: Chronic inflammatory and metabolic disorders may produce myocardial calcification. CT helps diff erentiate between pericardial and myocardial distribution of calcified plaques.

Essential Facts

Currently, the most common causes are previous surgery and radiation therapy.Other possible causes are infectious pericarditis (tuberculosis, viral), collagen vascular disease, and uremia.The physiologic eff ect and clinical presentation of constrictive pericarditis and restrictive cardiomyopathy are similar.A ff ected pericardium usually exceeds 4 mm in thickness, up to 10 or 12 mm.Irregular calcification may occur anywhere over the surface of the heart, but the largest accumulation is usually at the atrioventricular groove.Other imaging findings are ventricular deformity with tubular small ventricles and dilated atria.After surgery, complete normalization of cardiac hemodynamics is reported in 60% of patients.

Other Imaging Findings

Signs of impaired diastolic filling include dilatation of the inferior vena cava and hepatic veins, hepatosplenomegaly, and ascites.

Pearls & Pitfalls

Differentiation between constrictive pericarditis and restrictive cardiomyopathy is crucial, as definitive treatment of restrictive cardiomyopathy is surgical (pericardiectomy or pericardial stripping).

Constrictive pericarditis may be seen in patients with normal pericardial thickness.

Transthoracic echocardiography is limited for evaluating pericardial thickening.

Case 10

Clinical Presentation

A 63-year-old man presents with ST wave elevation on electrocardiogram (ECG).

Imaging Findings