CMR and MDCT in Cardiac Masses

CMR and MDCT in Cardiac Masses

 

Alexis Jacquier

CMR and MDCT in Cardiac Masses

Author Alexis Jacquier, M.D., Ph.D. Service d’imagerie Médicale Adulte CHU la Timone 264 rue Saint-Pierre 13385 Marseille, Cedex 05 France Centre de Résonance Magnétique Biologique et Médicale (CRMBM) Faculté de Médecine de Marseille Université de la Méditerranée France [email protected]

Translation from the French language edition: Imagerie en coupes des masses cardiaques by Alexis Jacquier Copyright © Springer-Verlag France, Paris 2009 Springer-Verlag France is part of Springer Science+Business Media All Rights Reserved

ISBN  978-3-642-18456-7 e-ISBN  978-3-642-18457-4 DOI  10.1007/978-3-642-18457-4 Springer Heidelberg Dordrecht London New York Library of Congress Control Number: 2011928408 © Springer-Verlag Berlin Heidelberg 2011 This work is subject to copyright. All rights are reserved, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilm or in any other way, and storage in data banks. Duplication of this publication or parts thereof is permitted only under the provisions of the German Copyright Law of September 9, 1965, in its current version, and permission for use must always be obtained from Springer. Violations are liable to prosecution under the German Copyright Law. The use of general descriptive names, registered names, trademarks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. Product liability: The publishers cannot guarantee the accuracy of any information about dosage and application contained in this book. In every individual case the user must check such information by consulting the relevant literature. Cover design: eStudioCalamar, Figueres/Berlin Printed on acid-free paper Springer is part of Springer Science+Business Media (www.springer.com)

To Mariangela, Chiara and Antoine

 

Foreword

Cardiac masses pose difficult diagnostic challenges. Although many cardiac tumours are today operable, the complexity of any surgery involved requires accurate pre-operative imaging. Several imaging modalities including cardiac magnetic resonance and computed tomography are used for this assessment, often used in combination. Because cardiac tumours are relatively rare, there is a great demand for textbooks providing guidance on imaging protocols and typical imaging findings for different tumours and cardiac masses. The textbook CMR and MDCT in Cardiac Masses edited by A. Jacquier is an outstanding contribution to this field. It provides a practical guide to the typical CT and MRI features of cardiac masses, is enriched with high quality case examples and provides tables summarizing important imaging findings and gives useful diagnostic algorithms. As such it will make an invaluable everyday companion to cardiac imagers and other clinicians involved in the care of patients with cardiac masses. Leeds, January 2011

Sven Plein, M.D., Ph.D.

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Contents

1  Introduction............................................................................................................

1

2  Technical Aspects...................................................................................................

3

2.1  Cardiac Magnetic Resonance Imaging Techniques.................................... 3 2.2  Multidetector Computed Tomography Image Acquisition........................ 4 3  Anatomic Pitfalls....................................................................................................

7

3.1  Deep Atrioventricular Groove...................................................................... 8 Philippe Germain and Gilles Goyault

3.2  Lipomatous Hypertrophy of the Interatrial Septum.................................. 11 Laurence Monnier-Cholley and Lionel Arrivé

3.3  Flow Artifact in the Right Atrium............................................................... 14 Laurence Monnier-Cholley and Lionel Arrivé

3.4  Crista Terminalis........................................................................................... 17 Arthur Varoquaux, Vincent Vidal, Jean Michel Bartoli,   Jean-Yves Gaubert, Guy Moulin, and Alexis Jacquier

3.5  Juxtacaval Fat Collection.............................................................................. 19 Philippe Dory-Lautrec, Frédéric Cohen, Guillaume Louis,   Jean-Yves Gaubert, Guy Moulin, and Alexis Jacquier

4  Cardiac Thrombus................................................................................................. 21 4.1  Thrombus Complicating the Evolution of Myocardial Infarction............ 23 Armelle Renaud, Maxime Lalisse, Trung Le-Thanh, Stéphanie Lemaire,   Marie-Aurélie Delesalle, Jean Paul Beregi, and Christophe Lions

4.2  Thrombus in Dilated Cardiopathy............................................................... 25 Cyril Muller, Arthur Varoquaux, Vincent Vidal, Jean Michel Bartoli,   Jean-Yves Gaubert, Guy Moulin, and Alexis Jacquier

4.3  Thrombus and Heart Transplantation......................................................... 27 Dominique Grisoli, Alberto Riberi, Vladimir Gariboldi,   Frédréric Collart, Guy Moulin, and Alexis Jacquier

4.4  Thrombus During Pulmonary Embolism.................................................... 29 Jean-Yves Gaubert, Vincent Vidal, Jean Michel Bartoli,   Guy Moulin, and Alexis Jacquier

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Contents

4.5  Thrombus and Endomyocardial Fibrosis.................................................... 31 Nicolas Amabile, Philippe Dory-Lautrec, Jean Michel Bartoli,   Jean-Yves Gaubert, Guy Moulin, and Alexis Jacquier

4.6  Thrombus and Central Venous Catheter..................................................... 34 Arthur Varoquaux, Vincent Vidal, Jean Michel Bartoli,   Guy Moulin, and Jean-Yves Gaubert

4.7  Thrombus and Uptake of Contrast Medium................................................ 37 Pierre Cassagneaux, Guillaume Louis, Arthur Varoquaux, Vincent Vidal,   Jean Michel Bartoli, Guy Moulin, Jean-Yves Gaubert,   and Alexis Jacquier

5  Benign Tumors....................................................................................................... 41 5.1  Myxoma......................................................................................................... 43 Julie Mayer, Valérie Chabbert, and Hervé Rousseau

5.2  Atypically Located Myxoma........................................................................ 47 Gwenaelle Pouliquen, Karine Warin-Fresse, and Dominique Crochet

5.3  Papillary Fibroelastoma of the Mitral Valve.............................................. 50 Gwenaelle Pouliquen, Karine Warin-Fresse, and Dominique Crochet

5.4  Intramyocardial Fibroma............................................................................ 53 Eric Stephan and Philippe Douek

5.5  Coronary Fistula........................................................................................... 57 Patrick Mailleux

5.6  Intracardiac Venous Malformation (Formerly Hemangioma)................. 59 Marianne Jolibert, Guillaume Louis, Arthur Varoquaux,   Vincent Vidal, Jean Michel Bartoli, Jean-Yves Gaubert,   Guy Moulin, and Alexis Jacquier

5.7  Lipoma........................................................................................................... 63 Mathieu Rodiere and Frederic Thony

5.8  Calcification of the Mitral Annulus............................................................. 66 Gwenaelle Pouliquen, Karine Warin-Fresse, and Dominique Crochet

5.9  Cardiac Paraganglioma................................................................................ 69 Antoine Micheau, Sébastien Bommart, Claudine Bousquet,   and Hélène Vernhet Kovacsik

5.10  Castelman’s Disease..................................................................................... 74 Archid Azarine, Suzana Castela, and Elie Mousseaux

5.11  Neurofibromatosis Involving the Pericardium........................................... 77 Jean-Yves Gaubert, Philippe Dory-Lautrec, Guillaume Louis, and Alexis Jacquier

5.12  Erdheim–Chester’s Disease with Mediastinal Involvement..................... 80 Arthur Varoquaux, Vincent Vidal, Jean Michel Bartoli, and Alexis Jacquier

5.13  Ante and Postnatal Bronchogenic Cyst...................................................... 82 Katia Chaumoitre and Michel Panuel

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Contents

5.14  Esophageal Duplication................................................................................ 85 Katia Chaumoitre and Michel Panuel

5.15  Ante and Postnatal Rhabdomyoma............................................................ 87 Guillaume Gorincour, Alain Potier, Beatrice Guidicelli, and Nicole Philip

5.16  Ante and Postnatal Teratoma...................................................................... 90 Guillaume Gorincour, Alain Potier, Marianne Capelle,   and Bernard Kreitmann

6  Infectious Lesions................................................................................................... 93 6.1  Cardiac Hydatidosis..................................................................................... 94 Flavie Bratan and Vivien Thomson

6.2  Pseudotumoral Endocarditis....................................................................... 97 Franck Thuny, Philippe Dory-Lautrec, Gilbert Habib, Jean-Yves Gaubert,   Guy Moulin, and Alexis Jacquier

6.3  Cardiac Actinomycosis................................................................................. 99 Jean-Yves Gaubert, Philippe Dory-Lautrec, Katia Chaumoitre,   Vincent Vidal, Jean Michel Bartoli, Guy Moulin, Michel Panuel,   and Alexis Jacquier

7  Malignant Tumors.................................................................................................. 101 7.1  Metastasis Inside the Heart Chamber........................................................ 103 Flavie Bratan and Vivien Thomson

7.2  Myocardial Metastasis of Bronchial Tumor............................................... 105 Armelle Renaud, Maxime Lalisse, Trung Le-Thanh, Stéphanie Lemaire,   Marie-Aurélie Delesalle, Jean Paul Beregi, and Christophe Lions

7.3  Right Ventricular Metastasis of a Hepatocellular Carcinoma.................. 107 Aurélie Chabrol, Brahim Harbaoui, and Vivien Thomson

7.4  Pericardial Metastasis.................................................................................. 109 Flavie Bratan and Vivien Thomson

7.5  Lymphoma Inside the Heart Chamber....................................................... 113 Julie Mayer, Valérie Chabbert, and Hervé Rousseau

7.6  Lymphoma Developing in the Epicardial Space........................................ 116 Antonin Flavian, Jean Michel Bartoli, Jean-Yves Gaubert, Guy Moulin,   and Alexis Jacquier

7.7  Large Cell Lymphoma Involving the Pericardium.................................... 119 Laurence Monnier-Cholley and Lionel Arrivé

7.8  Undifferentiated Sarcoma Inside the Heart Chamber.............................. 122 Julie Mayer, Valérie Chabbert, and Hervé Rousseau

7.9  Fibrosarcoma................................................................................................. 125 Hend Belhiba, Jerome Caudron, Jeannette Fares,   and Jean Nicolas Dacher

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Contents

7.10  Angiosarcoma of the Left Atrium............................................................. 128 Eric Stephan and Philippe Douek

7.11  Angiosarcoma Developing Outside the Heart Chambers........................ 129 Olivier Monnet, Jean Michel Bartoli, Jean-Yves Gaubert,   Guy Moulin, and Alexis Jacquier

8  Synoptic Tables....................................................................................................... 133 Appendix....................................................................................................................... 139 Index.............................................................................................................................. 143

Contributors

Nicolas Amabile Department of Cardiology, Centre Marie Lannelongue, Le Plessis-Robinson, France

Claudine Bousquet Department of Radiology, Hôpital Arnaud Villeneuve, Montpellier, France

Lionel Arrivé Department of Radiology, Assistance Publique-Hôpitaux de Paris and Faculté de Médecine Pierre et Marie Curie, Hôpital Saint-Antoine, Paris, France

Flavie Bratan Department of Radiology, Hôpital de la Croix Rousse, Lyon, France

Archid Azarine Department of Cardiovascular Radiology, Université Paris-Descartes, APHP, Hôpital Européen Georges Pompidou, Paris, France Jean Michel Bartoli Department of Radiology, Université de Marseille Méditerranée, CHU la Timone, Marseille, France Hend Belhiba Department of Medical Imaging,   CHU de Rouen, Hôpital Charles Nicolle, Rouen, France Jean Paul Beregi Service d’Imagerie et de Radiologie Cardiaque et Vasculaire, Hôpital Cardiologique, Lille, France Sébastien Bommart Department of Radiology, Hôpital Arnaud Villeneuve, Montpellier, France

Marianne Capelle Hôpital de la Conception, Maternité, Marseille, France Pierre Cassagneaux Department of Radiology, Université de Marseille Méditerranée, CHU la Timone, Marseille, France Suzana Castela Department of Cardiovascular Radiology, Université Paris-Descartes, APHP, Hôpital Européen Georges Pompidou, Paris, France Jerome Caudron Department of Medical Imaging,   CHU de Rouen, Hôpital Charles Nicolle, Rouen, France Valérie Chabbert Department of Radiology, Hôpital Rangueil, Toulouse, France Aurélie Chabrol Department of Radiology, Hôpital de la Croix Rousse, Lyon, France xiii

xiv

Katia Chaumoitre Department of Radiology, CHU Nord, Marseille, France Frédéric Cohen Department of Radiology, Université de Marseille Méditerranée, CHU la Timone, Marseille, France Frédréric Collart Department of Cardiac Surgery,   Université de Marseille Méditerranée, CHU la Timone, Marseille, France Dominique Crochet Institut du Thorax, Centre Hospitalier Universitaire de Nantes, Hôpital Guillaume et René Laënnec, Nantes, France Jean Nicolas Dacher Department of Medical Imaging,   CHU de Rouen, Hôpital Charles Nicolle, Rouen, France Marie-Aurélie Delesalle Service d’Imagerie et de Radiologie Cardiaque et Vasculaire, Hôpital Cardiologique, Lille, France Philippe Dory-Lautrec Department of Radiology, Université de Marseille Méditerranée, CHU la Timone, Marseille, France

Contributors

Antonin Flavian Department of Radiology, Université de Marseille Méditerranée, CHU la Timone, Marseille, France Vladimir Gariboldi Department of Cardiac Surgery,   Université de Marseille Méditerranée, CHU la Timone, Marseille,   France Jean-Yves Gaubert Department of Radiology, Université de Marseille Méditerranée, CHU la Timone, Marseille, France Philippe Germain Nouvel Hôpital Civil, Strasbourg, France Guillaume Gorincour Service d’ Imagerie Pédiatrique   et Prénatal, Université de Marseille Méditerranée, CHU la Timone,   Marseille, France Gilles Goyault Nouvel Hôpital Civil, Strasbourg, France Dominique Grisoli Department of Cardiac Surgery,   Université de Marseille Méditerranée, CHU la Timone, Marseille,   France

Philippe Douek Service d’imagerie cardio-vasculaire,   CHU Louis Pradel, Lyon, France

Beatrice Guidicelli Centre Plurisciplinaire de Diagnostic Prénatal, Université de Marseille Méditerranée, CHU la Timone,  Marseille, France

Jeannette Fares Department of Medical Imaging,   CHU de Rouen, Hôpital Charles Nicolle, Rouen, France

Gilbert Habib Department of Cardiology, Université de Marseille Méditerranée, CHU la Timone, Marseille, France

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Contributors

Brahim Harbaoui Service de Cardiologie, Hôpital de la Croix Rousse, Lyon, France Alexis Jacquier Service d’imagerie Médicale Adulte, CHU la Timone, Marseille, Cedex,   France Marianne Jolibert Department of Radiology, Université de Marseille Méditerranée, CHU la Timone, Marseille, France Hélène Vernhet Kovacsik Department of Radiology, Hôpital Arnaud Villeneuve, Montpellier, France Bernard Kreitmann Service de Chirurgie Thoracique Cardiovasulaire Infantile, CHU La Timone Enfants, Marseille, France Maxime Lalisse Service d’Imagerie et de Radiologie Cardiaque et Vasculaire, Hôpital Cardiologique, Lille, France Stéphanie Lemaire Service d’Imagerie et de Radiologie Cardiaque et Vasculaire, Hôpital Cardiologique, Lille, France

Guillaume Louis Department of Radiology, Université de Marseille Méditerranée, CHU la Timone, Marseille, France Patrick Mailleux Clinical St Luc Bouge, Bouge,   Belgium Julie Mayer Department of Radiology,   Hôpital Rangueil, Toulouse, France Antoine Micheau Department of Radiology, Hôpital Arnaud Villeneuve, Montpellier, France Olivier Monnet Department of Radiology, Université de Marseille Méditerranée, CHU la Timone, Marseille, France Laurence Monnier-Cholley Department of Radiology, Assistance Publique-Hôpitaux de Paris and   Faculté de Médecine Pierre et   Marie Curie, Hôpital Saint-Antoine,   Paris, France Guy Moulin Department of Radiology, Université de Marseille Méditerranée, CHU la Timone, Marseille, France

Trung Le-Thanh Service d’Imagerie et de Radiologie Cardiaque et Vasculaire, Hôpital Cardiologique, Lille, France

Elie Mousseaux Department of Cardiovascular Radiology, Université Paris-Descartes, APHP,   Hôpital Européen Georges Pompidou, Paris, France

Christophe Lions Service d’Imagerie et de Radiologie Cardiaque et Vasculaire, Hôpital Cardiologique, Lille, France

Cyril Muller Department of Radiology, Université de Marseille Méditerranée, CHU la Timone, Marseille, France

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Michel Panuel Department of Radiology, CHU Nord, Marseille, France Alain Potier Centre Pluridisciplinaire de Diagnostic Prénatal, Université de Marseille Méditerranée, CHU la Timone,   Marseille, France Nicole Philip Centre Pluridisciplinaire de Diagnostic Prénatal, Université de Marseille Méditerranée, CHU la Timone,   Marseille, France Gwenaelle Pouliquen Institut du Thorax, Centre Hospitalier Universitaire de Nantes, Hôpital Guillaume et René Laënnec, Nantes, France Armelle Renaud Service d’Imagerie et de Radiologie Cardiaque et Vasculaire, Hôpital Cardiologique, Lille, France Alberto Riberi Department of Cardiac Surgery and Radiology, Université de Marseille Méditerranée, CHU la Timone,   Marseille, France Hervé Rousseau Department of Radiology, Hôpital Rangueil, Toulouse, France

Contributors

Mathieu Rodiere CHU Grenoble, Grenoble, France Eric Stephan Service d’imagerie cardio-vasculaire,   CHU Louis Pradel, Lyon, France Vivien Thomson Department of Radiology, Hôpital de la Croix Rousse, Lyon, France Frederic Thony CHU Grenoble, Grenoble, France Franck Thuny Department of Cardiology, Université de Marseille Méditerranée, CHU la Timone, Marseille, France Arthur Varoquaux Department of Radiology, Université de Marseille Méditerranée, CHU la Timone, Marseille, France Vincent Vidal Department of Radiology, Université de Marseille Méditerranée, CHU la Timone, Marseille, France Karine Warin-Fresse Institut du Thorax, Centre Hospitalier Universitaire de Nantes, Hôpital Guillaume et René Laënnec, Nantes, France

Introduction

1

The prevalence of primary heart tumors ranges between 0.001% and 0.030% in the autopsy series [1]. Cardiac metastases are usually found in end-stage disease and their prevalence is 20–40 times higher than primary tumors. It is difficult to define the frequency of thrombi with any accuracy because they develop as the result of an underlying disorder; however for patients whose ejection fraction is below 50% the prevalence of thrombi is assessed at 7% [2], and at 4% in patients suffering from pulmonary embolism [3]. Thrombi and tumors can both cause serious complications requiring a specific treatment, which, once again, will depend on the etiology of the underlying disorder. Discriminating between variations from the normal anatomy, thrombi and benign or malignant tumors is the basis to set out a therapeutic strategy and make a prognosis. Multidetector computed tomography (MDCT) and cardiac magnetic resonance (CMR) are techniques that yield a functional and morphological analysis of these lesions, giving details of perfusion and enhancement with spatial definition and contrast that no other imaging technology is capable of equaling today. CMR and MDCT have now become the first-line examinations used to explore this type of heart disorder [4]. The goal of this book is (1) to provide a quick overview of the different MRI sequences and CT-scan acquisitions used to explore cardiac masses, (2) to present a collection of clinical cases compiled in cooperation with a number of teams of Frenchspeaking radiologists who are members of SFICV and (3) to provide a series of synoptic tables and decision-making trees for use in the everyday practice of radiology.

A. Jacquier, CMR and MDCT in Cardiac Masses, DOI: 10.1007/978-3-642-18457-4_1, © Springer-Verlag Berlin Heidelberg 2011

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Technical Aspects

2

2.1  Cardiac Magnetic Resonance Imaging Techniques Each cardiac magnetic resonance imaging (CMR) sequence must be adapted to the patient in terms of heart rate and duration of apnea. Cardiac gating is a prerequisite in a CMR study. Electrocardiogram leads have to be MR compatible and positioned to provide a clear, strong electrocardiogram signal. Peripheral vein access must be available to inject contrast medium during the scan session. Different CMR techniques at 1.5T, proposed for the evaluation of a cardiac mass, are described further on [1–6].

Cine Sequences Steady-state free precession cine sequences are considered as the gold standard for assessing left ventricular volume, ejection fraction and chamber anatomy [7]. The high contrast between the myocardium (low signal) and the blood (high signal) is excellent on cine sequences and gives an accurate delineation of the endocardial wall, showing the intracavity border of a cardiac mass. Temporal resolution is also excellent, providing high ­resolution cine sequences, and single shot images covering the whole chest in the axial plane in one or two breath-holds. The examination should include cine sequences in the two-chamber, four-chamber and short axis views, with the option of measuring left and right ventricle volumes, ejection fraction and mass.

T1- and T2-Weighted Sequences These are mainly used to image the great vessels and they can also be used to delineate anatomical features and characterize different types of tissue. These sequences are very sensitive to flow artifact and a black blood pulse is usually performed before acquisition to null the signal of flowing blood. They can also be used with a fat-suppressed pre-pulse and are of great interest in assessing differential diagnoses for thrombus such as lipoma, fatty infiltration or anatomic variations.

A. Jacquier, CMR and MDCT in Cardiac Masses, DOI: 10.1007/978-3-642-18457-4_2, © Springer-Verlag Berlin Heidelberg 2011

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2  Technical Aspects

First Pass Perfusion Imaging Gradient echo, steady-state free precession and echo planar imaging based sequences can be used to assess first pass myocardial perfusion. These sequences are T1-weighted, have a high temporal resolution and provide images on three or four different slice levels (usually three different short axis views, and one long axis view) in one RR interval. These MR techniques are used to measure myocardial perfusion [8] after gadolinium chelate injection, but can be used to assess cardiac mass perfusion [5].

Look-Locker Sequences Look-locker sequences consist in performing electrocardiogram-synchronized look-locker trains in one breath hold on consecutive heart beats (echo planar imaging with slice selective inversion recovery pulse). These sequences have the advantage of setting the inversion time of normal myocardium that is subsequently used for the delayed contrast-enhanced MR images [9]. Look-locker [10, 11] and, more recently, MOLLI sequences have also been used to measure T1 of the myocardium before and after contrast injection to assess the presence of enhancement within a mass [12].

Delayed Contrast Enhancement Gradient echo with inversion recovery in 2D and, more recently, in 3D is the gold standard sequence for assessing myocardial enhancement [9]. This sequence must be performed 5–20 min after the administration of an extracellular contrast medium for measuring myocardial infarcts [13–15]. Delayed contrast-enhanced MR images can also be performed to assess myocardial mass enhancement [1] and earlier acquisitions should be made (at 1–5  min) to assess the quality of mass enhancement. With gradient echo inversion recovery, inversion time must be set to null normal myocardium before each acquisition to provide a high contrast to noise ratio [9]. Phase sensitive inversion recovery images can now be used to assess late enhancement without the need to set inversion time [16, 17].

2.2  Multidetector Computed Tomography Image Acquisition Multidetector computed tomography (MDCT) yields high temporal resolution isotropic voxel images. Other benefits include improved quality of multiplanar and 3D reconstruction and the ability to combine other protocols with coronary CT angiography while still using a single dose of contrast medium. Thin slices give this imaging modality the capacity to visualize the cardiac and coronary anatomy in any spatial orientation with equal resolution. The same acquisition also provides both morphological and functional information.

2.2  Multidetector Computed Tomography Image Acquisition

5

Images Acquisition Cardiac MDCT is a technical challenge because image acquisition must be synchronized with the heart rate using the minimum dose of radiation. The scanning parameters must be adapted to the patient’s heart rate and morphology in order to achieve perfect image quality with the lowest possible radiation exposure for the patient. In clinical protocols, images are acquired in two different phases [18]. The arterial phase is synchronized with the arrival of the contrast bolus in the cardiac chambers and aortic roots. This acquisition is used to assess the coronary anatomy and myocardial perfusion and to differentiate early perfusion defects that are picked up as hypoenhanced areas in the normal myocardial tissue and to measure left ventricular (LV) volume and ejection fraction [19, 20]. The delayed enhancement phase is performed 5 min after contrast injection and image parameters must be adapted to show delayed myocardial enhancement [21–25].

Acquisition Parameters For the arterial phase, the acquisition parameters (detector collimation, tube voltage and tension) are set to assess the coronary anatomy and require the highest technical potential of the CT hardware and software. These acquisitions demand a high radiation dose, although the dose required may decrease as the technology progresses [26]. Acquisition parameters for the arterial rule-out phase depend on the available scan hardware and are described in detail in several papers [25, 27–29]. For the delayed enhancement phase the acquisition parameters must be adapted to show myocardium enhancement and most investigators set the tube voltage around 80 kV [21, 25, 30–32] in human studies assessing delayed myocardial enhancement. The tube voltage is adjusted to a low setting (80 kV) to decrease radiation exposure and increase contrast to noise ratio. The tube voltage should be set at 100 kV to assess delayed myocardial enhancement in patients with a body weight above 80 kg [30]. Detector collimation can be increased to 1.2 or 1.5 mm because the spatial definition required for assessing delayed myocardial enhancement is not the most essential aspect of this acquisition [25, 30, 32]. Increasing the detector collimation decreases the noise and subsequently increases the signal to noise ratio (SNR) and the control to noise ratio (CNR) thus allowing dose reduction [21]. The medium kernel convolution used for late enhancement reconstruction must be selected to enhance the contrast resolution [25].

Contrast Injection MDCT assessment of delayed myocardial enhancement requires an increased dose of ­iodinated contrast medium – between 120 and 140 mL compared to the dose used in coronary anatomy assessment (70–80 mL for 64-slice technology) [21, 25, 31, 32]. In the studies mentioned above, the concentrations of contrast media vary from 300 to 400 mg of iodine per mL and the total amount of iodine injected varies from 44 to 56 g per patient,

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2  Technical Aspects

which means a quantity between 0.44 and 0.77 mg of iodine per kg of body weight for a body weight of 80 kg. MDCT has advantages over CMR including a direct proportionate linear relationship between enhanced X-ray absorption and the concentration of the contrast agent [33]. An increase in the dose of iodine injected will increase the CNR, SNR and the contrast resolution. There is no recommended dose for MDCT in the literature but a dose of iodine around 0.6–0.7 mg of iodine per kg of body weight yields images of good diagnostic value. The delay between injection and image acquisition varies substantially in the literature for the delayed enhancement phase, ranging from 5 [32] to 15 min [25] after intravenous injection; this delay can increase to 24 ± 11 min if the iodine is injected directly into the coronary tree during coronarography with revascularization [30]. Lardo et al [20] measured the enhancement kinetics of iodine contrast media in vivo in a pig infarct model. Investigators showed that the infarct area was clearly delineated and reached peak enhancement 5 min after injection and then washed out showing the progressive renal clearance of the contrast medium. It was recently shown in humans that a delayed enhancement acquisition 5 min after contrast medium injection provided a higher CNR and SNR compared with the 10 min time point. This is explained by the rapid decrease in iodine concentration in the blood due to renal clearance. This study shows that delayed enhancement acquisitions should be performed 5 min after contrast injection to improve image quality [15].

Anatomic Pitfalls

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Contents 3.1  D  eep Atrioventricular Groove............................................................................ 8 Philippe Germain and Gilles Goyault 3.2  L  ipomatous Hypertrophy of the Interatrial Septum........................................ 11 Laurence Monnier-Cholley and Lionel Arrivé 3.3  F  low Artifact in the Right Atrium...................................................................... 14 Laurence Monnier-Cholley and Lionel Arrivé 3.4  C  rista Terminalis.................................................................................................. 17 Arthur Varoquaux, Vincent Vidal, Jean Michel Bartoli, Jean-Yves Gaubert, Guy Moulin, and Alexis Jacquier 3.5  J uxtacaval Fat Collection.................................................................................... 19 Philippe Dory-Lautrec, Frédéric Cohen, Guillaume Louis, Jean-Yves Gaubert, Guy Moulin, and Alexis Jacquier

A. Jacquier, CMR and MDCT in Cardiac Masses, DOI: 10.1007/978-3-642-18457-4_3, © Springer-Verlag Berlin Heidelberg 2011

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3  Anatomic Pitfalls

3.1  Deep Atrioventricular Groove Philippe Germain and Gilles Goyault

Case Report A 51-year-old male was referred to our department for exploration of a hyperechogenic mass in the right atrium. The lesion was discovered on a trans-thoracic echocardiography examination performed during a routine checkup. The patient was asymptomatic and the ultrasound exploration revealed no other anomaly apart from the mass. He was explored by contrast-enhanced CMR and cardiac MDCT.

Diagnosis Deep atrioventricular groove, confirmed on the cardiac MDCT and CMR; this is an anatomic pitfall yielding a hyperechogenic tumor-mimicking image in the right atrium on the transthoracic echocardiography findings.

Fig. 1  CMR, T1 SE black blood weighted image, four-chamber view, showing a deep, wide, right atrioventricular groove (arrow). The right atrioventricular groove contains epicardial fat (hypersignal) and the right coronary vessels

3.1  Deep Atrioventricular Groove Fig. 2  Cardiac MDCT, four-chamber view. (a) Deep, fatty atrioventricular groove (arrow); the right coronary artery is visible (arrowhead). (b) Surface rendering: deep atrioventricular groove (arrow)

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3  Anatomic Pitfalls

Table summarizing the radiological findings for deep atrioventricular groove: Age of discovery

Variable

Clinical presentation

Asymptomatic

Developing on

Right AV groove

Type

Fat and right coronary vessels

Borders

Regular

Extension

No

Calcifications

No

Density without contrast

Hypodense

T1 SE signal

Hypersignal

T2 SE signal

Hypersignal

Uptake of contrast

No

Differential diagnosis

Lipoma

Pathognomonic sign

Morphological features

3.2  Lipomatous Hypertrophy of the Interatrial Septum

11

3.2  Lipomatous Hypertrophy of the Interatrial Septum Laurence Monnier-Cholley and Lionel Arrivé

Case Report Ms Y. a 62-year-old female was under surveillance for ovarian cancer with peritoneal carcinosis. She had a cardiac MDCT as part of her routine follow-up during chemotherapy and the images showed a mass developing in the interatrial septum.

Diagnosis Lipomatous hypertrophy of the interatrial septum.

Fig. 3  Cardiac MDCT, axial slice through the cardiac chambers, showing a mass with regular borders located on the interatrial septum (arrows), sparing the fossa ovalis; the low density of the mass on the image suggests that it is made up of adipose tissue. There is also an increase in the adipose tissue around the heart and in the mediastinum

12 Fig. 4  The cardiac MDCT shows that the fossa ovalis (arrow) is not affected, thus giving the mass its typical shape

Fig. 5  Cardiac MDCT at a lower level. The adipose tissue is infiltrating along the coronary sinus into a proeminent Eustachian valve remnant (arrow)

3  Anatomic Pitfalls

13

3.2  Lipomatous Hypertrophy of the Interatrial Septum

Background The incidence of this disorder is around 2% and increases with age; it is mainly diagnosed in overweight patients. Lipomatous hypertrophy of the interatrial septum is a form of hypertrophy of the preexisting fatty tissue in the interatrial septum and is often associated with hypertrophy of the epicardial fat [34, 35]. Table summarizing the radiological findings in lipomatosis of the interatrial septum: Age of discovery

Adult

Clinical features

Asymptomatic

Developing on

Interatrial septum

Tissue

Brown fat

Borders

Regular

Extension

No

Calcifications

No

Density without contrast

Hypodense

Signal T1 SE

Hypersignal

Signal T2 SE

Hypersignal

Uptake of contrast

No

Differential diagnosis

Lipoma

Pathognomonic sign

No involvement of the fossa ovalis

14

3  Anatomic Pitfalls

3.3  Flow Artifact in the Right Atrium Laurence Monnier-Cholley and Lionel Arrivé

Case Report A 54-year-old female patient was referred for a non-gated thoracic CT scan to screen for suspected pulmonary embolus; the clinical examination revealed atrial fibrillation, precordalgia and breathlessness; the patient’s case history included surgery to correct a septal defect at the age of 17. Fig. 6  Contrast-enhanced thoracic CT scan without cardiac gating: no pulmonary embolus is visible. In the right atrium there is a round-shaped image developing against the interatrial septum; this image is hypodense in comparison to the right ventricle

3.3  Flow Artifact in the Right Atrium Fig. 7  The CT scan acquisitions with MPR reconstruction show that the hypodense signal picked up on the right atrium is located on the terminal portion of the inferior vena cava

Fig. 8  Contrast-enhanced CT scan 5 min after injection of contrast medium showing that the contrast medium is now evenly distributed in the vena cava and the right atrium and no mass is distinguishable

15

16

3  Anatomic Pitfalls

Fig. 9  On CMR, the SSFP cine sequences in the four-chamber plane confirm that there is no mass in the right atrium

Diagnosis Flow artifact inside the right atrium at the inferior vena cava junction, mimicking right atrial thrombus in the early enhancement phase.

Background The contrast medium can sometimes distribute unevenly in the right atrium immediately after injection because of the complex flow patterns and turbulence in this part of the heart. Multiple plane reconstructions and further acquisitions at a later stage can be helpful to correct the diagnosis. Table summarizing the radiological findings in flow artifact of the right atrium: Clinical

Asymptomatic

Developing on

Right atrium

Type

Physiological swelling

Borders

Regular

Arterial phase

The artifact is visible

Venous or later phase

Whole chamber homogenously enhanced

Pathognomonic sign

Late homogenization of contrast

3.4  Crista Terminalis

17

3.4  Crista Terminalis Arthur Varoquaux, Vincent Vidal, Jean Michel Bartoli, Jean-Yves Gaubert, Guy Moulin, and Alexis Jacquier

Case Report A 50-year-old female was referred to our department for the exploration of a mass pro­ jecting from the lateral wall of the right atrium discovered on an echocardiographic examination.

Diagnosis Crista terminalis.

Fig. 10  Post-contrast cardiac MDCT, axial view. The mass depicted on the echocardiogram is developing from the lateral wall of the right atrium; its borders are clear and regular (arrow)

18

3  Anatomic Pitfalls

Fig. 11  SSFP cine image, four-chamber view. The mass described above is visible on the lateral wall of the right atrium; it has regular borders and sends the same signal as the myocardium (arrow)

Background The crista terminalis is a vertical ridge of smooth myocardium that protrudes into the right atrium. It is located on the lateral wall, running from the right side of the orifice of the superior vena cava to the right side of the inferior vena cava. It marks the line where the anterior trabeculated portion of the right atrium and the smooth posterior wall of the venous sinus merge. The crista terminalis is often visualized in the right atrium in the course of a routine contrast-injected CT scan, or CMR and can sometimes be quite prominent. The sinoatrial node is located in the upper portion of the crista terminalis [36]. Table summarizing the radiological findings for crista terminalis: Developing on

Lateral wall of the right atrium

Type

Physiological muscular swelling

Borders

Regular

Location

Between the two vena cava, in the right atrium

Calcification

No

Density without contrast

Hypodense

T1 SE signal

Isosignal/muscle

T2 SE signal

Isosignal/muscle

Uptake of contrast

No

Differential diagnosis

Tumoral mass

Pathognomonic sign

Morphological findings

3.5  Juxtacaval Fat Collection

19

3.5  Juxtacaval Fat Collection Philippe Dory-Lautrec, Frédéric Cohen, Guillaume Louis, Jean-Yves Gaubert, Guy Moulin, and Alexis Jacquier

Case Report An obese female patient, age 45 years, was explored for abdominal pain and a mass was found in the retrohepatic portion of the inferior vena cava (IVC) on her CT scan. A CMR and a non-gated CT scan were ordered to explore the mass.

Diagnosis Juxtacaval fat collection. Fig. 12  CMR T1-weighted axial image in the upper part of the liver showing a hypersignal indicating a mass in the lumen of the IVC

20

3  Anatomic Pitfalls

Fig. 13  CT scan 60 s after contrast injection showing a fat-suppressed mass with regular borders, developing in the lumen of the retrohepatic IVC

Background Juxtacaval fat collection is caused by part of the fatty tissue located around the retrohepatic segment of the IVC invaginating into the lumen of the vessel. The image is positiondependent and also varies according to the patient’s respiratory phase. The frequency of this anatomical variation is 0.5%. It is located in a posteromedial position on the IVC, either on or below the confluence of the SHV. It is usually round or oval in shape, clearly delineated, measuring 5–25 mm in diameter and its density varies between −140 and −30 HU. There are many possible assumptions regarding its pathophysiology: angulation due to anatomical variation, obesity, diabetes or steroid treatment [37]. Table summarizing the radiological findings for juxtacaval fat collection: Age of discovery

Adult

Clinical

Asymptomatic

Developing on

IVC junction of the RA

Type

Fatty tissue around vena cava and esophagus

Borders

Regular

Extension

No

Calcifications

No

Density without contrast

Hypodense

T1 SE signal

Hypersignal

T2 SE signal

Hypersignal

Uptake of contrast

No

Differential diagnosis

Lipoma

Pathognomonic sign

Position-dependent and varies with breathing

Cardiac Thrombus

4

Contents 4.1  T  hrombus Complicating the Evolution of Myocardial Infarction.................. 23 Armelle Renaud, Maxime Lalisse, Trung Le-Thanh, Stéphanie Lemaire, Marie-Aurélie Delesalle, Jean Paul Beregi, and Christophe Lions 4.2  T  hrombus in Dilated Cardiopathy..................................................................... 25 Cyril Muller, Arthur Varoquaux, Vincent Vidal, Jean Michel Bartoli, Jean-Yves Gaubert, Guy Moulin, and Alexis Jacquier 4.3  T  hrombus and Heart Transplantation............................................................... 27 Dominique Grisoli, Alberto Riberi, Vladimir Gariboldi, Frédréric Collart, Guy Moulin, and Alexis Jacquier 4.4  T  hrombus During Pulmonary Embolism.......................................................... 29 Jean-Yves Gaubert, Vincent Vidal, Jean Michel Bartoli, Guy Moulin, and Alexis Jacquier 4.5  T  hrombus and Endomyocardial Fibrosis.......................................................... 31 Nicolas Amabile, Philippe Dory-Lautrec, Jean Michel Bartoli, Jean-Yves Gaubert, Guy Moulin, and Alexis Jacquier 4.6  T  hrombus and Central Venous Catheter........................................................... 34 Arthur Varoquaux, Vincent Vidal, Jean Michel Bartoli, Guy Moulin, and Jean-Yves Gaubert 4.7  T  hrombus and Uptake of Contrast Medium...................................................... 37 Pierre Cassagneaux, Guillaume Louis, Arthur Varoquaux, Vincent Vidal, Jean Michel Bartoli, Guy Moulin, Jean-Yves Gaubert, and Alexis Jacquier

A. Jacquier, CMR and MDCT in Cardiac Masses, DOI: 10.1007/978-3-642-18457-4_4, © Springer-Verlag Berlin Heidelberg 2011

21

22

4  Cardiac Thrombus

Cardiac thrombi are more frequent than cardiac tumors. Making a differential diagnosis between a tumor and thrombus is an important issue in clinical practice [2, 3, 38, 39]. Imaging findings in thrombus are variable and depend on several factors: mobility, size, the age of the thrombus, the chamber in which it has developed and the underlying cause of thrombus formation. All thrombi are the result of an underlying disease that can be either local (infarction scar tissue, akinetic chamber) or general (pulmonary embolism etc.). The goal of this chapter is to present the different radiological findings that thrombi can present with.

4.1  Thrombus Complicating the Evolution of Myocardial Infarction

23

4.1  Thrombus Complicating the Evolution of Myocardial Infarction Armelle Renaud, Maxime Lalisse, Trung Le-Thanh, Stéphanie Lemaire, Marie-Aurélie Delesalle, Jean Paul Beregi, and Christophe Lions

Case Report A female, age 36 years, presented with sudden-onset aphasia D1 after childbirth by vaginal delivery; the diagnostic workup revealed a stroke consecutive to left sylvian artery occlusion. The patient’s cardiovascular risk factors were: mixed dyslipidemia, tobacco use at 40 packets/year (she had not stopped smoking), a family history of cardiovascular disease and obesity. The echocardiographic findings included dyskinesia of the apex of the left ventricle (LV); the ultrasound examination of the supraaortic trunk vessels was normal. Her cardiac enzyme levels were normal. A CMR was performed to look for LV thrombi.

Diagnosis LV apical thrombus complicating the evolution of a myocardial infarct in the territory of the anterior interventricular artery. The stroke was due to migration of a part of the thrombus into the main circulation.

24 Fig. 1  Late enhancement images in the four-chamber view (a) and the two-chamber view (b), 10 min after contrast injection showing late transmural hyper enhancement of the apex of the LV, indicating transmural myocardial necrosis (arrows). The thrombus is adhering to the infarcted myocardium inside the LV cavity and appears as a hypoenhanced mass (arrowhead)

4  Cardiac Thrombus

a

b

Background The prevalence of myocardial infarct-related thrombus is around 5%. It is interesting to note that the incidence of these thrombi increases as the LV ejection fraction decreases and is significantly higher in patients with a left ventricular ejection fraction below 40% [1, 39].

4.2  Thrombus in Dilated Cardiopathy

25

4.2  Thrombus in Dilated Cardiopathy Cyril Muller, Arthur Varoquaux, Vincent Vidal, Jean Michel Bartoli, Jean-Yves Gaubert, Guy Moulin, and Alexis Jacquier

Case Report Mr. F., age 80 years, was admitted to hospital for heart failure. The patient’s echocardiographic examination showed LV enlargement and decreased ejection fraction. The coronarogram did not reveal any anomalies of the coronary vessels. A CMR was performed to assess the etiology of his recently revealed LV failure.

Diagnosis Dilated cardiomyopathy complicated by the presence of a thrombus in the left ventricle.

Fig. 2  The patient’s left ventricle is dilated (enddiastolic volume: 200 mL/m²) and hypokinetic (LVEF: 8%), the cine images also revealed a marked asynchronization between the contractions of the interventricular septum and the lateral LV wall. Note the pericardial effusion (arrow)

26

4  Cardiac Thrombus

Fig. 3  On the late enhancement images there are several, small microthrombi adhering to the endocardium on the upper and lower lateral walls of the LV (arrows)

Background Thrombus is a standard complication of dilated cardiomyopathy. Thrombi develop as the heart dilates due to stasis of the blood secondary to a decrease in the patient’s ejection fraction. The prevalence of this disorder in a population with a left ventricular ejection fraction below 50% is 7%. The incidence of thrombus increases as the ejection fraction decreases. The presence of myocardial scarring and/or an akinetic area is an independent factor increasing the risk of thrombus [39]. CMR cine and late enhancement sequences are more sensitive and specific than transthoracic and transesophageal echocardiography to diagnose thrombi.

4.3  Thrombus and Heart Transplantation

27

4.3  Thrombus and Heart Transplantation Dominique Grisoli, Alberto Riberi, Vladimir Gariboldi, Frédréric Collart, Guy Moulin, and Alexis Jacquier

Case Report A 68-year-old male patient who had undergone heart transplantation surgery was given a routine echocardiographic examination. A mobile, pedicled mass was discovered in his right atrium. A CMR was ordered to explore the mass and make a differential diagnosis between thrombus and a lymphoproliferative lesion.

Diagnosis Right atrial thrombus developing in the akinetic and fibrotic area of the surgical suture between the atria of the donor and host.

Fig. 4  CMR cine images in the long axis four-chamber view showing a bulky, round-shaped mass developing in the right atrium (arrow), moving during the cardiac cycle

28

4  Cardiac Thrombus

Fig. 5  Late enhancement images 10 min after injection of gadolinium chelate, revealing no visible enhancement of the lesion (arrow)

Background Thrombus is a complication that occurs frequently in standard orthoptic heart transplantation. In orthoptic transplantation a substantial portion of the host’s atria is left in situ, which can lead to thrombus formation. More recently, complete orthoptic transplantation has replaced standard orthoptic transplantation; this method leaves only a small portion of the host’s atrium in situ and in some cases only the venous ostia. The second type of procedure gives rise to fewer complications [40–43].

4.4  Thrombus During Pulmonary Embolism

29

4.4  Thrombus During Pulmonary Embolism Jean-Yves Gaubert, Vincent Vidal, Jean Michel Bartoli, Guy Moulin, and Alexis Jacquier

Case Report A female patient, age 45 years, was admitted to hospital for severe, acute pulmonary embolism. She was given an echocardiographic examination, and a heterogeneous mass was found in her right ventricle. A CMR was performed.

Diagnosis Right heart thrombus occurring during pulmonary embolism.

Fig. 6  CMR short axis cine images at the end-diastolic phase (a) then at the end-systolic phase (b), showing a mobile mass attached to the trabeculation of the right ventricle (arrow)

a

30 Fig. 6  (continued)

4  Cardiac Thrombus

b

Background The prevalence of thrombus during pulmonary embolism is around 4% (based on an echocardiographic study [44]). Thrombi are often found in the right heart chambers during severe pulmonary embolism; this is usually due to part of a thrombus traveling up from the lower limb veins into the pulmonary network becoming caught in the right  atrial or ventricular structures and adhering to their wall. These thrombi are extremely mobile.

4.5  Thrombus and Endomyocardial Fibrosis

31

4.5  Thrombus and Endomyocardial Fibrosis Nicolas Amabile, Philippe Dory-Lautrec, Jean Michel Bartoli, Jean-Yves Gaubert, Guy Moulin, and Alexis Jacquier

Case Report A female patient, age 46  years, was given a cardiac ultrasound examination before she started chemotherapy for mammary neoplasm. A nonmobile mass was found on the apex of the left ventricle; it was hypoechogenic and the left heart chambers were enlarged. The laboratory tests revealed a severe inflammatory syndrome but her blood count was normal. A CMR was ordered to explore the mass.

Diagnosis LV thrombus complicating the evolution of endomyocardial fibrosis. Fig. 7  Cine images, four-chamber view at the end-diastolic (a) and end-systolic (b) phases, revealing a large, heterogeneous mass at the apex of the LV

32 Fig. 7  (continued)

Fig. 8  Late enhancement image 10 min after gadolinium injection confirming the presence of a large thrombus (arrowhead) and showing significant enhancement of the layer of endocardium in the apical portion of the LV (arrows)

4  Cardiac Thrombus

4.5  Thrombus and Endomyocardial Fibrosis

33

Background There are three different stages of cardiac involvement in idiopathic eosinophilia: (1) a necrotic stage, which is due to eosinophils infiltrating the endocardium and causing microabscesses; (2) an intermediate thrombonecrotic stage during which thrombi appear on the surface of the necrotic myocardium of both ventricles; (3) and later a fibrous stage during which the myocardium and the chordae tendineae become fibrotic and the patient develops restrictive cardiomyopathy. The cardiac lesion caused by hypereosinophilia can also develop without eosinophilia: (1) as part of a paraneoplastic syndrome or because the eosinophil levels in the blood decrease although the heart is still affected [45, 46].

34

4  Cardiac Thrombus

4.6  Thrombus and Central Venous Catheter Arthur Varoquaux, Vincent Vidal, Jean Michel Bartoli, Guy Moulin, and Jean-Yves Gaubert

Case Report A 64-year-old female undergoing chemotherapy for bladder cancer had an ultrasound ­examination on which a large heterogeneous mass was found adhering to the wall of the right atrium. The patient had an implantable chamber for her treatment. A complementary CMR examination was ordered to make a differential diagnosis between thrombus and metastasis.

Diagnosis Thrombus of the right atrium on an implantable venous catheter. The lesion completely disappeared with appropriate anticoagulant treatment.

Fig. 9  The short axis cine image shows a large mobile mass filling the right atrium, developing from the lower wall on a narrow pedicle (arrow)

4.6  Thrombus and Central Venous Catheter Fig. 10  Late enhancement image after injection of contrast medium in short axis. No visible uptake of the contrast medium by the lesion, which is clearly seen as a hyposignal

Fig. 11  Cine image 3 months after starting anticoagulant treatment. The lesion has completely disappeared

35

36

4  Cardiac Thrombus

Background Thrombi develop on lesions of the endocardium either as a result of mechanical stress or due to the products injected via the catheter (chemical stress). In the latter case the lesion can be located at a distance from the end of the catheter. It can be very tricky to diagnose catheter-induced thrombi because these patients often have a potentially metastatic disorder. Anticoagulant treatment is sometimes required to confirm the diagnosis [44].

4.7  Thrombus and Uptake of Contrast Medium

37

4.7  Thrombus and Uptake of Contrast Medium Pierre Cassagneaux, Guillaume Louis, Arthur Varoquaux, Vincent Vidal, Jean Michel Bartoli, Guy Moulin, Jean-Yves Gaubert, and Alexis Jacquier

Case Report A male, age 65 years, was admitted to hospital for the management of heart failure secondary to chronic alcohol intoxication. The initial CMR findings showed evidence of an apical thrombus. The patient was seen again 3 months after having been weaned off alcohol and given an anticoagulant treatment. A CMR was ordered to explore the thrombus and assess his myocardial function.

Diagnosis Thrombus of the LV picking up the contrast medium at a late stage. Fig. 12  CMR late enhancement images with acquisitions at 1 min (a), 7 min (b) and 10 min (c) after contrast injection: 1 min, the apical thrombus in the LV is visible as white spot surrounded by dark rim (arrows); 7 min after injection the thrombus is gradually becoming enhanced; at 10 min the thrombus is completely enhanced and a bright mass is visible at the apex of the left ventricle

a

38 Fig. 12  (continued)

4  Cardiac Thrombus

b

c

Background Some thrombi are enhanced by the contrast medium; it can take several minutes for the dye to spread and they gradually become enhanced from the edge to the center. It is advisable to make early acquisitions immediately after injection of the contrast medium to assess these lesions. Contrast uptake in thrombus was described by other investigators and can occur in organized thrombus [2, 3].

39

4.7  Thrombus and Uptake of Contrast Medium

Table summarizing the radiological findings for thrombus: Age of discovery

Variable

Clinical

Asymptomatic, embolus or related to etiology

Developing on

Inside the heart chamber – location depends on etiology

Borders

Highly variable

Extension

Inside the heart chamber

Calcifications

Possible for old thrombi

Density without contrast

Isodense, depends on age

T1 SE signal

Highly variable

T2 SE signal

Highly variable

Uptake of contrast

Rare but possible for organized thrombus

Differential diagnosis

Any other mass

Benign Tumors

5

Contents 5.1  M  yxoma................................................................................................................ 43 Julie Mayer, Valérie Chabbert, and Hervé Rousseau 5.2  A  typically Located Myxoma............................................................................... 47 Gwenaelle Pouliquen, Karine Warin-Fresse, and Dominique Crochet 5.3  P  apillary Fibroelastoma of the Mitral Valve..................................................... 50 Gwenaelle Pouliquen, Karine Warin-Fresse, and Dominique Crochet 5.4  I ntramyocardial Fibroma................................................................................... 53 Eric Stephan and Philippe Douek 5.5  C  oronary Fistula.................................................................................................. 57 Patrick Mailleux 5.6  I ntracardiac Venous Malformation (Formerly Hemangioma)........................ 59 Marianne Jolibert, Guillaume Louis, Arthur Varoquaux, Vincent Vidal, Jean Michel Bartoli, Jean-Yves Gaubert, Guy Moulin, and Alexis Jacquier 5.7  L  ipoma.................................................................................................................. 63 Mathieu Rodiere and Frederic Thony 5.8  C  alcification of the Mitral Annulus.................................................................... 66 Gwenaelle Pouliquen, Karine Warin-Fresse, and Dominique Crochet 5.9  C  ardiac Paraganglioma....................................................................................... 69 Antoine Micheau, Sébastien Bommart, Claudine Bousquet, and Hélène Vernhet Kovacsik

A. Jacquier, CMR and MDCT in Cardiac Masses, DOI: 10.1007/978-3-642-18457-4_5, © Springer-Verlag Berlin Heidelberg 2011

41

42

5  Benign Tumors

5.10 Castelman’s Disease............................................................................................. 74 Archid Azarine, Suzana Castela, and Elie Mousseaux 5.11 Neurofibromatosis Involving the Pericardium.................................................. 77 Jean-Yves Gaubert, Philippe Dory-Lautrec, Guillaume Louis, and Alexis Jacquier 5.12 Erdheim–Chester’s Disease with Mediastinal Involvement............................ 80 Arthur Varoquaux, Vincent Vidal, Jean Michel Bartoli, and Alexis Jacquier 5.13 Ante and Postnatal Bronchogenic Cyst.............................................................. 82 Katia Chaumoitre and Michel Panuel 5.14 Esophageal Duplication....................................................................................... 85 Katia Chaumoitre and Michel Panuel 5.15 Ante and Postnatal Rhabdomyoma.................................................................... 87 Guillaume Gorincour, Alain Potier, Beatrice Guidicelli, and Nicole Philip 5.16 Ante and Postnatal Teratoma............................................................................. 90 Guillaume Gorincour, Alain Potier, Marianne Capelle, and Bernard Kreitmann

43

5.1  Myxoma

5.1  Myxoma Julie Mayer, Valérie Chabbert, and Hervé Rousseau

Case Report A female patient age 44 years was admitted to hospital in an emergency setting for chest pain and hemoptysis. She had an angioscan and was diagnosed with pulmonary embolism. By chance the scan also revealed a mass in the patient’s left atrium. A cardiac MDCT and a CMR were ordered as part of the preoperative workup.

Diagnosis Myxoma of the left atrium.

Fig. 1  Cardiac MDCT, MPR short-axis view of a reconstruction of the fossa ovalis (Fig. a) and MIP reconstruction in the two-chamber plane (Fig. b). A pediculated mass is visible inside the left atrium, attached to the septum. The borders of the mass are irregular

a

44 Fig. 1  (continued)

Fig. 2  Four-chamber cine image: the septal implantation of the lesion is clearly visible; it is mobile and moves through the mitral valve during the diastole, yielding an intermediate signal

5  Benign Tumors

b

5.1  Myxoma Fig. 3  T1-weighted black blood image, four-chamber view: the mass is picked up as a hyposignal with a narrow septal base of attachment

Fig. 4  T2-weighted black blood image, four-chamber view: the mass is picked up as a homogenous hypersignal

45

46 Fig. 5  Delayed enhanced image after gadolinium injection. No visible uptake of the contrast medium on this slice

5  Benign Tumors

5.2  Atypically Located Myxoma

47

5.2  Atypically Located Myxoma Gwenaelle Pouliquen, Karine Warin-Fresse, and Dominique Crochet

Case Report A chest auscultation for a viral illness revealed a heart murmur in a young female patient aged 12. She was given an ultrasound examination, which showed a mass located in the infundibulum of the right ventricle (RV), moving on each systole.

Diagnosis The mass was surgically removed; the histology slides confirmed that it was a myxoma.

Fig. 6  Short axis cine image in the plane of the RV infundibulum. An oval shaped, mobile, clearly delineated mass is visible in the RV under the pulmonary valve. The pediculated mass is inserted in the RV infundibulum under the pulmonary valve

48 Fig. 7  Cine image parasagittal view on the level of the main pulmonary artery taken on the diastole. The mass is obstructing the blood flow

Fig. 8  Late enhancement images after gadolinium injection in the plane of the infundibulum of the pulmonary artery showing a marked enhancement of the mass

5  Benign Tumors

49

5.2  Atypically Located Myxoma

Background Myxomas are benign and they are the primary heart tumors that most frequently affect adults with a slight predominance in females [47]. The mean age at diagnosis is 50, and 90% of patients are aged 30–60 years. They develop on the endocardium and usually arise from the fossa ovalis region. Three quarters of these tumors are located in the left atrium, 15–20% in the right atrium (with no particular preference for the fossa ovalis implantation) and 5% in the left or right ventricles. Most of the cases are sporadic. Some can be part of Carney’s complex, which is an autosomal dominant disease, associating abnormal pigmentation of the skin, endocrine hyperactivity (acromegaly, Cushing’s syndrome, testicular tumors) and myxoma (heart, skin or breast). Two thirds of the patients affected present with one or several cardiac myxomas. Some very specific features will suggest the diagnosis of Carney complex: multiple myxoma, atypical topography, recurrence after resection, younger age of onset and male gender [48, 49]. Most myxomas have a broad base of attachment, although a few have narrow pedicles that are characteristically attached to the interatrial septum. Table summarizing the radiological findings for myxomas: Age of discovery

Adult (mean age 50 years)

Clinical

Signs of obstruction, emboli, general signs; Carney complex in rare cases

Heart chamber

Left > right atrium

Tissue

Endocardium

Borders

Regular, broad base or pediculated

Extension

Inside the heart chamber

Calcifications

Possible

Density without contrast

Hypodense

T1 SE signal

Hyposignal or isosignal on myocardium

T2 SE signal

Hypersignal frequent

Mobility

Highly mobile mass that can prolapse into the ventricle

Uptake of contrast

Heterogeneous, sometimes difficult to obtain

Differential diagnosis

Thrombus

50

5  Benign Tumors

5.3  Papillary Fibroelastoma of the Mitral Valve Gwenaelle Pouliquen, Karine Warin-Fresse, and Dominique Crochet

Case Report A 72-year-old male was explored by echocardiography to assess the sudden onset of a sight disorder. The echocardiographic findings showed a small-sized mobile mass implanted close to the third segment of the posterior leaflet of the mitral valve. Surgery was indicated because of the risk of embolism. A cardiac MDCT was scheduled as part of the preoperative workup. Fig. 9  Cardiac MDCT with reconstruction performed after injection of contrast medium, in the four-chamber view (a), two-chamber view (b) and short axis view (c). A small-sized hypodense mass is visible (see arrows) attached by a pedicle to the surface endothelium of the left ventricle close to the posterior leaflet of the mitral valve

a

5.3  Papillary Fibroelastoma of the Mitral Valve Fig. 9  (continued)

51

b

c

Diagnosis The path lab findings confirmed the diagnosis as papillary fibroelastoma. It was difficult  to determine exactly where this mass was implanted because the pedicle was thin and in close contact with the valve endothelium and the surface of the heart chamber.

52

5  Benign Tumors

Background Papillary fibroelastoma is rare, accounting for only 10% of all the benign heart tumors. Some investigators believe that the incidence of papillary fibroelastoma is underestimated because the lesion is usually small, asymptomatic and therefore easily missed [47]. However it is the most frequent tumor involving the heart valves, affecting exclusively the endocardium. About 80–90% of papillary fibroelastoma are found on the endocardium of the aortic and mitral valves, followed by the tricuspid valves and the endocardium. One hypothesis is that an underlying endothelial lesion may explain why it is predominantly found on the heart valves (80%) [47]. Fibroelastoma affects mainly adults (mean age 60 years); the mass is generally very small and mobile, which explains why it is so difficult to characterize. Table summarizing the radiological findings for papillary fibroelastoma: Age of discovery

Adult

Clinical

Asymptomatic, systemic emboli

Size

Usually <15 mm

Heart chamber

Aortic or mitral valve

Developing on

Endocardium

Borders

Irregular

Extension

No

Calcifications

No

Density without contrast

–

T1 SE signal

–

T2 SE signal

–

Uptake of contrast

–

Differential diagnosis

Endocarditis

5.4  Intramyocardial Fibroma

53

5.4  Intramyocardial Fibroma Eric Stephan and Philippe Douek

Case Report A 9-year-old child, in good general health, was given a chest X-ray to investigate a cough. A bulge was noted on the left apex of his heart and an echocardiography examination was therefore prescribed. The echocardiographic findings showed a mass on the lateral wall of the left ventricle, but its apical extension was not clear. A CMR and a cardiac MDCT were performed to complete the exploration.

Diagnosis Intramyocardial fibroma. Fig. 10  CMR cine image, two-chamber view, showing a round-shaped mass depicted as a hyposignal arising from the apex of the LV

54 Fig. 11  On the fat-suppressed T1 image, the mass appears as a heterogeneous hyposignal

Fig. 12  CMR late enhancement image 10 min after gadolinium injection showing homogenous enhancement of the mass

5  Benign Tumors

5.4  Intramyocardial Fibroma Fig. 13  Cardiac MDCT, arterial phase acquisition, MPR reconstruction, two-chamber view. The examination shows that there are polymorphic calcifications inside the tumor

Fig. 14  Cardiac MDCT at the late enhancement phase (5 min after injection) with thick, two-chamber MPR reconstruction. The lesion is clearly enhanced, mainly around the edges

55

56

5  Benign Tumors

Background Fibroma is the second most frequent primary cardiac tumor and the most frequent in ­children after rhabdomyoma. Considered by some as a hamartoma rather than a true tumor it is sometimes known as a fibroelastic hamartoma because of its histology that includes mature fibroblasts, collagen fibers and a few elastic fibers. One third of all fibromas are diagnosed before the age of 1, and 15% are diagnosed in adults or adolescents. The mean age of discovery is 13  years. A fibroma can occur as an isolated lesion or as part of Gorlin’s syndrome or basal cell naevomatosis, which is an autosomic dominant hereditary disease with complete penetrance and variable expression. Forty percent of the mutations of the gene that causes the disease occur spontaneously. The disease associates developmental anomalies (odontogenic keratocysts, poroker­ atosis of the palms of the hands and soles of the feet, cardiac fibroma, ectopic intracranial calcifications) and a predisposition for some forms of cancer (basal cell carcinoma). It can sometimes be difficult to distinguish a fibroma from hypertrophic cardiomyopathy, but perfusion images and late enhancement images can be helpful to make the diagnosis [50]. Table summarizing the radiological findings in myocardial fibroma: Age of discovery

Childhood (mean age = 13 years)

Clinical

Arrhythmia, heart failure

Size

Large: 2–10 cm

Heart chamber

LV, RV

Developing on

Myocardium

Extension

In the myocardium

Borders

Regular, sometimes difficult to distinguish from normal myocardium

Calcifications

++

Density without contrast

Hypodense

T1 SE signal

Isosignal

T2 SE signal

Hyposignal

Uptake of contrast

Usually marked

Differential diagnosis

Hypertrophic cardiomyopathy

5.5  Coronary Fistula

57

5.5  Coronary Fistula Patrick Mailleux

Case Report A vascular mass developing in the right atrioventricular sulcus was discovered in a 72-yearold patient with no previous case history. A cardiac MDCT was performed to research the etiology of this mass.

Diagnosis Arteriovenous fistula between the circumflex artery and the coronary sinus.

Fig. 15  Cardiac MDCT after pulsed injection of contrast medium. The axial slice at the base of the heart chambers shows an aneurysm in the coronary sinus (arrowhead)

58

5  Benign Tumors

Fig. 16  Surface reconstruction of the root of the aorta and the coronary network: a large bulge is visible on the left coronary and circumflex arteries (arrowhead). The anterior interventricular artery is thin (arrow). The orifice of the fistula between the circumflex artery and the coronary sinus is visible on the reconstruction (open arrow)

Background These fistulae can also develop on the right ventricle. If they are large they can cause ­pulmonary artery hypertension. Table summarizing the radiological findings for arteriovenous fistulae: Age of discovery

Variable

Clinical

Asymptomatic, pulmonary hypertension

Developing on

Circumflex artery and coronary sinus or RV

Borders

Regular

Type

Vascular

Density without contrast

Hypodense

Uptake of contrast

Vascular

5.6  Intracardiac Venous Malformation (Formerly Hemangioma)

59

5.6  Intracardiac Venous Malformation (Formerly Hemangioma) Marianne Jolibert, Guillaume Louis, Arthur Varoquaux, Vincent Vidal, Jean Michel Bartoli, Jean-Yves Gaubert, Guy Moulin, and Alexis Jacquier

Case report A 55-year-old patient was referred to our department for a CMR to explore a mass discovered in the right atrium. The patient was asymptomatic and had no previous case history.

Diagnosis The findings concluded that the patient had a venous type vascular malformation.

Fig. 17  Cine image, short axis view. A large, round-shaped, clearly delineated mass is developing on the roof of the right atrium

60 Fig. 18  Perfusion image (SR flash) at an early stage (a), at a later stage (b) and on the short axis. The gradual uptake of the contrast medium is visible, spreading from the edges to the center of the lesion

5  Benign Tumors

a

b

5.6  Intracardiac Venous Malformation (Formerly Hemangioma)

61

Fig. 19  Late enhancement image (IR GRE), four­chamber view. The uptake of the contrast medium is visible and persists at a later stage. The uptake of the contrast is uneven and is more marked around the edges of the lesion and at its point of attachment in the heart tissue

Background These vascular malformations are benign lesions made up of vessels with a dysplastic architecture [51]. They are characterized by the type of vessel they arise from (artery, capillary, vein, lymph vessel, mixed) and by the velocity of the blood flow inside them (slow or fast). They are rarely found in the heart. Vascular malformations affecting the heart account for less than 2% of heart tumors. All age groups can be affected; the symptoms of these lesions are nonspecific. Vascular malformations are found in all three layers of the heart’s tissue (endocardium, myocardium or epicardium). Malformations that develop from the endocardium are usually of the capillary or mixed type (capillary and cavernous) and present as clearly delineated polypoid masses that develop inside the heart chamber. Intramyocardial malformations are less  clearly circumscribed and can contain fatty or fibrous tissue. Epicardial vascular malformations are frequently associated with a bloodtainted effusion in the pericardium.

62

5  Benign Tumors

Table summarizing the radiological findings for vascular malformations: Age of discovery

Any

Clinical

Asymptomatic, nonspecific

Developing on

All the heart tunics

Type

Artery, vein, capillary, lymph vessel, mixed, slow and fast flows

Borders

Regular

Extension

No

Calcifications

Possible if venous

Density without contrast

Hypodense

T1 SE signal

Variable

T2 SE signal

Variable

Uptake of contrast

Variable

5.7  Lipoma

63

5.7  Lipoma Mathieu Rodiere and Frederic Thony

Case Report A 64-year-old patient was admitted to hospital in an emergency setting for sudden ­dyspnea. An angioscan of the pulmonary arteries confirmed the presence of bilateral pulmonary emboli suggested by the clinical data, revealing by chance a cardiac mass.

Diagnosis Cardiac lipoma.

Fig. 20  Non-gated CT scan performed after contrast injection showing a hypodense mass (−96 UH) measuring 19 mm on its long axis arising from the right ventricle (white star)

64 Fig. 21  CMR T1-weighted image. The mass appears as a hypersignal (white arrow heads)

Fig. 22  T1-weighted sequence, fat-suppressed image in the short axis showing that the signal inside the mass is nulled, thereby confirming that it contains fat (arrowheads)

5  Benign Tumors

65

5.7  Lipoma

Background Cardiac lipoma is a benign heart tumor that occurs relatively frequently, accounting for 8–12% of primary tumors of the heart and pericardium. It is often discovered by chance in adults and in most cases remains asymptomatic and does not require surgical treatment. Cardiac lipomas are located under the endocardium in half of the cases, under the epicardium in 25% of the cases and in the myocardium in another 25%. Lipomas located under the epicardium are generally larger in size and can impair cardiac function or have an adverse impact on the coronary network. Table summarizing the radiological presentation of cardiac lipoma: Age of discovery

Adult

Clinical

Asymptomatic

Heart chamber

All

Tissue

Subendocardial

Type

Fatty

Borders

Regular

Extension

No

Calcifications

No

Density without contrast

Hypodense

T1 SE signal

Fat signal

T2 SE signal

Fat signal

Uptake of contrast

No

Differential diagnoses

Fatty hypertrophy of the interatrial septum liposarcoma

66

5  Benign Tumors

5.8  Calcification of the Mitral Annulus Gwenaelle Pouliquen, Karine Warin-Fresse, and Dominique Crochet

Case Report A 67-year-old male in general good health, with no particular past history, consulted as an emergency in the ophthalmology department for sudden blindness in the left eye. He was diagnosed with thrombosis of the central artery of the retina. The echocardiogram revealed a cyst-like mass, located behind the annulus of the mitral valve in the atrioventricular groove. The patient’s lab tests were normal; his serum tested negative for hydatidosis. A CMR was performed. Fig. 23  T1-weighted fat-suppressed image, four-chamber view, showing a mass attached to the mitral annulus, picked up as an isosignal arising from the atrioventricular groove (arrows)

5.8  Calcification of the Mitral Annulus Fig. 24  T2-weighted fat-suppressed image, four-chamber view. The mass appears as a homogenous hypersignal

Fig. 25  Late enhancement image after contrast injection in the four­chamber view showing no enhancement inside the mass

67

68

5  Benign Tumors

Diagnosis The patient had surgery; the final results of the path lab findings confirmed the diagnosis of calcification of the mitral annulus.

Background Valve calcifications occur frequently, especially in elderly women and renal failure patients. They can affect the mitral valve or the aortic valve and show that the valve system is affected by a degenerative process. When they are located on the mitral valve these calcifications can sometimes be large, involving the three posterior segments of the valve. On imaging studies the picture will be specific to the age of the lesion. At an early stage of the disease the picture usually presents as a calcified mass located on the mitral annulus. The lesion is hypoechoic with a cone-shaped shadow in the background on the ultrasound findings, very dense on the MDCT and sends out a hyposignal on all the CMR sequences. At a later stage the center of the lesion appears as a hypodense area with a calcified shell on the MDCT. This stage of the lesion is called necrotic liquefaction of a mitral annulus calcification. Table summarizing the radiological findings for mitral annulus calcification: Age of discovery

Elderly subjects

Clinical

Asymptomatic, mitral insufficiency in many cases

Tissue

Mitral annulus

Type

Variable ranging from calcified tissue to a thick, yellowish fluid

Extension

Mitral annulus

Calcifications

Central initially and peripheral in the necrotic stage

T1 SE signal

Hyposignal

T2 SE signal

Hyposignal

Uptake of contrast

The contrast does not spread readily throughout the lesion

5.9  Cardiac Paraganglioma

69

5.9  Cardiac Paraganglioma Antoine Micheau, Sébastien Bommart, Claudine Bousquet, and Hélène Vernhet Kovacsik

Case Report An asymptomatic patient, age 67 years, was referred to our department for a cardiac lesion discovered on a routine echocardiography examination. He was explored by cardiac-gated MDCT and CMR.

Diagnosis The lesion was surgically removed and the path lab findings concluded that it was a paraganglioma located in the pericardium. Fig. 26  Cardiac MDCT, four-chamber view, showing a round-shaped mass arising from the interatrial sulcus behind the right atrium. The lesion is highly vascularized and unevenly enhanced

70 Fig. 27  SSFP cine image, end-diastolic phase, four-chamber view showing a mass picked up as a heterogeneous signal

Fig. 28  T1-weighted image, the mass appears as an isosignal in comparison to the myocardial muscle

5  Benign Tumors

5.9  Cardiac Paraganglioma Fig. 29  T2-weighted fat-suppressed image: the lesion appears as a marked hypersignal

Fig. 30  First pass perfusion image during gadolinium injection. The lesion is highly vascularized and picks up the contrast medium rapidly and clearly

71

72

5  Benign Tumors

Fig. 31  Late enhancement image 10 min after gadolinium injection showing substantial uptake of the contrast medium

Background A paraganglioma is a tumor that develops from the neuroectodermally derived paraganglionic cells that are dispersed along the autonomic ganglia. A distinction is usually made between non-secreting paraganglioma, sometimes known as chemodectoma and secreting paraganglioma, which occur more frequently and are known as pheochromocytoma. Cardiac paraganglioma is extremely rare (less than 50 cases have been described in the English-language literature). In most cases they are benign tumors, which explains why they are covered in this chapter, but some rare cases of invasive forms with metastases (lymph nodes, bones and viscera) have been described. Most of the cases of paraganglioma described in the literature affect adults aged 15–85, the mean age being around 40. Ten to 20% of secreting paraganglioma belong to an inherited family disorder; type 2 multiple endocrine neoplasia, Von Hippel–Lindau syndrome, type 1 neurofibromatosis or familial paraganglioma. In the latter case they are often multiple and tend to be recurrent. However, most cases remain sporadic.

73

5.9  Cardiac Paraganglioma

Table summarizing the radiological findings for paraganglioma: Age of discovery

Adult

Clinical: inconstant Calcifications

Headache, palpitations, sweating, paroxystic arterial hypertension No

Borders

Regular

Density without contrast

–

T1 SE signal

Hyposignal to isosignal

T2 SE signal

Clear hypersignal

Uptake of contrast

Intense, sometimes with central necrosis

Differential diagnosis

Sarcoma, lymphoma (usually the lymphoma is less vascularized)

74

5  Benign Tumors

5.10  Castelman’s Disease Archid Azarine, Suzana Castela, and Elie Mousseaux

Case Report A 59-year-old male was referred for CMR exploration of a dilatation of his ascending aorta. The findings showed a mass encompassing the anterior interventricular artery.

Fig. 32  Cine image, short axis view, showing an isolated mass growing around the interventricular artery

5.10  Castelman’s Disease Fig. 33  T2-weighted image: the mass appears as a discrete, round, clearly delineated hypersignal

Fig. 34  Late enhancement image after injection of contrast medium. The mass shows moderate uptake of the contrast medium

75

76

5  Benign Tumors

Diagnosis The patient had surgical resection of the lesion and a bypass. On the path lab findings we diagnosed an inflammatory tumor related to Castelman’s disease.

Background Castelman’s disease is a complex lymphoproliferative syndrome that can present with disseminated or circumscribed lesions, as in this patient. The patient was seen again a year later with no recurrence of the lesion. Table summarizing the radiological findings for Castelman’s disease: Heart chambers

All

Calcifications

No

Density without contrast

–

T1 SE signal

Hyposignal to isosignal

T2 SE signal

Hypersignal

Uptake of contrast

Moderate

Differential diagnosis

Lymphoma

5.11  Neurofibromatosis Involving the Pericardium

77

5.11  Neurofibromatosis Involving the Pericardium Jean-Yves Gaubert, Philippe Dory-Lautrec, Guillaume Louis, and Alexis Jacquier

Case Report A 42-year-old patient treated for Recklinghausen syndrome was admitted to hospital with dyspnea that was gradually becoming worse. The workup showed that she had a pericardial effusion that had substantially increased over the 15-day period she had been in hospital. A cardiac MDCT was prescribed to explore the pericardial effusion. Fig. 35  Cardiac MDCT, arterial phase acquisition, axial view (a) and coronal view (b). A substantial quantity of pericardial effusion is present and is slightly heterogenous

a

b

78 Fig. 36  Cardiac MDCT, late tissular phase acquisition 5 min after contrast acquisition axial view (a) and coronal view (b) showing a peripherally enhanced mass with a serpiginous border arising from the pericardium

5  Benign Tumors

a

b

Diagnosis The patient had surgery to treat her pericardial lesion. The histological slides of the surgical specimen confirmed the diagnosis of neurofibroma.

79

5.11  Neurofibromatosis Involving the Pericardium

Background Lesions of this type are rare in the pericardium and it was the patient’s background of Recklinghausen’s disease that suggested the diagnosis in this case. The case report shows how essential it is to make late acquisitions on a cardiac MDCT when a pericardial or cardiac mass is suspected. Table summarizing the radiological findings for neurofibroma involving the pericardium: Layer involved

Pericardium

Calcifications

No

Density without contrast

Between 30 and 40 HU

T1 SE signal

Heterogeneous isosignal

T2 SE signal

Heterogeneous hypersignal

Uptake of contrast

Substantially heterogeneous

Differential diagnosis

Lymphoma, neurofibrosarcoma

80

5  Benign Tumors

5.12  Erdheim–Chester’s Disease with Mediastinal Involvement Arthur Varoquaux, Vincent Vidal, Jean Michel Bartoli, and Alexis Jacquier

Case Report A patient age 32 years was admitted to hospital in an emergency setting for spinal cord compression. Her spinal cord had been compressed by epidural infiltration of an invasive process that had spread through the intervertebral foramina. After decompression surgery the patient had a cardiac MDCT and a CMR examination.

Diagnosis The final diagnosis made on the basis of the histological findings from the surgical specimen was Erdheim–Chester’s disease. Fig. 37  Cardiac MDCT performed after pulsed iodine injection, axial view at the origin of the coronary vessels. A thickening process is visible around the aorta and the coronary arteries causing extrinsic stenosis of the coronary vessels. The descending aorta is also thickened

5.12  Erdheim–Chester’s Disease with Mediastinal Involvement

81

Fig. 38  Cardiac MDCT, MPR reconstruction in the parasagittal plane: the perivascular structures are thickened along the whole thoracic aorta

Background Erdheim–Chester disease is a rare, non-Langerhans cell form of histiocytosis of unknown origin. It is characterized by xanthomatous or xanthogranulomatous infiltration of tissues by spumous histiocytes. Erdheim–Chester disease is characterized by heterogeneous systemic signs and symptoms: bone pain, diabetes insipidus, exophthalmia and can even include central signs. The cardiovascular form can affect the periaortic tissue causing periaortic thickening also affecting all the other layers of heart tissue and causing one third of the deaths [52]. Erdheim–Chester disease is diagnosed on the basis of an association of pathological features – (1) lab findings: the presence of foamy histiocytes inside a granuloma, combined with fibrosis and CD 68 histiocyte proliferation; (2) radiological data: bilateral, symmetrical osteosclerosis affecting the metaphyses and diaphysis of the long bones and/or a hypersignal picked up in the osteosclerotic areas on the technetium99-labeled bone scan. Table summarizing the radiological findings in Erdheim–Chester disease: Age of discovery

Adult

Heart chamber

All, mediastinum, aorta

Type

Histiocyte and fibrosis

Borders

Regular

Extension

Parietal arterial thickening

Density without contrast

Hypodense

T1 SE signal

Isosignal

T2 SE signal

Isosignal or hypersignal

Uptake of contrast

Yes

Differential diagnoses

Inflammatory aortitis, lymphoma

82

5  Benign Tumors

5.13  Ante and Postnatal Bronchogenic Cyst Katia Chaumoitre and Michel Panuel

Case Report A fetal ultrasound image in the third trimester showed a mediastinal mass close to a fetus’s heart. Fig. 39  Fetal ultrasound, axial slice through the heart chambers. A clearly delineated round, hypoechoic mass can be seen (arrow) located under the tracheal bifurcation of the right and left bronchial trunks (arrowhead)

5.13  Ante and Postnatal Bronchogenic Cyst Fig. 40  Antenatal MRI, sagittal T2-weighted image (Haste). The mass appears as a hypersignal with clear borders (arrow). It is located under the trachea and its bifurcation (arrowhead)

Fig. 41  Contrast-enhanced CT image acquired a few days after birth showing a round, clearly delineated mass with a liquid density

83

84

5  Benign Tumors

Conclusion The diagnosis of bronchogenic cyst was confirmed by the histological analysis of the surgical specimen.

Background It is difficult to make a differential diagnosis between an esophageal duplication cyst, bronchogenic cyst and pericardial cyst. The anatomical location may be helpful to differentiate between these three diagnoses. There is frequently still some doubt between the three even when the histological analysis results are available. Table summarizing the findings for ante- or postnatal bronchogenic cyst: Age of discovery

Before or after birth

Heart chamber

Posterior mediastinal paracardiac mass

Type

Cyst lined with GI endothelium

Borders

Regular

Density

Liquid

T1 SE signal

Hyposignal

T2 SE signal

Hypersignal

Uptake of contrast

No

Differential diagnosis

GI duplication

5.14  Esophageal Duplication

85

5.14  Esophageal Duplication Katia Chaumoitre and Michel Panuel

Case Report Fetal ultrasound image in the third trimester showing a mediastinal mass developing behind the fetus’s heart.

Diagnosis The diagnosis of esophageal duplication was confirmed by the histological analysis of the surgical specimen.

Fig. 42  Fast T2-weighted MR image in the axial plane showing a thin-walled, fluid-filled mass developing behind the aorta and the heart chambers

86

5  Benign Tumors

Table summarizing the radiological findings for esophageal duplication: Age of discovery

Ante- or postnatal

Heart chamber

Posterior mediastinal paracardiac mass

Type

Cyst lined with GI endothelium

Borders

Regular

Density without contrast

Liquid

Signal T1 SE

Hyposignal

Signal T2 SE

Hypersignal

Uptake of contrast

No

Differential diagnosis

Bronchogenic cyst

5.15  Ante and Postnatal Rhabdomyoma

87

5.15  Ante and Postnatal Rhabdomyoma Guillaume Gorincour, Alain Potier, Beatrice Guidicelli, and Nicole Philip

Case Report Several left ventricular cardiac masses were discovered on a fetal ultrasound examination performed at 32 weeks of gestation.

Diagnosis These lesions suggest a cardiac rhabdomyoma associated with tuberous sclerosis.

Fig. 43  Antenatal ultrasound in the four-chamber view showing several heterogeneous hyperechoic masses located on the lateral wall of the left ventricle, the septum and the upper part of the right ventricle (arrows)

88

5  Benign Tumors

Fig. 44  Antenatal T1-weighted MR image shows two masses picked up as a hypersignal on the lateral part of the left ventricle wall (arrows)

Background Rhabdomyoma is the most frequent heart tumor in children, usually developing at an early stage of fetal life; it grows in utero and can often be multiple [53, 54]. After birth over half of these tumors regress spontaneously, leaving a fatty scar. Rhabdomyoma can occur as an isolated lesion, but in 50% of the cases it is associated with tuberous sclerosis. Tuberous sclerosis is a disease with high penetrance that is inherited via a dominant autosomal pattern and can be expressed in different ways in the same family. The cutaneous signs often suggest the diagnosis: achromic patches, facial angiofibroma, and Koenen’s periungueal tumors. It can also be useful to look for cysts and renal angiomyolipoma, astrocytoma of the retina and aortic aneurysms. An antenatal diagnosis can be made on the obstetrical ultrasound findings. Over 50% of the cases are diagnosed before the age of 1, the mean age of diagnosis is around 18 months. Early diagnosis is not correlated with a higher incidence of heart complications.

89

5.15  Ante and Postnatal Rhabdomyoma

Table summarizing the radiological findings for rhabdomyoma: Age of discovery

Before birth or newborn infant

Clinical

Bourneville’s tuberous sclerosis

Number

Multiple

Size

1 mm to 10 cm

Heart chamber

All

Tissue

Myocardium

Extension

No

Calcifications

No

Density without contrast

Hyperdense

T1 SE signal

Isosignal to hypersignal

T2 SE signal

Isosignal

Uptake of contrast

Minimal

Differential diagnosis

Fibroma

90

5  Benign Tumors

5.16  Ante and Postnatal Teratoma Guillaume Gorincour, Alain Potier, Marianne Capelle, and Bernard Kreitmann

Case Report A mediastinal mass was discovered on a fetal ultrasound examination performed at 33 weeks gestational age.

Diagnosis The diagnosis of teratoma was confirmed by the histological findings.

Fig. 45  Fetal ultrasound in the oblique coronal plane showing a large mass developing close to the heart chambers (white arrow head). The mass is located high in the mediastinum (black arrows) with tissue-like components and several cystic formations. There are also signs of pericardial effusion. The two possible diagnoses suggested by these findings are teratoma and cystic lymphangioma. The presence of pericardial effusion is suggestive of teratoma

5.16  Ante and Postnatal Teratoma Fig. 46  Antenatal MR coronal image showing a lesion in the upper part of the mediastinum, close to the heart chambers. This mass is made up of tissue-like components and several fluid-filled formations (arrow)

Fig. 47  The postnatal MR image show a mass with the same characteristics (arrow)

91

92

5  Benign Tumors

Background Pericardial teratoma is a benign tumor that is frequent in infancy. It accounts for 2% of the primary heart tumors in children. In exceptional cases a teratoma can be locally immature and malignant. In most cases pericardial teratoma are discovered in infancy. The number of cases discovered has increased with the routine use of obstetrical ultrasound examinations. A few rare cases of teratoma in adults have been reported in the literature [55]. Table summarizing the radiological findings for teratoma: Age of discovery

Ante or postnatal

Clinical

Tamponade

Heart chamber

Right

Type

Complex

Borders

Irregular/indented

Extension

No

Calcifications

+++ (teeth)

Density without contrast

–

T1 SE signal

Heterogeneous

T2 SE signal

Multicystic appearance

Uptake of contrast

Yes

Differential diagnosis

Cystic lymphangioma

Infectious Lesions

6

Contents 6.1  C  ardiac Hydatidosis............................................................................................ 94 Flavie Bratan and Vivien Thomson 6.2  P  seudotumoral Endocarditis.............................................................................. 97 Franck Thuny, Philippe Dory-Lautrec, Gilbert Habib, Jean-Yves Gaubert, Guy Moulin, and Alexis Jacquier 6.3  C  ardiac Actinomycosis........................................................................................ 99 Jean-Yves Gaubert, Philippe Dory-Lautrec, Katia Chaumoitre, Vincent Vidal, Jean Michel Bartoli, Guy Moulin, Michel Panuel, and Alexis Jacquier

A. Jacquier, CMR and MDCT in Cardiac Masses, DOI: 10.1007/978-3-642-18457-4_6, © Springer-Verlag Berlin Heidelberg 2011

93

94

6  Infectious Lesions

6.1  Cardiac Hydatidosis Flavie Bratan and Vivien Thomson

Case Report A 55-year-old patient from North Africa had been suffering from various symptoms including dyspnea, chronic coughing and chest pain. She had a plain X-ray that showed several pulmonary nodules and was therefore given a CT scan, which revealed a number of walled, cyst-like lesions, scattered in her right lung, mediastinum, heart, liver and ­retroperitoneum, invading the superior vena cava and compressing it.

Diagnosis Hydatidosis, echinococcus granulosus infection, was confirmed by blood tests.

Fig. 1  CMR, True Fisp short-axis cine image at end diastole (a) and end systole (b) showing a septated cystic mass developing on the right ventricle infundibulum (arrows). Two other septated cystic masses are also visible in the liver, extending toward the inferior vena cava (arrowheads)

a

95

6.1  Cardiac Hydatidosis Fig. 1  (continued)

Fig. 2  CMR, T2-weighted images showing a clear hypersignal inside the masses

b

96

6  Infectious Lesions

Fig. 3  First-pass perfusion images after gadolinium chelate injection showing no enhancement inside the lesion

Background The standard treatment for cardiac hydatidosis is surgery as early as possible even if there is a high risk of the cyst rupturing inside the heart chamber. Because this patient had a disseminated form and was in a poor state of health, we simply decided to treat her with Albendazole. After 2 years of treatment the patient had no further cardiac symptoms, the cyst-like lesions seemed stable on the various examinations she was given and her lab tests were negative. In the patient’s right heart chambers the lesions tended to expand inside the chamber and the endocardium, whereas in the left heart chambers the cysts expanded in the epicardium, the myocardium being thicker and denser. Table summarizing the radiological findings for cardiac hydatidosis: Clinical

Variable, compression of chambers, emboli

Heart chamber

All

Type

Variable, ranging from cyst to tissue-like lesion

Borders

Regular

Calcifications

Possible

Density without contrast

Variable according to the age of the lesion

T1 SE signal

Cyst-like, pseudo-tissue or mixed

T2 SE signal

Cyst-like, pseudo-tissue or mixed

Uptake of contrast

No

Differential diagnosis

6.2  Pseudotumoral Endocarditis

97

6.2  Pseudotumoral Endocarditis Franck Thuny, Philippe Dory-Lautrec, Gilbert Habib, Jean-Yves Gaubert, Guy Moulin, and Alexis Jacquier

Case Report A 32-year-old HIV + male was admitted to hospital for severe sepsis with heart failure. A heterogeneous mass was visible on the echocardiographic examination, developing between the tricuspid valve and the infundibulum of the pulmonary artery. The patient was referred in our department for CMR.

Diagnosis Pseudotumoral endocarditis was diagnosed on the basis of the histology and bacterial ­culture of the biopsies taken from the lesions.

Fig. 4  Cine image, ­four-chamber view showing a broad-based mass (arrowhead) d­ eveloping on the free wall of the RV. Another smaller mass is visible in the upper part of the right atrium (arrow). The patient also has bilateral pleural effusion

98

6  Infectious Lesions

Fig. 5  Late enhancement image 10 min after injection of contrast medium showing heterogeneous enhancement of the mass, with a non-enhanced portion in each affected area

Background As a general rule vegetations are difficult to pick up on CMR because they are small in size and highly mobile. Endocardial and valvular vegetations can present as bulky cardiac masses, especially in patients with compromised immune systems. These anomalies are rare and only a few cases have been described in the literature. Table summarizing the radiological findings in pseudotumoral endocarditis: Age of discovery

Adult

Clinical

Endocarditis

Number

Multiple

Extension

Possible in the valve annuli

Calcifications

No

Density without contrast

–

T1 SE signal

–

T2 SE signal

–

Uptake of contrast

Yes

Differential diagnosis

Thrombus, metastasis inside heart chamber

6.3  Cardiac Actinomycosis

99

6.3  Cardiac Actinomycosis Jean-Yves Gaubert, Philippe Dory-Lautrec, Katia Chaumoitre, Vincent Vidal, Jean Michel Bartoli, Guy Moulin, Michel Panuel, and Alexis Jacquier

Case Report A 54-year-old immigrant male presented with fever, dyspnea and recent weight loss. His chest X-ray revealed a diseased area in the upper part of his right lung. The echocardiographic examination revealed a mobile mass on the posterior wall of the right atrium.

Diagnosis Mediastinal actinomycosis with cardiac involvement was diagnosed on the basis of the findings of the transbronchial biopsy of the pulmonary lesion. Fig. 6  Cine image, ­four-chamber view showing a mass arising from the posterior wall of both atria and the interatrial septum (white arrowhead). A mass developing on a pedicle attached to the interatrial septum can be seen protruding into the right atrium (black arrowhead)

100

6  Infectious Lesions

Fig. 7  Late enhancement MR image showing heterogeneous enhancement of the lesion involving the atrium; the thrombus in the right atrium does not pick up the contrast medium

Background Actinomycosis is a chronic infection featuring the formation of pus and fibrosis. It affects the deeper tissues of the face, the chest and the central nervous system. It is caused by an anaerobic Gram + bacillus of the actinomycosis species. Table summarizing the radiological findings for cardiac actinomycosis: Age of discovery

Adult

Clinical

Subacute or acute infectious syndrome

Localization

Multiple, pulmonary, mediastinal, cardiac

Calcifications

No

Density without contrast

Isosignal

Signal T1 SE

Isosignal

Signal T2 SE

Heterogeneous

Uptake of contrast

Yes, heterogeneous

Differential diagnosis

Lymphoma, tuberculosis

Malignant Tumors

7

Contents 7.1  M  etastasis Inside the Heart Chamber................................................................ 103 Flavie Bratan and Vivien Thomson 7.2  M  yocardial Metastasis of Bronchial Tumor...................................................... 105 Armelle Renaud, Maxime Lalisse, Trung Le-Thanh, Stéphanie Lemaire, Marie-Aurélie Delesalle, Jean Paul Beregi, and Christophe Lions 7.3  R  ight Ventricular Metastasis of a Hepatocellular Carcinoma......................... 107 Aurélie Chabrol, Brahim Harbaoui, and Vivien Thomson 7.4  P  ericardial Metastasis......................................................................................... 109 Flavie Bratan and Vivien Thomson 7.5  L  ymphoma Inside the Heart Chamber.............................................................. 113 Julie Mayer, Valérie Chabbert, and Hervé Rousseau 7.6  L  ymphoma Developing in the Epicardial Space............................................... 116 Antonin Flavian, Jean Michel Bartoli, Jean-Yves Gaubert, Guy Moulin, and Alexis Jacquier 7.7  L  arge Cell Lymphoma Involving the Pericardium........................................... 119 Laurence Monnier-Cholley and Lionel Arrivé 7.8  U  ndifferentiated Sarcoma Inside the Heart Chamber..................................... 122 Julie Mayer, Valérie Chabbert, and Hervé Rousseau 7.9  F  ibrosarcoma........................................................................................................ 125 Hend Belhiba, Jerome Caudron, Jeannette Fares, and Jean Nicolas Dacher

A. Jacquier, CMR and MDCT in Cardiac Masses, DOI: 10.1007/978-3-642-18457-4_7, © Springer-Verlag Berlin Heidelberg 2011

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7.10  A  ngiosarcoma of the Left Atrium.................................................................... 128 Eric Stephan and Philippe Douek 7.11  A  ngiosarcoma Developing Outside the Heart Chambers............................... 129 Olivier Monnet, Jean Michel Bartoli, Jean-Yves Gaubert, Guy Moulin, and Alexis Jacquier

7.1  Metastasis Inside the Heart Chamber

103

7.1  Metastasis Inside the Heart Chamber Flavie Bratan and Vivien Thomson

Case Report A 77-year-old male, under surveillance for a melanoma that had been surgically removed in July 2003, had a routine ultrasound examination in March 2008 revealing a mobile mass in the right atrium. A complete CMR and cardiac MDCT exploration was performed to complete the patient’s workup before surgery.

Diagnosis The path lab analysis of the surgical specimen confirmed that the tumor in the right atrium was an intracardiac metastasis of malignant melanoma with parietal neoplastic emboli. Malignant melanoma is the tumor that sends metastases to the heart the most frequently (46% of the cases according to autopsy data), mainly via the blood stream through the coronary arteries or the inferior vena cava. These metastases are often ubiquitous and usually invade the myocardium of the heart chambers. Fig. 1  Thoracic CT scan, axial view, after injection of iodine-based contrast medium showing a mass filling the right atrium

104 Fig. 2  Cardiac MDCT, two-chamber view of the right ventricle, showing a hypodense, multilobular mass hanging from the roof of the right atrium that has not prolapsed into the right ventricle

Fig. 3  CMR, cine image, four-chamber view, showing a tumor depicted as a hyposignal

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7.2  Myocardial Metastasis of Bronchial Tumor

105

7.2  Myocardial Metastasis of Bronchial Tumor Armelle Renaud, Maxime Lalisse, Trung Le-Thanh, Stéphanie Lemaire, Marie-Aurélie Delesalle, Jean Paul Beregi, and Christophe Lions

Case Report A 65-year-old male who was a tobacco user was referred to our department for the ­radiological exploration of a pulmonary mass discovered on a routine chest X-ray. The injected thoracic CT scan confirmed the mass in the pulmonary parenchyma and also revealed a mass developing in the left ventricle. A CMR was performed to complete the exploration.

Diagnosis Myocardial metastasis of a bronchial tumor. Fig. 4  Thoracic CT scan without cardiac gating, mediastinal window 1 min after injection of contrast medium. There is a hypodense mass infiltrating the lateral wall of the myocardium at the apex of the left ventricle (arrows). No pericardial effusion can be seen

106 Fig. 5  CMR, T1-weighted turbo spin-echo image with black blood pulse, short axis view. A mass is depicted as a hypersignal, infiltrating the anterolateral wall of the left ventricle

Fig. 6  CMR, late enhancement image performed 5 min after gadolinium injection. There is a central area of necrosis inside the myocardial mass and peripheral uptake of the contrast medium. The mass and the pulmonary parenchyma have the same characteristics (arrows)

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7.3  Right Ventricular Metastasis of a Hepatocellular Carcinoma

107

7.3  Right Ventricular Metastasis of a Hepatocellular Carcinoma Aurélie Chabrol, Brahim Harbaoui, and Vivien Thomson

Case Report A 79-year-old male presented with subacute right heart failure on a local picture of hepatocellular carcinoma. Initially pulmonary embolism was suspected but was not confirmed by the thoracic angioscan on which there were a number of artifacts. An echocardiographic examination revealed a right ventricular mass associated with pericardial effusion. The patient was given a CMR. Fig. 7  CMR, cine image, four-chamber view showing a mass developing in the right ventricular chamber (3 × 5 cm) involving both the heart chamber and the epicardial space. The patient has a substantial amount of pericardial and pleural effusion

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Fig. 8  CMR, perfusion image in the short axis after gadolinium injection. The contrast is picked up heterogeneously from the borders of the lesion to the center

Diagnosis The diagnosis was right ventricular metastasis of a hepatocellular carcinoma. These metastases spread directly by intravascular extension. This mechanism seems the most probable in this patient who had tumoral thrombosis of a suprahepatic vessel when he presented for his previous abdominal ultrasound check-up. Other malignant tumors (kidney, adrenal glands) can also spread to the heart in the same way via the inferior vena cava.

7.4  Pericardial Metastasis

109

7.4  Pericardial Metastasis Flavie Bratan and Vivien Thomson

Case Report A 55-year-old female was under regular radiological surveillance for a scapular melanoma that had been surgically removed in 1997, with pulmonary metastases treated by lobectomy and chemotherapy in 2005. A thoracic CT scan performed in June 2007 revealed a mass behind her heart to the left, although the patient was completely asymptomatic. Her left ventricular function was normal.

Diagnosis The diagnosis was intrapericardial metastasis of malignant melanoma. The patient died shortly after diagnosis. Metastases involving the heart and pericardium are far more Fig. 9  Thoracic CT scan after injection of contrast medium. A mass (arrow) is developing under and behind the left atrium (arrowhead). The mass is heterogeneously enhanced after injection and the left atrium is pushed upward

110 Fig. 10  Cardiac MDCT, sagittal reconstruction. The mass is developing from the lower aspect of the pericardium

Fig. 11  CMR, cine two­chamber view showing a 5-cm mass developing from the pericardium and spreading forward. The mass is picked up as an isosignal

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7.4  Pericardial Metastasis Fig. 12  CMR, T2-weighted image. The mass is clearly depicted as a hypersignal

Fig. 13  CMR, late enhancement image, the edges of the lesion are strongly enhanced

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f­ requent than primary heart tumors and the prognosis is often very poor because they are usually connected to end-stage cancer. Only 10% of the patients present with symptoms, 90% of which are due to pericardial involvement and 10% to involvement of the myocardium or heart chambers.

General Background on Cardiac Metastasis Metastases to the heart are 20–40 times more frequent than primary heart tumors [56, 57]. Several autopsy series in cancer patients show that metastases develop in the heart in 10–12% of the cases [56–58]. The primary malignancies that spread to the heart the most frequently are lung cancer, hematological tumors (lymphoma, leukemia), breast cancer, esophagus cancer and melanoma. The heart and pericardium can be invaded by local extension, through the blood stream, the lymph nodes or by venous extension (inferior vena cava or pulmonary veins). The patients often have pericardial effusion although it is not necessarily of the neoplastic type. This can be caused by idiopathic pericarditis induced by chemotherapy (doxorubicin, cyclophosphamide) or consecutive to radiotherapy. All the lymph that circulates through the heart drains through a lymph node at the root of the aorta and the invasion of this lymph node can also cause pericardial effusion. Table summarizing the radiological findings for cardiac metastases: Age of discovery

Adult

Clinical

Variable

Number

Multiple

Size

Variable

Heart chamber

All the chambers

Tissue

Pericardium, myocardium

Borders

Irregular

Extension

Yes

Calcifications

–

Density without contrast

Variable

T1 SE signal

Hyposignal

T2 SE signal

Hypersignal

Uptake of contrast

+++

Differential diagnosis

7.5  Lymphoma Inside the Heart Chamber

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7.5  Lymphoma Inside the Heart Chamber Julie Mayer, Valérie Chabbert, and Hervé Rousseau

Case Report A patient age 60 years was referred to our department for CMR exploration of a superior vena cava syndrome.

Diagnosis Type B large cell lymphoma.

Fig. 14  Cine image, four-chamber view showing a mass filling the right atrium and infiltrating the interatrial septum and the left atrium. A pericardial effusion is visible

114 Fig. 15  Cine image two­chamber views of the right ventricle showing the extension of the mass in the superior vena cava

Fig. 16  T2-weighted image. The mass is picked up as a homogenous hypersignal

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7.5  Lymphoma Inside the Heart Chamber Fig. 17  Shows the ventriculogram performed to locate the lesion. The right atrium has been filled by the bulky mass growing in the posterior aspect of the upper part of the right atrium

Fig. 18  Percutaneous fluoroscopy-guided biopsy of the mass

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7.6  Lymphoma Developing in the Epicardial Space Antonin Flavian, Jean Michel Bartoli, Jean-Yves Gaubert, Guy Moulin, and Alexis Jacquier

Case Report A 65-year old male was admitted to hospital to be assessed for rapidly progressing dyspnea. His echocardiographic exploration revealed the presence of a right cardiac mass and bilateral masses on the adrenal glands. He was explored by CMR to complete the assessment.

Diagnosis Type B lymphoma. Fig. 19  Cine image, four-chamber view. The mass is developing around the right coronary artery in the atrioventricular groove. It is compressing the right heart chambers. There is a substantial amount of fluid collecting around the pericardium

7.6  Lymphoma Developing in the Epicardial Space Fig. 20  Cine image short axis view. The progression of the mass follows the right coronary artery in the atrioventricular groove. The orifice of the tricuspid valve has shrunk (star)

Fig. 21  First pass perfusion image with gadolinium injection. The lesion is slightly enhanced

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118 Fig. 22  Late enhancement image. The lesion is homogeneously enhanced with no areas of necrosis

Fig. 23  T1-weighted gradient echo after gadolinium injection in the upper part of the abdomen showing the presence of a mass located on each of the adrenal glands. These lesions are enhanced, have regular borders and no central necrosis

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7.7  Large Cell Lymphoma Involving the Pericardium

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7.7  Large Cell Lymphoma Involving the Pericardium Laurence Monnier-Cholley and Lionel Arrivé

Case Report An HIV positive patient, age 50 years, with a severely compromised immune system (15 CD4/mm3) was admitted to hospital in a very poor state of health. Upon palpation the clinical examination revealed numerous enlarged superficial lymph nodes; a CT scan was performed to research deep enlarged lymph nodes.

Diagnosis There are several masses in all, one of which is located on the pericardium. The diagnosis was made by transesophageal biopsy and the lesion was a lymphoma located on the pericardium. Fig. 24  Cardiac MDCT, slice in the plane of the pulmonary artery revealing an anterior pericardial mass of the same density as the surrounding tissues located between the ascending aorta and the trunk of the pulmonary artery; its footprint is visible on the pulmonary artery

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General Background on Lymphomas Complete clinical and radiological staging will distinguish primary cardiac lymphoma from cardiac involvement in generalized lymphoma [47]. Primary cardiac lymphoma is a rare entity, defined by (1) the absence of lymphoma outside the pericardial sac after a complete autopsy examination and (2) the bulk of the neoplasm is confined to the pericardium Fig. 25  Cardiac MDCT, slice in the plane of the heart chambers. A small mass can be seen behind the heart against the inferior vena cava and the esophagus (arrow)

Fig. 26  Cardiac MDCT, slice in the plane of the heart chambers. There is also a small mass in front of the right atrium (arrow)

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7.7  Large Cell Lymphoma Involving the Pericardium Fig. 27  CMR black blood image, axial slice on the level of the pulmonary artery. The anterior pericardial mass can be seen compressing the ascending thoracic aorta and the trunk of the pulmonary artery

or the patient has cardiac symptoms from lymphomatous cardiac infiltration at the time of the initial diagnosis. Primary cardiac lymphoma affects adults, with a slight predominance in males (3 males for 2 females). Cardiac metastases of extra-cardiac forms of lymphoma that have spread are far more frequent (16–28% of the patients with lymphoma have ­associated cardiac involvement). The prevalence of cardiac lymphoma is higher in immunocompromised patients and in particular those who have AIDS and who have had a transplantation procedure. However, immunocompetent patients can also be affected. Table summarizing the radiological findings for lymphoma: Age of discovery

Adult

Clinical

Variable

Heart chamber

All

Borders

Clearly delineated

Extension

Yes

Calcifications

No

Density without contrast

–

T1 SE signal

Isosignal

T2 SE signal

Isosignal

Uptake of contrast

In general little but homogenous

Differential diagnosis

Other malignant tumors

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7.8  Undifferentiated Sarcoma Inside the Heart Chamber Julie Mayer, Valérie Chabbert, and Hervé Rousseau

Case Report A male patient, age 38, with no previous case history was explored by ultrasound for superior vena cava syndrome, revealing a mass in his right atrium. He had a CMR to complete the exploration.

Diagnosis The lesion was completely resected; the tumor was invading the floor of the RA and ­progressing toward the interatrial septum, the surrounding epicardial fat and a small ­portion of the inferior vena cava. The path lab tests on the surgical specimen revealed a high-grade malignant pleomorphic sarcoma. Fig. 28  Cine image, four-chamber view showing a mass depicted as an isosignal in relation to the myocardium entirely filling the right atrium. The mass is polylobular, measuring 5 cm along its longest axis with clear borders and does not seem to be invading the structures outside the heart

7.8  Undifferentiated Sarcoma Inside the Heart Chamber Fig. 29  Cine image, axial view showing the extension of the mass into the superior vena cava

Fig. 30  Four-chamber T1-weighted black blood image showing the mass as an isosignal compared to the myocardium

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Fig. 31  T2-weighted fat-suppressed image; the mass is visualized as a clear hypersignal. Note the pericardial fluid collection at the apex of the right ventricle”

Fig. 32  Late enhancement in short axis view image showing that the mass is strongly, evenly enhanced

Background Sarcomas without specific histological patterns, ultrastructural features or specific immunohistochemical findings are regarded as undifferentiated or unclassifiable and account for 0–24% of sarcomas. The mean age of presentation is 44 years with no predilection for either sex.

7.9  Fibrosarcoma

125

7.9  Fibrosarcoma Hend Belhiba, Jerome Caudron, Jeannette Fares, and Jean Nicolas Dacher

Case Report A 70-year-old patient came to consult for dyspnea. The ECG revealed atrial fibrillation although there were no abnormal findings on her chest X-ray. Her transthoracic echocardiogram showed a mass containing calcifications on the lateral wall of the left atrium (LA), extending to the mitral valve. The patient was explored by CMR and cardiac MDCT to support the diagnosis.

Fig. 33  The True Fisp image in the long axis of the left ventricle shows a sessile triple-lobed mass developing from the lesser mitral valve, infiltrating the posterior wall of the LA and the left superior vena cava. On the diastole the mass prolapses into the mitral valve

126 Fig. 34  T2-weighted black blood image showing an oval lesion sending out a heterogeneous T2 hyposignal

Fig. 35  Late enhancement image in the short axis view. The lesion shows heterogeneous late enhancement

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7.9  Fibrosarcoma

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Fig. 36  Cardiac MDCT, four-chamber view reconstruction, showing a mass of hypodense tissue containing small calcifications but no adipose layer of its own

Diagnosis The tumor was surgically removed and the patient’s mitral valve was replaced with a bioprosthetic graft. The tumor was infiltrating the wall of the left atrium and extending toward the left superior pulmonary vein. The immunohistochemical and pathology tests showed that the tumor was a fibrosarcoma.

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7.10  Angiosarcoma of the Left Atrium Eric Stephan and Philippe Douek

Case Report A 58-year-old female was admitted to hospital to be explored for asthenia and exercise dyspnea. She was given an echocardiographic examination, which diagnosed a mass developing in the left atrium. To complete the presurgical workup the patient had a cardiac MDCT.

Diagnosis Angiosarcoma. The clinical presentation and the patient’s age were suggestive of a ­malignant tumor. Surgical exeresis showed a solid tumor with necrotic and hemorrhagic components. Fig. 37  Cardiac MDCT late tissular phase acquisition, MPR reconstruction (5 mm) showing a mass filling the left atrium; it has several lobes, clear borders and is attached to the interatrial septum, prolapsing into the left ventricle

7.11  Angiosarcoma Developing Outside the Heart Chambers

129

7.11  Angiosarcoma Developing Outside the Heart Chambers Olivier Monnet, Jean Michel Bartoli, Jean-Yves Gaubert, Guy Moulin, and Alexis Jacquier

Case Report A male, age 68 years, was admitted to hospital to be explored for dyspnea and a poor state of general health. The ultrasound examination revealed a mass in his right heart. He was given a CMR to assess the mass and prepare a presurgical workup.

Diagnosis Cardiac angiosarcoma.

Fig. 38  SSFP four-chamber cine image. The mass is developing against the right atrium, the atrioventricular groove and the lateral aspect of the base of the right ventricle. It is pushing the heart chambers and the right coronary artery backward (arrow). The borders are irregular and polylobular. The signal is heterogeneous (arrow)

130 Fig. 39  SSFP, short axis cine image. The mass is depicted as a heterogeneous signal with an anterior fluid component shown as a hypersignal

Fig. 40  T1-weighted first-pass perfusion image. The lesion is heterogeneously enhanced, predominantly around its edges

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7.11  Angiosarcoma Developing Outside the Heart Chambers

131

Fig. 41  Late enhancement image 10 min after contrast injection. The lesion is very heterogeneously enhanced with areas of central necrosis picked up as a hyposignal and areas of intense enhancement around the edges

Background Cardiac sarcomas are the most frequent primary malignant tumors. Many different histological types have been described with different incidences in adults: angiosarcoma (37%), non-­differentiated sarcoma (27%), malignant fibrous histiocytoma (11–24%), leiomyosarcoma (8–9%), osteosarcoma (3–9%) and more rarely liposarcoma, fibrosarcoma and synovialosarcoma. Primary heart sarcomas affect mainly middle-aged adults and are rare in the pediatric population. Only rhabdomyosarcomas are more frequently found in children. With the exception of angiosarcoma, which more readily affect the right atrium, the other sarcomas are usually found in the left atrium but they can arise in any part of the heart [47]. Metastases develop in 47–89% of patients usually in the lungs. Table summarizing the radiological findings for cardiac sarcoma: Age of discovery

Middle age

Clinical

Generally impaired condition, right ventricle, atrium compression

Heart chamber

Atrium

Borders

Irregular

Extension

Yes

Calcifications

Possible

Density without contrast

Heterogeneous

T1 SE signal

Isosignal

T2 SE signal

Heterogeneous

Uptake of contrast

Yes, heterogeneous, with marked changes

Differential diagnosis

Metastasis

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Synoptic Tables

Table 1  Summary of the distinctive signs discriminating thrombus and tumors Thrombus

Tumors

Perfusion/enhancement

–

+/++

Dye diffusion from edges to center

Possible

–

Pericardial effusion

−/+

+

Myocardial spread

–

++

Adjacent tissue spread

–

++

Underlying cause of thrombus

+++

–

Akinesia or dyskinesia

++

–

Myocardial scar

++

–

A. Jacquier, CMR and MDCT in Cardiac Masses, DOI: 10.1007/978-3-642-18457-4_8, © Springer-Verlag Berlin Heidelberg 2011

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Usually too small to be characterized

Isosignal

Depends on type of malformation

Fat signal

No signal

Hyposignal/isosignal

Uneven

Isosignal

Isosignal

Isosignal

Isosignal/hypersignal

Uneven

Depends on stage of development

Fibroelastoma

Fibroma

Vascular malformation

Lipoma

Mitral annulus calcification

Paraganglioma

Neurofibroma

Erdheim–Chester

Bronchogenic cyst

Esophageal duplication

Rhabdomyoma

Teratoma

Hydatidosis

Cystic

Isosignal

Hypersignal

Hypersignal

Isosignal/ hypersignal

Uneven

Strong hypersignal

Hyposignal

Hypersignal

Isosignal

Myxoma

Variable

Variable

Thrombus

Table 2  Summarizing the classical radiological features of cardiac masses T1 T2

No

Yes

Yes, tinny

No

No

Yes

Yes

Yes central necrosis possible

No

No

Important

Yes

Late diffusion, no perfusion

Enhancement

Yes

Yes, tooth or calcification

No

No

No

No

No

No

Early stage: diffuse; late: peripheral

No

Possible if venous type

Yes

–

Possible

Possible

Calcification

Association with tuberous sclerosis

Diffuse mediastinal infiltration

Other location

–

–

Mobile

Mobile

Pattern depends on the underlying cause

Note

134 8  Synoptic Tables

Isosignal

Isosignal

Isosignal

Isosignal

Uneven

Pseudo-tumoral endocarditis

Actinomycosis

Metastases

Lymphoma

Sarcoma

Uneven

Isosignal

Isosignal/ hypersignal

–

Yes with necrosis and hemorrhage

Yes

Yes

Heterogeneous

Yes

Possible

No

No

Usually the patient is symptomatic

Other locations frequent

Immunocompromised patients

8  Synoptic Tables 135

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8  Synoptic Tables

Table 3  Summarizing the diagnosis of intracavitary mass Intracavitary mass Underlying cause of thrombus formation ?

YES: • Scar tissue (LV thrombus) • Pulmonary embolus (RV, RA, thrombus) • Central venous catheter (RA) • Mitral stenosis (LA) • Endomyocardial Fibrosis (RV,LV) • Cardiac graft (OD, G) • Segmetal akinesia, dyskinesia

No

This is probably a tumor

Confirm the lack of contrast uptake after gadolinium injection (2–5 min post gado)

Located in the LA growing from the fossa ovalis on a pedicle

Thrombus

Myxoma

Only fat

Lipoma

• The tumor spreads into the myocardium • More than one cardiac chamber is involved • Pericardial and / or pleural effusion • Asthenia

No = This is probably a benign mass: atypical myxoma, fibroelastoma, atypical thrombus or rare etiology

Yes= this is probably a malignant tumor: lymphoma, sarcoma, metastasis

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8  Synoptic Tables

Table 4  Summary of the diagnosis of intramyocardial mass Intra myocardial mass

Infants

Adults

• Extension to pericardium and or the cavity Prenatal or neonatal

pediatric

• More than one cardiac chamber is involved • Pericardial and / or pleural effusion • Asthenia

Rhabdomyoma

Fibroma

Bourneville tuberous sclerosis

No = probably a benign mass: Fibroma, paraganglioma (systemic hypertension in 1/3 of cases), vascular malformation Rare cases

Yes = malignant lesion: Lymphoma, sarcoma and metastasis

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8  Synoptic Tables

Table 5  Summary of the diagnosis of pericardial or paracardiac mass Pericardial or paracardiac location

Infants

Complex cyst (multilobular, calcifications…)

Adults

Cyst

• Extension to pericardium and / or the cavity • More than one cardiac chamber are involved • Pericardial and / or pleural effusion • Asthenia

Teratoma

Close to the oesophagus: esopheagal duplication

Close to the pleura or the pericardium: Pleuro-pericardial cyst

No = probably a benign mass: Fibroma, paraganglioma, vascular malformation Rare cases

Close to the bronchus: Bronchogenic cyst

Sometimes it is impossible to differentiate between these 3 diagnoses

Multiple cyst, calcification, intramyocardial location, positive echinococcus serology: hydatidosis

Yes = malignant lesion: Lymphoma, sarcoma, metastasis, mesothelioma

Appendix

Last Cover Page This book results from the cooperation between a number of teams of radiologists working under the aegis of the French Society of Cardiovascular Imaging (SFICV). Its goal is to review the different MRI sequences and CT acquisitions used to explore cardiac masses. It was designed as a teaching tool and offers a fully illustrated compendium of clinical cases, tables summarizing data and decision-making trees essential in everyday practice. It is presented as a practical handbook and can either be read cover to cover or consulted whenever needed during a cardiac imaging assignment. It is for all students and experienced practitioners, whether they are radiologists or not, who are interested in cardiac or thoracic pathology.

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Index

A Actinomycosis cine image, four-chamber, 99 clinical presentation, 99 diagnosis, 99 late enhancement MR image, 100 radiological findings, 100 Anatomic pitfalls crista terminalis, 17–18 deep atrioventricular groove (see Deep atrioventricular groove) juxtacaval fat collection, 19–20 lipomatous hypertrophy, interatrial septum cardiac MDCT, 11–12 diagnosis, 11 epicardial fat, 13 incidence, 13 radiological findings, 13 right atrium, flow artifact (see Right atrium, flow artifact) Angiosarcoma left atrium, 128 outside the heart chamber clinical presentation, 129 late enhancement image, 131 SSFP, 129–130 T1-weighted first-pass perfusion image, 130 radiological findings, 131 Ante and postnatal tumors bronchogenic cyst antenatal MRI, 83 CT image, 83 diagnosis, 84 fetal ultrasound, 82 radiological findings, 84 rhabdomyoma antenatal ultrasound, four chamber view, 87 radiological findings, 89

tuberous sclerosis, 88 T1-weighted MR image, 88 teratoma antenatal MR coronal image, 91 fetal ultrasound examination, 90 postnatal MR image, 91 radiological findings, 92 Arteriovenous fistulae, 58 B Benign tumors ante and postnatal tumors (see Ante and postnatal tumors) Castelman’s disease, 74–76 coronary fistula, 57–58 Erdheim–Chester disease, 80–81 intracardiac venous malformation (see Intracardiac venous malformation) intramyocardial fibroma (see Intramyocardial fibroma) lipoma (see Lipoma) mitral annulus calcification (see Mitral annulus calcification) myxoma (see Myxoma) neurofibromatosis, 77–79 papillary fibroelastoma, 50–52 paraganglioma (see Paraganglioma) Bronchial tumor, myocardial metastasis clinical presentation, 105 CMR, 106 diagnosis, 105 thoracic CT scan, 105 Bronchogenic cyst antenatal MRI, 83 CT image, 83 diagnosis, 84 fetal ultrasound, 82 radiological findings, 84

A. Jacquier, CMR and MDCT in Cardiac Masses, DOI: 10.1007/978-3-642-18457-4, © Springer-Verlag Berlin Heidelberg 2011

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144 C Cardiac hydatidosis pulmonary nodules CMR, 94–95 diagnosis, 94 radiological findings, 96 treatment, 96 Cardiac sarcomas, 131. See also Sarcoma Castelman’s disease CMR cine image, 74 Late enhancement image, 75 T2 weighted image, 75 lymphoproliferative syndrome, 76 radiological findings, 76 Coronary fistula arteriovenous fistulae, 58 cardiac MDCT, 57–58 clinical presentation, 57 diagnosis, 58 Crista terminalis MDCT, 17 radiological findings, 18 SSFP cine image, 18 D Deep atrioventricular groove diagnosis, 9 hyperechogenic mass CMR, right coronary vessels, 8 MDCT, coronary artery, 9 radiological findings, 10 Dilated cardiopathy cine images, 25 late enhancement images, 26 LV enlargement, 25 prevalence and incidence, 26 E Endomyocardial fibrosis cine images, 31 clinical presentation, 31 diagnosis, 31 idiopathic eosinophilia, 33 late enhancement image, 32 mammary neoplasm, 31 Erdheim–Chester disease diagnosis, 81 MDCT, 80–81 radiological findings, 81 signs and symptoms, 81

Index Esophageal duplication radiological findings, 86 T1-weighted MR image, 85 F Fibrosarcoma cardiac MDCT, 127 clinical presentation, 125 diagnosis, 127 late enhancement image, 126 True Fisp image, 125 T2-weighted black blood image, 126 Flow artifacts, right atrium. See Right atrium, flow artifact H Heart transplantation clinical presentation, 27 CMR cine images, 27 diagnosis, 27 late enhancement images, 28 orthoptic transplantation, 28 Hepatocellular carcinoma, 107–108 High-grade malignant pleomorphic sarcoma cine image axial view, 123 four-chamber, 122 clinical presentation, 122 late enhancement image, 124 T2-weighted fat-suppressed image, 124 T1-weighted image, four-chamber, 123 I Idiopathic eosinophilia, 33 Infectious lesions actinomycosis, 99–100 cardiac hydatidosis, 94–96 pseudotumoral endocarditis, 97–98 Intracardiac venous malformation clinical presentation, 59 CMR cine image, short axis view, 59 late enhancement image, 61 perfusion image, 60 diagnosis, 61 radiological findings, 62 vascular malformations, 61 Intracavitary mass, 136 Intramyocardial fibroma cardiac MDCT, 55

145

Index clinical presentation, 53 CMR fat-suppressed T1 image, 54 late enhancement image, 54 two-chamber view, 53 developmental anomalies, 56 hamartoma, 56 radiological findings, 56 Intramyocardial mass, 137 J Juxtacaval fat collection radiological findings, 20 retrohepatic mass CMR, 19 CT scan, 20 IVC invaginating, 20 L Lipoma clinical presentation, 63 CMR T1-weighted image, 64 epicardium, 65 location, 65 non-gated CT scan, 63 primary tumors, 65 radiological findings, 65 Lipomatous hypertrophy, interatrial septum cardiac MDCT, 11–12 diagnosis, 11 epicardial fat, 13 incidence, 13 radiological findings, 13 Lymphoma epicardial space cine image, four-chamber, 116 cine image short axis view, 117 clinical presentation, 116 late enhancement image, 118 perfusion image, 117 T1-weighted image, 118 inside the heart chamber cine image, four-chamber, 113 cine image two-chamber, 114 clinical presentation, 113 percutaneous fluoroscopy, 115 T2-weighted image, 114 large cell lymphoma, pericardium cardiac MDCT, 119–120 clinical presentation, 119 CMR black blood image, 121

diagnosis, 119 radiological findings, 121 vs. primary cardiac lymphoma, 120–121 M Malignant melanoma cardiac MDCT, 104 CMR, 104 CT scan, 103 diagnosis, 103 Malignant tumors angiosarcoma (see Angiosarcoma) bronchial tumor, 105–106 fibrosarcoma (see Fibrosarcoma) hepatocellular carcinoma, 107–108 high-grade malignant pleomorphic sarcoma, 122–124 lymphoma (see Lymphoma) malignant melanoma, 103–104 pericardial metastasis (see Pericardial metastasis) type B lymphoma (see Type B lymphoma) Mitral annulus calcification CMR Late enhancement image, 67 T1 weighted fat-suppressed image, 66 T2 weighted fat-suppressed image, 67 MDCT, 68 necrotic liquefaction, 68 radiological findings, 68 Myocardial infarction clinical presentation, 23 diagnosis, 23 incidence, 24 late enhancement images, 24 risk factors, 23 Myxoma atypically located myxoma cine image parasagittal view, 48 clinical presentation, 47 diagnosis, 49 late enhancement images, 48 short axis cine image, RV infundibulum, 47 Carney complex, 49 left atrium clinical presentation, 43 delayed enhanced image, 46 four-chamber cine image, 44 MDCT, 43–44 T1-weighted black blood image, 45 T2-weighted black blood image, 45 radiological findings, 49

146 N Neurofibromatosis diagnosis, 78 MDCT, 77 arterial phase acquisition, 77 axial view, 78 coronal view, 78 radiological findings, 79 O Orthoptic transplantation, 28 P Papillary fibroelastoma cardiac MDCT, 50–51 clinical presentation, 50 diagnosis, 51 incidence, 52 radiological findings, 52 Paraganglioma chemodectoma, 72 diagnosis, 69 fat suppressed image, 71 first pass perfusion image, 71 late enhancement image, 72 MDCT, four chamber view, 69 pheochromocytoma, 72 radiological findings, 73 SSFP cine image, 70 T1 weighted image, 70 Pericardial metastasis cardiac MDCT, 110 clinical presentation, 109 CMR cine two-chamber, 110 late enhancement image, 111 T2-weighted image, 111 CT scan, 109 diagnosis, 109 pericardial effusion, 112 primary malignancy, 112 radiological findings, 112 Pericardial/paracardiac mass, 138 Pericardial teratoma, 92. See also Teratoma Pseudotumoral endocarditis clinical presentation, 97 endocardial and valvular vegetations, 98 heterogeneous mass cine image, four-chamber, 97 diagnosis, 97

Index late enhancement image, 98 radiological findings, 98 Pulmonary embolism, 29–30 R Radiological features, 134–135 actinomycosis, 100 angiosarcoma, 131 bronchogenic cyst, 84 cardiac hydatidosis, 96 Castelman’s disease, 76 crista terminalis, 18 deep atrioventricular groove, 10 Erdheim–Chester disease, 81 esophageal duplication, 86 intracardiac venous malformation, 62 intramyocardial fibroma, 56 juxtacaval fat collection, 20 lipoma, 65 lipomatous hypertrophy, interatrial septum, 13 mitral annulus calcification, 68 myxoma, 49 neurofibromatosis, 79 papillary fibroelastoma, 52 paraganglioma, 73 pericardial metastasis, 112 pseudotumoral endocarditis, 98 rhabdomyoma, 89 right atrium, flow artifact, 16 teratoma, 92 Rhabdomyoma antenatal ultrasound, four chamber view, 87 diagnosis, 88 radiological findings, 89 tuberous sclerosis, 88 T1-weighted MR image, 88 Right atrium, flow artifact pulmonary embolus contrast medium, 15 CT scan, 14 MPR reconstruction, 15 SSFP cine sequences, 16 radiological findings, 16 S Sarcoma, 124 angiosarcoma (see Angiosarcoma) fibrosarcoma (see Fibrosarcoma)

147

Index undifferentiated sarcoma (see High-grade malignant pleomorphic sarcoma) T Technical aspects CMR cine sequences, 3 delayed contrast enhancement, 4 first pass perfusion imaging, 4 look-locker sequences, 4 T1-and T2-weighted sequences, 3 MDCT acquisition parameters, 5 contrast injection, 5–6 images acquisition, 5 Teratoma antenatal MR coronal image, 91 fetal ultrasound examination, 90 postnatal MR image, 91 radiological findings, 92 Thrombi, 1 Thrombus, 22 central venous catheter bladder cancer, 34 catheter lesion, 36 cine image, 34, 35 clinical presentation, 34 diagnosis, 36 late enhancement image, 35 contrast medium uptake late enhancement images, 37, 38

radiological findings, 39 dilated cardiopathy, 25–26 endomyocardial fibrosis cine images, 31 clinical presentation, 31 diagnosis, 31 idiopathic eosinophilia, 33 late enhancement image, 32 mammary neoplasm, 31 heart transplantation, 27–28 myocardial infarction, 23–24 pulmonary embolism, 29–30 vs. tumors, 1, 133 Type B lymphoma epicardial space cine image, four-chamber, 116 cine image short axis view, 117 clinical presentation, 116 late enhancement image, 118 perfusion image, 117 T1-weighted image, 118 large cell cine image, four-chamber, 113 cine image two-chamber, 114 clinical presentation, 113 percutaneous fluoroscopy, 115 T2-weighted image, 114 V Valve calcifications, 68. See also Mitral annulus calcification