Comparative Cardiac Imaging E-Book

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 532

Veröffentlichungsjahr: 2018

Beschreibung

Provides the information necessary to guide clinicians to more efficient and appropriate use of the cardiac imaging modalities at their disposal Most books currently available on cardiac imaging focus on just modality. As the number of imaging options has increased, the choice of procedure has become more complicated. This comprehensive book will guide the practitioner in choosing the most appropriate test when confronted by various cardiac symptoms and diseases and to understand the benefits and limitations of each imaging modality. It demonstrates the advantages and disadvantages of various imaging modalities such as echocardiography, computer tomography, MRI, and nuclear cardiology in the evaluation of various disease states both commonly and infrequently seen in a standard practice. Comparative Cardiac Imaging--A Case-based Guide utilizes actual case examples to demonstrate the state of the art in comparative cardiac imaging. It offers in-depth chapter coverage of Aortic Diseases; Aortic Valvular Diseases; Mitral Valvular Diseases; Prosthetic Valves; Coronary Artery Disease; Pulmonary Artery Diseases; Congenital Heart Disease; Cardiac Tumor; Infective Disease; Cardiomypathy; and Cardiac Trauma. * Uniquely focuses on and compares the many different modalities for cardiac imaging * Breaks the topic down by anatomy and pathophysiology in order to cover all aspects of non-invasive cardiac imaging * Covers newer and lesser known modalities like speckle tracking and velocity vector imaging * Offers coverage of more controversial topics, such as CT angiography Comparative Cardiac Imaging--A Case-based Guide presents a level of data that is appropriate for the practicing cardiologist and cardiology trainee, as well as residents, internists, and other primary care clinicians.

Leseprobe

Table of Contents

Cover

Title Page

Notes on Contributors

Foreword

Preface

Abbreviations

About the Companion Website

Part I: Congenital Heart Disease in the Adult

1 Aneurysmal Aorto–Left Ventricular Tunnel and Bicuspid Aortic Valve with Severe Stenosis

History

Discussion

Diagnosis

Treatment

Key Points

References

2 Anomalous Origin of the Left Coronary Artery from the Pulmonary Trunk

History

Discussion

Imaging Diagnosis

Treatment

Conclusion

Key Points

References

3 Anomalous Origin of Right Coronary Artery

History

Discussion

Key Points

References

4 Interrupted Aortic Arch associated with Aortopulmonary Window

History

Discussion

Key Points

References

5 Congenitally Corrected Transposition of the Great Arteries

History

Discussion

Key Points

References

6 Coronary Fistula

History

Discussion

Key Points

References

7 Crista Terminalis Bridge Mimicking Right Atrial Mass

History

Discussion

Key Points

References

8 A Criss‐cross Heart with Double Outlet Right Ventricle

History

Discussion

Key Points

References

9 Double‐Chambered Right Ventricle with Ventricular Septal Defect

History

Discussion

Diagnosis

Key Points

References

10 Isolated Double‐Orifice Mitral Valve

History

Discussion

Key Points

References

11 The Gerbode Defect: A Ventriculo‐Atrial Defect

History

Discussion

Key Points

References

12 Intralobar Pulmonary Sequestration

History

Discussion

Treatment

Key Points

References

13 Partial Anomalous Pulmonary Venous Connection with Secundum Atrial Septal Defect

History

Discussion

Diagnostic Evaluation

Key Points

References

14 Pulmonary Arteriovenous Malformation

History

Discussion

Diagnosis

Complications

Treatment and Prognosis

Differential Diagnoses

Key Points

References

15 Right Pulmonary Agenesis associated with Congenital Heart Diseases

History

Discussion

Key Points

References

16 Compressive Giant Right Atrial Diverticulum

History

Discussion

Key Points

References

17 Shone’s Syndrome

History

Discussion

Conclusions

Key Points

References

18 Subaortic Membrane in the Adult

History

Discussion

Key Points

References

19 Supracardiac Total Anomalous Pulmonary Venous Connection

History

Discussion

Treatment

Prognosis

Key Points

References

20 Tricuspid Atresia

History

Discussion

Key Points

References

21 Isolated Congenital Tricuspid Valve Dysplasia in a 38‐year‐old Adult

History

Discussion

Key Points

References

22 Unroofed Coronary Sinus Defect

History

Discussion

Key Points

References

Part II: Artery Disease

23 Acute Aortic Regurgitation caused by Spontaneous Aortic Valve Rupture

History

Discussion

Key Points

References

24 Bicuspid Aortic Valve Complicated by Pseudo‐aneurysm of Aortic Root Abscesses

History

Discussion

Key Points

References

25 Coronary Artery Vasculitis in Patient with Systemic Lupus Erythematosus

History

Discussion

Key Points

Reference

26 Aortic Dissection

History

Discussion

Key Points

References

27 Large Thrombus in Giant Unruptured Noncoronary Sinus of Valsalva Aneurysm

History

Discussion

Key Points

References

28 Isolated Pulmonary Vasculitis

History

Discussion

Key Points

References

29 Giant Left Ventricular Pseudoaneurysm

History

Discussion

Key Points

References

30 Salmonela Aortitis:A Rare Cause of Fever and Back Pain in the Elderly

History

Discussion

Treatment

Key Points

References

31 Subepicardial Aneurysm of Left Ventricle:A Rare Complication of Acute Myocardial Infarction

History

Discussion

Key Points

Reference

32 Coronary Artery Disease and Systemic Vasculitis

History

Hospital Course

Discussion

Clinical Appearance

Diagnostic Approach

Imaging

Management

Monitoring and Follow Up

Key Points

References

Part III: Cardiac Mass

33 Primary Cardiac Angiosarcomain Left Atrium

History

Discussion

Key Points

References

34 Atypical Left‐Atrial Papillary Fibroelastoma

History

Discussion

Key Points

References

35 Cardiac Lipoma with Ventricular Arrhythmias

History

Discussion

Key Points

References

36 Primary Cardiac Pheochromocytoma

History

Discussion

Diagnosis

Treatment and Prognosis

Key Points

References

37 Cardiac Rhabdomyosarcoma of the Left Atrium

History

Discussion

Key Points

References

38 Unusual Cardiac Fibroelastoma

History

Physical Examination

Discussion

Management

Key Points

References

39 Pulmonary and Cardiac Inflammatory Myofibroblastic Tumor

History

Discussion

Key Points

Reference

40 Intravenous Leiomyomatosis with Cardiac Metastases

History

Discussion

Treatment

Key Points

References

41 Intramural Left Atrial Hematoma Complicating Catheter Ablation for Atrial Fibrillation

History and Hospital Course

Discussion

Key Points

References

42 Primary Cardiac Lymphoma: Two Rare Cases

History

Discussion

Key Points

Reference

43 Mass in Left Atrium and Appendage

History

Discussion

Key Points

References

44 Metastatic Cardiac Lymphoma

History

Discussion

Key Points

References

45 Metastatic Renal Carcinoma in Inferior Vena Cava

History

Discussion

Key Points

References

46 Pericardial Metastasis Mass from Thyroid Carcinoma

History

Discussion

Key Points

References

47 Spindle Cell Sarcoma: A Rare Case of Multicardiac Chamber Mass

History

Diagnosis

Discussion

Key Points

References

Part IV: Cardiomyopathy and Myocarditis

48 Fulminant Myocarditis

History

Discussion

Diagnosis

Classification

Management

Prognosis

Key Points

References

49 Cardiac Amyloidosis

History

Discussion

Diagnosis

Key Points

References

50 Hypertrophic Cardiomyopathy with Apical Aneurysm

History

Discussion

Key Points

References

51 Arrythmogenic Right Ventricular Dysplasia

History

Discussion

Diagnostic Evaluation

Diagnostic Tests

Prognosis and Management

Key Points

References

52 Danon Disease

History

Discussion

Key Points

References

53 Acute Eosinophilic Myocarditis

History

Discussion

Conclusion

Key Points

References

54 Noncompaction Cardiomyopathy with Apical Aneurysm

History

Discussion

Key Points

References

Part V: Diversification

55 A Fistula between Aortic Pseudoaneurysm and Right Atrium

History

Discussion

Key Points

References

56 Dual Aortic and Mitral Valve Aneurysms in a Patient with Infective Endocarditis

History

Physical Examination

Discussion

Key Points

References

57 Intracardiac Thrombus in Behçet’s Disease

History

Discussion

Key Points

References

58 Cardiac Hydatid Disease

History

Discussion

Key Points

References

59 Diagnosis of Constrictive Pericarditis with Multimodality Imaging

History

Discussion

Key Points

References

60 Inverted Left‐Atrial Appendage

History

Discussion

Key Points

References

61 Inferior Vena Stent Fracture and Multiple Heart Injuries caused by Migration

History

Discussion

Key Points

References

62 Anterior Mitral Valve Aneurysm: A Rare Complication of Aortic Valve Endocarditis

History

Discussion

Key Points

References

Index

End User License Agreement

List of Illustrations

Chapter 01

Figure 1‐1 Transthoracic echocardiogram showed: A. Aortic valves displayed severe calcification (Figure 1‐1.*). An aorto‐left ventricular tunnel (ALVT) (T) was seen with entry from the aorta (thin arrow) and exit (thick arrow) into the left ventricle (LV). B. The blood flow from the aorta into the ALVT (T) and out of the tunnel into the LV were seen with color Doppler. C. The outline of the tunnel (T) with the entrance from the aorta was clearly seen. D. A nonvalvular regurgitation (thick arrow) and a shunt from the aorta into the ALVT (thin arrow) were seen with color Doppler.

Figure 1‐2 Computer angiogram showed: A. Computed tomography scan, long‐axis view, showed the dilated ascending aorta, an aneurysmal ALVT (T) arising from aortic root and connected with the LV (*). B. The short‐axis view showed the aortic annulus with calcification, and calcificatiive connection (arrow) between the LV and tunnel (T). C. The short‐axis view showed the connection (*) between the aortic root and ALVT (T). D. Computed tomography three‐dimensional reconstruction imaging showed aneurysmal ALVT (arrow), left coronary artery (LCA) arising from the aortic root (arrow) behind the aneurysmal ALVT, and significantly dilated ascending AO.

Figure 1‐3 Intraoperative picture showed the entrance of tunnel (white arrow) arising from the left Valsalva sinus, located at below and in front of the LCA orifice in the ascending aorta.

Chapter 02

Figure 2‐1 A. Atypical parasternal short‐axis view showed anomalous left coronary artery with retrospective flow arrow (arrow). B. Continuous wave Doppler recorded from a short‐axis view showed coronary flow into septum during cardiac cycle, predominately in diastole.

Figure 2‐2 A. Apical four‐chamber view showed left atria and ventricle were significantly enlarged with a color Doppler flow in the ventricular septum (long arrow) communicating with the left ventricular cavity continuously. The blood flowed back to septum during systole (short arrow) and B. into the LV cavity during diastole (short arrow). C. A parasternal short‐axis view showed the intraseptal blood flow (long arrow) and the flow from the interventricular septal into the LV (short arrow).

Figure 2‐3 A series of angiograms showed that: A. The right coronary artery was original from aorta, B. plenty collateral arteries between right and left coronary, and C. anomalous origin of left coronary artery was from pulmonary artery, and plenty collateral arteries between right and left coronary, D. anomalous LAD with retrospective flow (arrow) from collateral arteries.

Figure 2‐4 Computed tomography reconstructive imaging: A. A three‐dimensional CT reconstruction image showed the RCA originating from the aorta, but the LCA originating from the pulmonary artery. B. A three‐dimensional CT reconstruction image showed numerous anastomosis branches between right and left coronary arteries, and the RCA originating from the aorta, but the LCA originating from the pulmonary artery.

Chapter 03

Figure 3‐1 The left main stem arose from the left coronary cusp, which then gave rise to the left anterior descending artery and left circumflex artery with normal caliber. The right coronary artery shared the common origin of the LMS, originating from the left coronary cusp.

Notes:

LMS, left main stem coronary; LAD, left anterior descending artery; LCX, left circumflex artery; RCA, right coronary artery.

Figure 3‐2 A. The right coronary artery shared the common origin of LMS, originating from the left coronary cusp. B. The proximal RCA run in an epicardial interarterial course between the aortic root and the right ventricular outflow tract, in which the sandwiched proximal segment is smoothly narrowed.

Note:

RVOT, right ventricular outflow tract.

Chapter 04

Figure 4‐1 Echocardiography: A. A parasternal short axis view showed a large aortopulmonary window (*) between the ascending aorta (AAO) and the pulmonary artery (PA), the right pulmonary artery was arising from ascending aorta. B. A suprasternal notch view showed an aortic arch (ARCH) interrupted at distal to the origin of the left subclavian artery (arrow). C. The parasternal short axis view showed a large patent ductus arteriosus (PDA) extending into the thoracic aorta (DAO).

Figure 4‐2 Computed tomography images: A. Axial maximum intensity projection image showed a large aortopulmonary window (arrow) between the ascending aorta (AAO) and the pulmonary artery (MPA), right and left pulmonary arteries and descending aorta (DAO). B. Lateral view showed right ventricle (RV), main pulmonary artery (MPA) with left pulmonary artery (LPA), and a patent ductus arteriosus (PDA) extending into the thoracic aorta (DAO). C. A posterior view with a three‐dimensional volume rendering image showed the main pulmonary artery with a patent ductus arteriosus extending in the thoracic aorta and aortic arch interruption distal to the origin of the left subclavian artery. D. Anterior view with three‐dimensional volume rendering showing a large aortopulmonary window (arrow) between the ascending aorta and the main pulmonary artery, and a type A interrupted aortic arch.

Notes:

APSD, aortopulmonary window; RPA, right pulmonary artery; LSCA, left subclavian artery; LCCA, left common carotid artery; IA, Innominate artery; RPA, right pulmonary artery; LPA, left pulmonary artery; LBCV, left brachiocephalic vein; AAO, ascending aorta; AA, aortic arch.

Chapter 05

Figure 5‐1 Electrocardiogram showing normal sinus rhythm with a left‐axis deviation, QS waves in II, III, AVF and absence of Q waves in leads V4–V6.

Figure 5‐2 Chest X ray. Posteroanterior chest X‐ray showing a cardiac silhouette. The ascending aortic shadow and the main pulmonary artery segment are absent.

Figure 5‐3 Echocardiography. In the apical four‐chamber view, there is reversed offsetting of the attachments of the atrioventricular valves to the septum, with the mitral valve on the right side attached appreciably higher than the tricuspid valve (TV) on the left side of the heart. The left atrium (LA) is connected to a morphological right ventricle, which is characterized by myocardial trabeculations; in addition, the morphological left ventricle (LV) is connected with the right atrium (RA), positioned on the right side.

Figure 5‐4 Computed tomography. A. Note the main pulmonary artery arising from the morphology left ventricle (MLV). B. The aorta arises from the anterior position of the morphology right ventricle (MRV), the pulmonary veins return to left atrium.

Figure 5‐5 Three‐dimensional volume‐rendered image shows spatial relationship of great arteries with ascending aorta locating at anterior and to left of main pulmonary artery. Anterior descending artery and circumflex artery arise from common left ventricular coronary artery off of anterior aortic sinus. Right coronary artery arises from posterior aortic sinus.

Chapter 06

Figure 6‐1 Two‐D Echocardiography showed: A. Parasternal short‐axis view at aortic level showed dilated RCA (*). B. Atypical apical four‐chamber view showed multiple shunts from RV free wall (long arrow) into RV cavity (small arrows). C. Parasternal short axis view at aortic valve level showed dilated LCA (*). D. Parasternal short‐axis view with color Doppler at papillary muscle level showed three fistula flows from ventricular septum into RV cavity. E. Parasternal short‐axis view with color Doppler at aortic valve level showed dilated LCA filling with color flow (arrow). F. Atypical apical two‐chamber view with color Doppler showed multiple fistula flows (arrow) from LV anterior wall into LV cavity.

Notes:

RA, right ventricle; LA, left atrium; AO, aorta; PA, pulmonary artery; LV, left ventricle and LMCA, left main coronary artery.

Figure 6‐2 Volume‐rendered image from computed tomography (CT) showed RCA dilated over the entire length (arrow); and the left main coronary artery derived into three branches (arrows), which are dilated over the entire length along the anterior surface of the ventricle.

Chapter 07

Figure 7‐1 Two‐dimensional echocardiography: A small mass/structure (1 × 0.9 cm, arrow) noted in the right atrial roof from an apical four‐chamber view (left), and right ventricular inflow view (right).

Figure 7‐2 MRI images showed a linear band–like structure in the roof of the right atrium with signal identical to myocardium with no evidence of thrombus. Appearance is compatible with a prominent crista terminalis (arrow).

Chapter 08

Figure 8‐1 Transthoracic echocardiography. A. An atypical apical view showed that the left atrium was connected with right ventricle through the tricuspid valve; the aorta and pulmonary artery arose from the right ventricle, but the pulmonary valves were thickened with stenosis (arrow). B. An apical view showed the right atrium was connected with left ventricle through the mitral valve. C. An apical four‐chamber view showed double outlets right ventricle with a ventricular septal defect. D and E. A super sternum notch view showed collateral circulation between aorta and pulmonary artery. F. The velocity of collateral circulation.

Figure 8‐2 Computed tomography multiplanar reconstruction images showed: A. Right atrium connected with left ventricle through the mitral valve, and a ventricular septal defect. B. Left atrium connected with the right ventricle. C. Left atrium located at upper left of right atrium. D. Right ventricle (RV) superiorly located and the left ventricle (LV) inferiorly located. These images indicated that the AV connection is discordant in this case.

Figure 8‐3 A. An echocardiography image showed that the left atrium was connected with the right ventricle through the tricuspid valve; the aorta and pulmonary artery arose from the right ventricle. B. The findings of CT images were consistent with echocardiography. C. Computed tomography image showed a plentiful collateral circulation between the aorta and the pulmonary artery.

Figure 8‐4 Computed tomography three‐dimensional reconstruction image displaying the aorta, which originated from the right ventricle, and plentiful collateral circulation between the aorta and pulmonary artery (arrows).

Chapter 09

Figure 9‐1 Echocardiographic findings (a modified view) in a patient with a double‐chambered right ventricle. A. A modified view showed an anomalous RV muscle bundle (large and small arrows), turbulent Doppler color flow velocity pattern in the right ventricular outflow tract (RVOT, *), which suggested RV obstruction between RV and RVOT. B. The high velocity by continuous wave Doppler in RVOT indicated obstruction within the RV.

Notes:

RV, right ventricle; RA, right atrium.

Figure 9‐2 A. Atypical four‐chamber view showed a dilated right atrium (RA), anomalous RV muscle bundle (*) from the RV free wall and septum hypertrophy resulting in RV obstruction. B. A parasternal long‐axis view showed significantly hypertrophy of the ventricular septal and right ventricle wall, and a ventricular septal defect; the arrow pointed to the subaortic membrane. C. A computed tomography image showed dilated RA and VSD with a left‐to‐right shunt; the thickness of the RV wall was significant increased. D. A CT atypical short‐axis image showed that RV wall was significantly hypertrophied; there is an obstruction (arrow) between the RV and the RVOT.

Notes:

RV, right ventricle; LV, left ventricle; RVOT, right ventricle outflow tract; AO, aorta; and PA, pulmonary artery.

Chapter 10

Figure 10‐1 Transthoracic two‐dimensional echocardiography. A parasternal short‐axis view showed distinctive morphology of an isolated double orifice mitral valve; two orifices are equal in size (A and B). An apical two‐chamber view showed that there was a single mitral annulus with the two valvular orifices separated by a central fibrous bridge (C). The same view with color Doppler showed that there are two normal laminar flows from double orifice into left ventricle separately (D).

Chapter 11

Figure 11‐1 A. A transthoracic parasternal short‐axis view showed the true or direct left‐ventricular to right‐atrial shunt. B. A transesopheageal four‐chamber view showed the direct left‐ventricular to right‐atrial shunt. C. A transesopheageal short‐axis view showed the ventricular septal defect. D. A transesopheageal short‐axis view showed the direct left‐ventricular to right‐atrial shunt.

Figure 11‐2 The continuance wave Doppler recording showed the high velocity of left ventricular‐to‐right atrial shunt; the instantaneous gradient in this patient was 76 mm Hg.

Figure 11‐3 A transesopheageal long‐axis view showed the vegetation attached to aortic valves during diastole (A), and systole (B).

Figure 11‐4 A computed tomography four‐chamber view indicated there is a Gerbode defect with shunting of blood from the left ventricle into the right atrium, via the membranous portion of the interventricular septum and at a level above the tricuspid annulus plane (arrow). The defect size is estimated as 1.1 cm on CT.

Chapter 12

Figure 12‐1 An irregular solid mass was shown in the thoracic cavity behind the heart.

Figure 12‐2 A. A maximal intensity projection (MIP) reconstructive image of thoracic CT scan shows normal main pulmonary artery (PA) and branches (yellow arrow). B. A transverse image of the venous phase showing dilated left inferior pulmonary vein and draining into the left atrium (yellow arrow). C. A transverse reconstructive image of thoracic CT scan shows the aberrant vascular structure originating from descending aorta (red arrow) and the dilated left inferior pulmonary veins (yellow arrow).

Figure 12‐3 A. In coronal reconstruction, the aberrant vascular structure originating from the descending aorta (red arrow) extends to the left inferior pulmonary sequestration (red arrow). The draining vein of the pulmonary sequestration is the left inferior pulmonary veins (yellow arrow). B. A sagittal reconstructive image of thoracic CT scan shows the aberrant vascular structure originating from descending aorta (red arrow).

Chapter 13

Figure 13‐1 A. A two‐dimensional image in the apical four‐chamber view showing that the right ventricle and atrium are markedly dilated, a secundum atrial defect is seen (arrow), and the right lower pulmonary vein can be visualized. B. A saline contrast echocardiographic image demonstrates that a small contrast negative filling area in the RA, which is consistent with left to right shunt through the atrial septum defect. C. Parasternal short‐axis view showing dilated RV and RA as well as the atrial septum defect (arrow). D. A suprasternal short‐axis view and Doppler color flow images revealed the superior vena cava is enlarged. E. There is a flow in red towards the left innominate vein and superior vena cava, suggested this flow is in a vertical vein. F. Tricuspid regurgitation evaluated by continuous wave Doppler; the estimating pulmonary arterial systolic pressure is about 51 mmHg.

Figure 13‐2 Three‐dimensional reconstruction of MDCT. A. An anterior view reveals anomalous drainage of the left upper pulmonary vein via a vertical vein into the brachiocephalic vein. B. A right‐anterior‐oblique view shows anomalous drainage of the right upper and middle pulmonary veins to the SVC. C. The left and right inferior pulmonary veins are normal connected to the left atrium.

Notes:

SVC, superior vena cava; VV, vertical vein; LUPV, upper pulmonary vein; RUPV, right upper pulmonary vein; RIPV, right inferior pulmonary vein; LIPV, left inferior pulmonary vein.

Chapter 14

Figure 14‐1 An apical four‐chamber view showed a positive agitated saline bubble test. Large amounts of bubbles appear at the left heart after five cardiac cycles, consistent with pulmonary arteriovenous malformations.

Figure 14‐2 Computed tomography with contrast injection demonstrates enhancement of the feeding artery, the aneurysmal part (arrow), and the draining vein on early phase sequences.

Chapter 15

Figure 15‐1 A. A chest X‐ray showed right hemithorax opacity (lung agenesis), leftward deviation of the mediastinal structure, dextrocardia, and abnormal T3 vertebra. B. A MinMip reconstruction of the airway showed a normal trachea and left bronchus, and absence of right lung and bronchus.

Figure 15‐2 A. Echocardiography found dextrocardia; an apical four‐chamber view showed the left atrial was small, and there was no pulmonary venous return. B. Left anomalous pulmonary venous drainage into the superior vena cava.

Notes:

RV, right ventricle; RA, right atrium; LV, left ventricle; LA, left atrium; SVC, superior vena cava; LPV, left pulmonary vein.

Figure 15‐3 Pulmonary artery and venous angiography by 64‐slice spiral computed tomography (CT) demonstrated: A. Both right pulmonary artery and right pulmonary vein were absent. The end of the left pulmonary vein was narrow and drained into the lower part of the right superior vena cava. B. There was a patent ductus arteriosus between the beginning of the descending aorta and the main pulmonary artery, but the right pulmonary artery was absent. C. Computed tomography reconstruction image showed dextrocardia; the left atrial was small, and the superior vena cava was dilated. There was a patent ductus arteriosus between the beginning of descending aorta and the main pulmonary artery, but the right pulmonary artery and vein were absent.

Notes:

RV, right ventricle; RA, right atrium; LV, left ventricle; LA, left atrium; SVC, superior vena cava; LPV, left pulmonary vein; MPV, main pulmonary artery; PDA, patent ductus arteriosus, DAO, descending aorta. LPA, left pulmonary artery.

Chapter 16

Figure 16‐1 A chest X‐ray showed marked cardiomegaly.

Figure 16‐2 A. Echocardiography: two‐dimensional transthoracic echocardiography revealed a giant diverticulum (13 cm × 8.9 cm × 13.8 cm) connected to the right atrial free wall by a large defect (5.8 cm × 3.2 cm). B. Spontaneous contrast but no thrombus could be seen within the diverticulum. There was free bidirectional flow between the right atrium and the diverticulum shown by color Doppler.

Figure 16‐3 Computed tomography confirmed a giant diverticulum adjacent to the right side of the right atrium compressing the right atrium and ventricle (A and B). A three‐dimensional reconstruction image shows the huge diverticulum adjacent to the right side of the heart (C).

Chapter 17

Figure 17‐1 Case 1. Left: Parasternal long‐axis view of a transthoracic echocardiogram showing the posterolateral papillary muscle. Middle: Parasternal short‐axis view showing a small mitral annulus. Right: apical long axis view showing a prominent posterolateral papillary muscle.

Figure 17‐2 Case 2. A. Two‐dimensional TTE apical three‐chamber view showed subaortic membrane and unicuspid aortic valve. a unicuspid aortic valve (arrow). B. Two‐dimensional TTE without (small one) and with color Doppler showed stenotic unicuspid aortic valve with high velocity (arrow). C. Three‐dimensional TEE showed a supravalvular ring in left atrium. D. Two‐dimensional TEE showed a supravalvular ring in left atrium (small arrow). E. Computed tomography aorta, long‐axis view, and multiplanar reconstruction of aortic long‐axis view showed that the ascending aorta was significantly dilated, and a mild to moderate coarctation of the descending aorta beyond the origin of the left subclavian artery (arrow) without poststenotic dilatation. F. The operative view showed subaorticvalvular membrane (*). G. The operative view showed the supravalvular ring (*).

Figure 17‐3 Computed tomography scan showed the coarctation of the thoracic descending aorta (0.5 mm) just distal to the left subclavian artery representing. The multiple collateral vessels were present, supplying the distal site of aortic coarctation.

Notes:

AO, ascending aorta; DAO, descending aorta.

Chapter 18

Figure 18‐1 A subtle tissue (arrow) attached to the ventricular septum in LVOT was seen in parasternal (A) and apical three‐chamber views (B).

Notes:

LV, left ventricle; LA, left atrium; RV, right ventricle; AO, ascending aorta.

Figure 18‐2 A.The long‐axis view of transesophageal two‐dimensional echocardiography showed a subaortic membrane attached to ventricular septum. B. The long‐axis view of transesophageal three‐dimensional echocardiography showed a subaortic membrane attached to ventricular septum. C. Three‐dimensional transoesophageal echocardiography examination showing a pyramidal volume on the LV outflow tract and the subaortic membrane (arrow) in the short‐axis view.

Notes:

LV, left ventricle; LA, left atrium; RV, AO, ascending aorta; MV, mitral valve.

Figure 18‐3 The continue wave Doppler spectrum showed: A. The maximal gradient was 27 mmHG during rest. B. The maximal gradient was 64 mmHG after treadmill exercise.

Chapter 19

Figure 19‐1 Echocardiography: A. An apical four‐chamber view showed that the right atrium and ventricle were significantly enlarged, the left atrium was small without pulmonary vein entrance. The entrances of pulmonary veins were not seen in the roof of left atrium. B. An apical four‐chamber view showed an atrial septal defect with right‐to‐left shunt. C. The subcostal view showed that the superior vena cava was significantly enlarged.

Notes:

RV, right ventricle; RA, right atrium; LA, left atrial; LV, left ventricle; ASD, atrial septal defect; SVC, superior vena cava.

Figure 19‐2 Ehocardiography: A. A supersternal notch view showed four pulmonary veins converging into a common pulmonary vein connected with the vertical vein and enter into innominate vein draining into the superior vena cava. B and C. Supersternal notch views with color Doppler showed the blood‐flow directions.

Notes:

CPV, common pulmonary vein; VV, vertical vein; LIV, left innominate vein.

Figure 19‐3 Computed tomography imaging: A. Four pulmonary veins entered into a common pulmonary vein. B. The common pulmonary vein connected with vertical vein; an innominate vein entered into a significantly enlarged superior vena cava. C. The relation among vertical vein, innominate vein, superior vena cava and right atrium was clearly presented. D. Three‐dimensional cardiac CT image showed the vertical vein, innominate vein, huge superior vena cava, and right atrium.

Notes:

CPV, common pulmonary vein; VV, vertical vein; LIV, left innominate vein; RA, right atrium.

Chapter 20

Figure 20‐1 Transthoracic echocardiography four‐chamber views without (A) and with color Doppler (B) showed: significantly dilated left (LA) and right atrium (RA) with spontaneous contrast, a large thrombus in right atrium and severe mitral valve regurgitation; tricuspid atresia and a hypoplastic right ventricle (RV). A modified view (C) showed tricuspid atresia (arrow), an occluded pulmonary artery (PA). A four‐chamber view (D) showed ventricular septal defect (VSD) and dilated left atrium.

Figure 20‐2 Computed tomography scan indicated a significantly dilated left atrium (LA) and right atrium (RA), and ventricular septal defect (VSD).

Chapter 21

Figure 21‐1 Transthoracic echocardiography: A and B. Apical four‐chamber view showed significantly dilated right atrium and ventricle and enlarged tricuspid valve annulus with severe tricuspid regurgitation (color Doppler). C and D. Magnetic resonance imaging indicated: The right ventricle and atrial were significantly dilated.

Chapter 22

Figure 22‐1 Parasternal long‐axis view showed the significantly enlarged left atrium and the drainage of unroofed coronary sinus into the left atrium, constituting a bidirection shunt – coronary sinus ASD (atrial septal defect) (A), with a LA‐to‐CS shunt (B) during LA contraction, and CS‐to‐LA (C) during LA relaxation.

Figure 22‐2 A. From three‐dimensional full‐volume imaging, a short‐axis surgical view obtained by cropping showed the long axis of the coronary sinus and the ostium of the significantly dilated middle coronary vein. B. A four‐chamber view of TTE presents a significantly enlarged LA, the defect (arrow) between the LA posterior‐lateral wall and the coronary sinus (*). C. An atypical parasternal short‐axis view indicated the long axis of CS and the defect between CS and LA and stenosis entrance of CS.

Figure 22‐3 Left: From three‐dimensional full‐volume imaging, short‐axis surgical views obtained by cropping showed a defect between the LA posterior lateral wall and the CS, as well as part of the CS long‐axis view. Right: A narrow entrance flow from CS to right atrium, the significantly dilated ostium of mid coronary vein, and the defect between the LA posterior wall and the CS.

Figure 22‐4 A. CT coronal view showed LA, RA and coronary sinus connected with LA. B. A three‐dimensional reconstructive image presents a significantly enlarged LA and a huge midcoronary vein, a narrow entrance of CS (arrow), and the coronary sinus (arrow).

Chapter 23

Figure 23‐1 The chest roentgenogram showed a bilateral ground‐glass pattern, which was consistent with pulmonary edema.

Figure 23‐2 Transesophageal echocardiography short axis view showed: A. prolapsed left coronary cusp (LCC, arrow); B. the regurgitant flow through the dissected LCC (arrow); C. TEE long axis view showing the prolapsed LCC, which mimicked a wreath drifting chaotically into the left ventricular outflow tract with severe aortic regurgitation (AR) (arrow).

Figure 23‐3 A. The intraoperative picture demonstrates the laceration at the bottom of left coronary (arrow shows point of laceration). B. The dissected LCC was transparent with another two pieces of rupture structures.

Chapter 24

Figure 24‐1 Transthoracic echocardiogram. Parasternal short axis view at great vessel level showed that the configuration of aortic leaflets was not clear but they were thickened with calcification; there was an aortic right coronary sinus aneurysm (about 19 mm × 42 mm), which pressed the right ventricular outflow tract (the narrower width was 6 mm). There was moderate pericardial effusion.

Figure 24‐2 A. Multiplanar reconstruction of aortic root short‐axis view showed that there were two aneurisms from the valve junction points of the bicuspid annulus respectively, which were filled with contrast agent. The cross‐section of larger one (∆, about 17 × 47 mm) was located at the front left of the aortic root, which oppresses right ventricular outflow tract (RVOT); the smaller one was located at the right rear of the aortic root (*, about 11 × 19 mm) and communicated with the right sinus. B. The oblique‐coronal of maximum intensity projection showed ascending aorta (AA) was dilated. Two aneurysms (∆ and *) from the bicuspid annulus could be seen in this view. C. Computed tomography volume rendering imaging showed that the ascending aorta (AA) was dilated. Two aneurysms (∆ and *) from the bicuspid annulus could be seen and the right coronary artery (RCA) originated from the superior margin of the right coronary sinus.

Figure 24‐3 Computed tomography virtual endoscopy (CTVE). A. The imaging showed an aortic bicuspid deformity with valve thickening and calcification. There was a small defect at the right anterior sinus (arrow). The right coronary artery originated from the superior margin of right anterior sinus, and the left coronary artery originated from the left coronary sinus (arrow). B. The opening of valves was restricted, which was consistent with stenosis (☆).

Figure 24‐4 The pathology result. The aortic valve contain fibrosis with hyalinization, myxoid degeneration and calcification, a large amount of neutrophils and lymphocytes infiltrating connective tissue; the results were consistent with chronic inflammation.

Chapter 25

Figure 25‐1 Electrocardiogram: sinus rhythm, Q‐wave presented with T‐wave inversion in leads II, III, aVF, V6‐V9.

Figure 25‐2 Coronary intravascular ultrasound imaging: A. Coronary artery intima were concentrically thickened, which was in line consistent with the change of vasculitis. B. Transthoracic echocardiography four chamber view showed that the left ventricle and atrium were enlarged.

Figure 25‐3 Cardiac magnetic resonance imaging (MRI). The ventricular short‐axis view showed the myocardial perfusion was significantly reduced (arrows) in the lateral and inferior walls of left ventricle (A). Gadolinium‐DTPA delayed‐enhancement magnetic resonance imaging identified the left ventricular multiple abnormal enhancement, consistent with myocardial fibrosis (arrows) (B).

Figure 25‐4 Computed tomography three‐dimensional reconstruction imaging showing that all coronary arteries are thinner than normal.

Chapter 26

Figure 26‐1 Parasternal long‐axis view (left) and short‐axis view (right) showed aortic intramural hematoma.

Figure 26‐2 A. Supersternal notch aortic long‐axis view showed that the aortic dissection was beginning at descending aorta, and formed true and false lumens. B. A flap was noted in the aortic arch. C. Supersternal notch short‐axis view showed flaps in aortic arch. D. Long‐axis views with color Doppler showed true and false lumens. Computed tomography imaging of descending aorta (E) and descending aorta short axis view by echocardiography (F) showed true and false lumens.

Figure 26‐3 A. Echocardiographic abdominal aortic long‐axis view with color Doppler showed three color flows from true lumen into false lumen. B and C. Computed tomograpy imaging showed the dissection of abdominal aorta with true and false lumina.

Figure 26‐4 Computed tomography images (different phase) showed the aortic dissection from beginning of descending aorta dawn to abdominal aorta (A, B, and C).

Chapter 27

Figure 27‐1 The transthoracic echocardiogram. Parasternal long axis view without (A) and with color Doppler (B) showed mild aortic regurgitation (arrow) and a giant cystic mass significantly pressed the left atria: the left ventricular inflow tract was almost obstructed by cystic mass resulting in high velocity inflow of the mitral valve. A two‐dimensional atypical apical four‐chamber view (C) showed a cystic mass (with spontaneous contrast and a big thrombus) compressing the right and left atria. The mass blocked both ventricle inflow tracts. A three‐dimensional apical five‐chamber view (D) showed the cystic mass compressing the right and left atria blocking mitral inflow tract.

Figure 27‐2 A. A two‐dimensional apical four‐chamber view with color Doppler showed the giant cystic mass was in position between the right and left atria, the velocity of tricuspid inflow was high by color Doppler. B. With the transesophageal echocardiography (TEE), the long‐axis view showed that the left atrium was significantly compressed by the aneurysm and the mitral inflow tract was blocked by the aneurysm. C and D. After operation, the TEE longitudinal view showed the mitral inflow tract and mitral valve were normal with a normal laminar flow.

Chapter 28

Figure 28‐1 Transthoracic echocardiography. A. Transthoracic echocardiographic four‐chamber view with color Doppler showed marked enlarged right atrium and ventricle with moderate to severe tricuspid regurgitation. B. Parasternal short‐axis view showed significant thickening of the intimal in left and right pulmonary arteries (arrow). C. Parasternal short‐axis view with color Doppler showed turbulence color signal in the left pulmonary artery (arrow) and no flow signals within the right pulmonary artery.

Notes:

LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle; AO, aorta.

Figure 28‐2 Computed tomographic pulmonary angiography and volume reconstruction images. A. Short‐axis view showed the occluded right main pulmonary artery (yellow arrow) and left main pulmonary artery stenosis (red arrow). B. Short‐axis view showed the right main pulmonary artery was opened with severe stenosis (yellow arrow) and left main pulmonary artery stenosis was improved (red arrow) after therapy. C. Same view showed right and left pulmonary stenosis become more severe after 2 years. D. Computed tomography reconstruction image showed left pulmonary artery stenosis (red arrow) and the occluded right main pulmonary artery (yellow arrow) at first admission.

Notes:

AO, aortic; PA, pulmonary artery; LPA, left pulmonary artery; RPA, right pulmonary artery; LPV, left pulmonary vein.

Chapter 29

Figure 29‐1 Transthoracic two‐ and three‐dimensional echocardiography: A. Apical three‐chamber view reveals the rupture (arrow) of LV lateral‐posterior wall. B. Apical three‐chamber view with color Doppler shows the shunt entering the pseudoaneurysm. C. Three‐dimensional echocardiography displays the orifice of rupture (arrow). D. Apical four‐chamber view shows the rupture hole and the pseudoaneurysm. E. Apical four‐chamber view with color Doppler indicates the shunt from LV into pseudoaneurysm. F. Three‐dimensional echocardiography illustrates the orifice of rupture (arrow).

Notes:

RV, right ventricle; LV, left ventricle, RA, right atria; LA, left atria; P‐An, pseudoaneurysm.

Figure 29‐2 Computed tomography image: A. The coronal plane of three‐dimensional reconstruction cardiac CT shows the basal segment of left ventricular lateral‐posterior wall has ruptured and a large pseudoaneurysm has formed. B. The front view indicates the pseudoaneurysm (8.7 × 7.8 cm) located beside the left ventricular posterior‐inferior wall.

Notes:

RV, right ventricle; LV, left ventricle, RA, right atria; LA, left atria; P‐AN, pseudo aneurysm; SVC, superior vena cava; AO, aorta; PA, pulmonary artery.

Chapter 30

Figure 30‐1 Transesophageal echocardiographic examination. A. Upper esophageal aortic arch long‐axis view demonstrating moderate atheroma (white double arrow) with a complex ulcer (black arrow). B. Cross‐sectional view of the aortic arch showing the ulcer (black arrow) and the atherosclerotic plaque (white double arrow). C. Color‐flow Doppler image showing flow through the complex ulcer at the aortic arch. D. Small mobile strand‐like densities (arrow) seen in the ulcer suggestive of vegetation along the margin of the defect.

Figure 30‐2 Contrast‐enhanced chest CT demonstrating: A. an ulcerated atherosclerotic plaque measuring 1.1 cm × 1.6 cm affecting the aortic arch (arrow). B. The ulcer progressively increased in size (1.5 cm × 2.9 cm) over 3 months despite antibiotics (double arrow). C. Poststenting CT showed the stent deployed at the aortic arch being patent (arrows) and the aneurysm remained stable in size a few months later.

Chapter 31

Figure 31‐1 Electrocardiography showed a complete right bundle branch block, and ST elevation on leads II, III, and aVF, V2‐V6.

Figure 31‐2 Angiogram showed the proximal segment of left anterior descending coronary was total occluded (arrow).

Figure 31‐3 Apical two‐chamber view showed apical myocardial perforation (2 mm in diameter) connected with a small apical aneurysm (10 × 5 mm) covered by an intact epicardium (A), which communicated with left ventricular cavity demonstrated by color Doppler (B). Follow‐up echocardiography was performed 8 days after infarction. There was a small thrombus at apex and the false aneurysm could not be seen (C).

Figure 31‐4 Cardiac MRI. A. Cine (SSFP) CMR imaging of a two‐chamber view in the diastolic phase. A diverticulum‐like cavity (arrowhead) with thrombus (white arrow) inside can be clearly observed. B. Cine imaging of a two‐chamber view in the systolic phase. A diverticulum‐like cavity disappeared, which indicated the formation of an aneurysm; the intact epicardia could be seen in this phase (white filled arrow), which was consistent with an subepicardial aneurysm. The thrombus (black arrow) still could be seen in LV apex. C. Late gadolinium enhancement imaging of the short axis. The scar (arrowhead) was demonstrated by enhanced myocardium, while significant microvascular obstruction (MVO) was detected as hypo‐enhancement (white arrow) within the necrotic area. D. Late gadolinium enhancement imaging of the two‐chamber view. Enhanced myocardium was detached in the apex. Thromboses (open arrow) can be seen in the LV and inside the aneurysm.

Figure 31‐5 Gross pathological examination showed that the epicardium of apical surface was integrity (1*) but the endocardium and muscle‐layer structure was ruptured (2, arrow) and covered by thrombus (3 and 4). Histological examination showed the epicardium was integrity (arrow) with fibrous tissue and a small amount of myocardial cells (5).

Chapter 32

Figure 32‐1 Transthoracic echocardiography. A mass was seen in the apex of the parasternal short‐axis view (A), the apical four‐chamber view (B), and in the three‐dimensional four‐chamber real‐time image (C). Cine cardiovascular magnetic resonance imaging delineates the apical thrombus; late gadolinium enhancement imaging clearly confirms the avascular nonenhancing thrombus (D–F small arrow) close to the transmural infarcted myocardium (bright hyper enhanced, longer arrows).

Chapter 33

Figure 33‐1 Transthoracic echocardiography showed a mural mass (16 × 53 mm) (A) attached to the left atrial posterior wall, which protruded across the mitral valve during diastole. Another mass (15 × 30 mm) was seen infiltrating the anterior mitral leaflet (B). M‐mode echocardiography of mitral valve of this case showed the mass filled in the mitral inflow tract. The two masses caused dynamic obstruction of the mitral inflow with high‐color Doppler velocity (C and D).

Figure 33‐2 Histologic photomicrograph. The tumor consists of spindle‐shaped cells with pleomorphic nuclei lining anastomosing vascular spaces. Mitotic figures and areas of hemorrhage and necrosis can also be found. These findings support the diagnosis of angiosarcoma.

Figure 33‐3 The follow‐up echocardiography found a recurrence of tumor attached to the anterior mitral leaflet.

Chapter 34

Figure 34‐1 The subxiphoid window of transthoracic echocardiography showed a suspicious mass (indicated by a white arrow) moving within the left atrium.

Figure 34‐2 The transesophageal echocardiography: A. View at 45° showed a 1 cm echogenic mass (indicated by a white arrow) attached to left atrial wall. B. The transesophageal echocardiography at the bicaval view clearly demonstrated a frond‐like mass with a stalk (indicated by a white arrow) attached to the left atrial wall. The features were compatible to papillary fibroelastoma.

Figure 34‐3 Computed tomography image. A. The four‐chamber view from multidetector computed‐tomography could not identify any suspicious mass in the left atrium. B. The four‐chamber view from cardiac magnetic resonance imaging should be more sensitive in detecting small cardiac structure but could not visualize any mass in the left atrium in our case.

Chapter 35

Figure 35‐1 An electrocardiogram showed ST elevation 0.1–0.2 mv with T‐wave bidirection on I, II, III, AVL, V2‐V6 leads with paroxysmal ventricular tachycardia (VT).

Figure 35‐2 Echocardiography: A. There was a large mass at left ventricular posterior‐lateral wall within pericardium. B. Computed tomography. There was a large fat density lesion with a size of 10.0 × 9.5 × 5.2 cm in the left ventricular lateral‐posterior wall. C. A cardiac MRI scan showed a large lesion with the size of 8.5 × 8.3 × 5.9 cm in the pericardium connected with the left ventricular and left atrial wall. D. Histological section shows mature adipose tissue intermixed with myocardium, and thinning fibrous connective tissue surrounding it.

Chapter 36

Figure 36‐1 A. Two‐dimensional echocardiography. A subcostal short axis view showed a mass between the right atrium and the left atrium. B. Contrast‐enhanced computed tomography showed a tumor located between the left atrium and right atrium. C. The coronary angiography showed the majority of the blood supply to the mass was from the branch of the right coronary artery.

Chapter 37

Figure 37‐1 Echocardiography: A. Parasternal long‐axis view showed a huge mass occupying most of the left atrium, with blood flow within the tumor on color‐Doppler examination. B. Modified four‐chamber view showed the mass protruding into the left ventricle during diastole. C. On postoperative day 38, a parasternal long‐axis view of echocardiography revealed a small mass attached to the atrial septum. D. A modified parasternal short‐axis view showed another mass in the left atrial appendage.

Figure 37‐2 Left. Gross appearance of the excised tumor showing hemorrhagic and necrotic areas. Right. Histology revealed roundish tumor cells with pleomorphic nuclei and large eosinophilic cytoplasm that are typical of rhabdomyosarcoma. Histological examination of the excised tumor mass revealed typical features of a rhabdomyosarcoma.

Figure 37‐3 There are several soft tissue masses in the left atrium demonstrated by CT 60 days after operation, which suggested recurrence of the tumor. A. A CTA four‐chamber view showed three masses in the left atrium. B. A CTA short‐axis view showed several masses in the left atrium.

Chapter 38

Figure 38‐1 A. The parasternal long‐axis view showed an echo‐dense mass attached to the left ventricular anterior papillary muscle (arrows), extended to the anterior mitral valvular chordae (oval arrows), LVOT, and aortic root (open arrows). B. The apical five‐chamber view demonstrated the mass in the LVOT extended into the aortic root through the aortic valves. C and D. The apical four‐chamber view illustrated that the mass was on the mitral valvular chordae and papillary muscle.

Figure 38‐2 The series of parasternal long axis views (A, B, C, D) illustrated the mass (diamond arrows) in aortic root was closed to the orifice of RCA (open arrows) and swung into the RCA during cardiac circle.

Figure 38‐3 A. Cardiac CT coronal view showed a big mass with a long tail (white arrows) extended from left mid‐ventricular via LVOT into the ascending aorta through the aortic valve. B. The CT cardiac long axis view clearly illustrated the mass on the papillary muscle, extended to the mitral valvular chordae, and appeared in the aortic root, invaded into right Valsalva sinus (*). C. The CT short‐axis view showed the mass was on the papillary muscle and mitral valvular chordae.

Figure 38‐4 The appearance of the cardiac mass (arrow) during operation.

Figure 38‐5 The gross appearance of the mass. Part 1 was on the papillary muscle. Part 2 was on the mitral valvular chordae. Part 3 was in the LVOT. Part 4 was in the aortic root.

Chapter 39

Figure 39‐1 Chest X‐ray. A. Posterior‐anterior view showed that the cardiothoracic ratio was increased, and a high density was noted behind the heart (arrow). B. A left lateral view showed an enlarged left atrium and an abnormally high density (arrow) at the region of the lower left pulmonary hilar.

Figure 39‐2 A. An echocardiographic parasternal long‐axis view showed a mass (*) in the left atrium and a blocked left ventricular inflow tract. B. An atypical four‐chamber view showed a mass (*) in the left atrium connected with mass in the left lower pulmonary vein. C. MRI 4‐chamber imaging showed a mass (*) in the left atrium and connected with mass in the left lung.

Figure 39‐3 Pathology: Left. Gross examination: left lung lower lobe and left atrial tumor with smooth surface, size of 3.5 cm × 2.5 cm. Middle: Gross examination: the left inferior pulmonary vein and left lower lung hilum, and mass with dumbbell shape and clear boundary but no capsule; the larger part was in the left atrium, the small part was in the lung, its size was 1.0 cm × 1.0 cm × 0.5 cm. The tumor sections were homogeneous solid, gray white, and hard. Right: Histologic examination revealed the tumor consisted of spindle‐shaped cells and myxoid stroma with infiltration of lymphocytes, plasma cells, and monocyte inflammatory cells.

Chapter 40

Figure 40‐1 Transthoracic echocardiography: A. A parasternal short‐axis view shows a soft echogenic mass in the right atrium and extending into the right ventricle to the right outflow tract. B. Apical four‐chamber views during diastole; the right inflow tract was obstructed by a mass. The right atrium was significantly enlarged. C. A long strip mass was seen in the inferior vena cava and extended into the right atrium.

Figure 40‐2 A computed tomography image showed a big mass in right atrium (A, *) extending into the right ventricle through the tricuspid valve (B, *). An abdominal CT scan showed a long strip mass in the inferior vena cava extending into the right atrium (C, arrows).

Chapter 41

Figure 41‐1 Cardiac CT showed a large hematoma (arrows) measuring 5.5 cm × 3.5 cm × 3.3 cm at the posteroinferior aspect of the left atrium, which was thought to be extracardiac.

Figure 41‐2 Transthoracic echocardiography. A parasternal long‐axis view (A), parasternal short‐axis view (B) and apical four‐chamber view (C) showed a smoothly contoured echogenic mass (*) measuring 3.0 cm × 4.2 cm in the posterior left atrial wall. The left atrial wall was clearly delineated (arrows), raising the possibility of left‐atrial haematoma. The outer cardiac border (black arrows) could be clearly delineated on the parasternal short‐axis view, making the diagnosis of extracardiac mass unlikely.

Figure 41‐3 A. Contrast echocardiography. A parasternal long‐axis view showed a nonenhancing mass in the posterior left atrial wall (arrows) and excluded the diagnosis of pseudoaneurysm of the left atrium. The mass measured 2.4 cm (double arrow). B. Contrast echocardiography. A parasternal long‐axis view demonstrated that a nonenhancing mass had reduced in size significantly. The mass measured 1.6 cm (double arrow).

Figure 41‐4 Transthoracic echocardiography. A parasternal long‐axis view (A), parasternal short‐axis view (B) and modified apical 4‐chamber view (C) showed a cystlike structure (*) measuring 2.3 cm × 3.9 cm. The dissection flap in the left atrial wall (arrows) was clearly visualized. Again, the outer cardiac border (white arrows) could be clearly visualized, excluding the diagnosis of extracardiac mass.

Chapter 42

Figure 42‐1 Case 1. Transthoracic echocardiogram. A. Parasternal short‐axis view at great‐vessel level showed a large mass almost completely filling right atrium, penetrated into right atrial free wall, tricuspid annulus (∆) and ventricular free wall (*), resulting in functional tricuspid stenosis (arrow). There was large amount of pericardial effusion. B. Contrast‐enhanced echocardiography of four‐chamber view showed a lobulated mass in right atrium and thickened right ventricular free wall (red *). C. The bright blood SSFP sequence MRI showed a large, lobulated mass fill in the right atrium, invading right ventricular free wall and tricuspid annulus. Case 2. Transthoracic echocardiogram. D. Four‐chamber view showed a large mass in the right atrium, penetrating the interatrial septum (*), right atrial lateral wall (arrow), and tricuspid annulus (∆). E. The atypical four‐chamber view showed the mass in the right atrial cavity and extended into the RA roof, the lateral wall and part of tricuspid annulus (Ф). F. The bright blood SSFP sequence MRI imaging showed a large mass in the right atrium, penetrating interatrial septum and tricuspid annulus. A small amount of pleural effusion was seen.

Notes:

LV, left ventricle; RV, right ventricle; LA, left atrium; RA, right atrium; AO, aortic valve; PA, pulmonary artery; IVC, inferior vena cava.

Figure 42‐2 Case 1. A. The surface of RA was dark red appearance (white arrow), which resulted from malignant tumor infiltration. B. The gross appearance of gelatinous, friable fragments in the kidney basin were cleared from right atrium. C. Histological examination confirmed that the mass was diffuse lymphoma (hematoxylin–eosin stain, original magnification × 400). D. Histological examination using immunochemical staining showed cytoplasmic expression of CD79a (original magnification × 200).

Notes:

RV, right ventricle; PA, pulmonary artery; RA, right atrium.

Chapter 43

Figure 43‐1 Case 1. Transesophageal echocardiography showed significant expansion of the left atrial appendage (4.7 × 2.6 cm

2

) with spontaneous echo contrast, and a pedunculated mass (3.6 × 1.8 cm

2

). After thrombolytic therapy, the mass was shrinking gradually and almost dissolved (A–D).

Figure 43‐2 Case 2. Transthoracic echocardiography indicated mitral stenosis with significantly dilated left atrium (LA) and a subtle echo density in the top of the LA closing to the atrial septum in the parasternal and apical four‐chamber views (A and B*); a definite mass in the LA could be seen in subcostal view (C*).

Figure 43‐3 Cardiac CT scan demonstrated a left atrial mass and left atrial enlargement.

Figure 43‐4 These images were obtained from several cases to show the atrial pouch on the left side (A and B, arrows) and right side (D, arrows). An image with contrast (C) shows there are no microbubbles through the atrial septum pouch. A patent foramen ovale with color flow (E). A contrast echo image showing microbubbles through PFO (F, arrow).

Figure 43‐5 This image was obtained from Case 3. It shows a thrombus (arrow) within the left atrial (LA) septal pouch (A, arrow). An image (Case 4) shows a tiny thrombus arising from the right atrial (RA) septal pouch (B, arrow).

Chapter 44

Figure 44‐1 Echocardiography: A. Apical four‐chamber view showed a huge heterogeneous mass (5.7 × 5.1 cm) filling the right atrium, and a positive agitated saline test with right to left shunting. B. Subcostal four‐chamber view with agitated saline contrast showed a huge mass in the right atrium. C. Subcostal view showed dilated inferior vena cava and hepatic vein.

Figure 44‐2 Computed tomography images showed there is a large (8 cm deep × 7 cm wide × 11 cm long) irregular mixed hypodence anterior mediastinal mass with fat density or cystic change. The mass invades and protrudes into the right atrium.

Chapter 45

Figure 45‐1 Echocardiography. A. Apical four‐chamber view demonstrates a long strip in the right atrium extending into ventricle. B. A subcostal view shows a long strip in the inferior vena cava extending into RA.

Figure 45‐2 Computed tomography image showed a large left renal cell carcinoma.

Figure 45‐3 Magnetic resonance image showed a long linear filling defect inside the left renal vein to the confluence of the left renal vein with the inferior vena cava, along the retro hepatic segment of IVC and extending into the right atrium and possibly to the tricuspid valve level.

Chapter 46

Figure 46‐1 A series of transthoracic echocardiography images obtained over 5 years was reviewed. A. Five years ago, a pericardial mass (1.0 × 1.2 cm) and moderate effusion were seen in parasternal short‐axis view. B. Four years ago, the mass had grown bigger (2 × 2 cm), partially compressing the right ventricle (RV). C. Two years ago, the mass had grown in size compressing the RV more, with a plentiful blood supply. D. One year ago, the parasternal long‐axis view showed the RV was severely pressed by the pericardial mass. E and F. After 5 years, the RV was almost completely compressed by the huge vascular pericardial mass (5.8 cm × 8 cm).

Figure 46‐2 Echocardiography. A. Atypical short axis view showed the size of the mass was 5.8 × 8 cm. B. The mass was clearly seen within the pericardial space without penetrating into the right ventricular wall. Apical four‐chamber view with color Doppler showed moderate tricuspid regurgitation. C. The Doppler recording showed the peak velocity of tricuspid regurgitation is mildly elevated.

Chapter 47

Figure 47‐1 Transthoracic 2‐D echocardiography examination revealed: A. The parasternal long‐axis view showed a large mass (*) in the left atria, obstructing into the mitral inflow tract and a small mass (*) in the right ventricle. The systolic function of the left and right ventricles was normal. B. An apical four‐chamber view showed a large mobile mass (*) obstructing into the mitral valve. A small round (*) mobile mass was seen in the left ventricle and the right atrium. C. A parasternal short‐axis view showed three mobile masses (*) within the left atrium, right ventricle and atrium separately.

Notes:

LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle; AO, aorta.

Figure 47‐2 The characteristic of histology examination from left buttock mass biopsy is consistent with undifferentiated spindle‐cell sarcoma.

Chapter 48

Figure 48‐1 Electrocardiogram showing sinus tachycardia with nonspecific ST segment changes.

Figure 48‐2 Chest X‐ray anteroposterior chest radiograph showed interstitial and alveolar pulmonary edema.

Figure 48‐3 The results of cardiac longitudinal strain showed that the LV global longitudinal strain was significantly impaired excepting apex (A); it partially recovered after 2 weeks (B) and totally recovered three month later (C).

Figure 48‐4 Cardiac magnetic resonance T2‐weighted short tau inversion recovery (STIR) imaging showed myocardial edema in the intraventricular septum, anterior and lateral wall of left ventricle (red arrow). Pericardial effusion is detected as hyperintense (A). Early T1‐weighted (early gadolinium enhancement [EGE]) images showed patch hyperintense in myocardia in the washout phase (B). Late gadolinium enhanced areas were detected in the subepicardial layers of the LV inferolateral wall and in the intraventricular septum of short‐axis image (C) and in LV lateral wall of four‐chamber image (D).

Chapter 49

Figure 49‐1 Case 1: Diffuse low voltages (presence of QRS voltage amplitude <0.5 mV) in all limb leads with QS pattern in pericardial leads V1‐4 (top). Case 2: Diffuse low voltages (≦0.5 mV) in all limb leads (bottom).

Figure 49‐2 Two‐D echocardiography images recorded from Case 1: A. The parasternal long‐axis view shows left atrial enlargement, severe concentric left‐ventricular hypertrophy. There were echogenetic dots diffusing in the myocardium. There is small amount pericardial effusion and moderate pleural effusion (PE). B. The aortic level of parasternal short axis view shows aortic valves and annulus are thickened and both of atriums are enlarge. C. The basal level of parasternal short‐axis view shows LV walls and mitral valves are thickened, there is small amount pericardial effusion. D. The middle level of the parasternal short‐axis view shows thickened LV walls and pericardial effusion. E. The apical four‐chamber view indicates both of atriums enlargement with thickened interatrial septum, and LV hypertrophy. F. An apical two‐chamber view shows concentrated LV hypertrophy. G. An apical three‐chamber view shows LV hypertrophy and pericardial effusion. H. An apical three‐chamber view with color Doppler shows aortic valvular regurgitation. I. The subcustal four‐chamber view indicates that the RV free wall is thickened.

Figure 49‐3 Doppler recordings of Case 1: A. The mitral inflow Doppler recording showed E/A >2.5, deceleration time = 116 ms. B. The peak velocity of mitral annulus was 2.3 cm/s, and E/e’ was 32.5. C. The peak velocity of tricuspid regurgitation was elevated (346 cm/s).

Figure 49‐4 Two‐D echocardiography images recorded from Case 2: A. The parasternal long axis view shows left atrial enlargement, mild concentric left ventricular hypertrophy. B. The aortic level of parasternal short axis view shows aortic valves and annulus are thickened. C. The basal level of parasternal short axis view shows LV walls and mitral valves are thickened. D. The apical level of parasternal short axis view shows thickened LV walls. E. The apical four‐chamber view indicates left atrial enlargement with thickened inter atrial septum, and concentrate LV hypertrophy; there is localized pericardial effusion. F. Apical three‐chamber view shows concentrate LV hypertrophy. G. Apical two‐chamber view shows LV hypertrophy.

Figure 49‐5 A two‐D strain image of Case 2 showed the LV longitudinal (A) and circumferential (B) strain reduced especially in septal and anterior walls; the basal and apical rotation were decreased and desynchronized resulting in a decreased LV twist (C); the radial strain rate showed that the velocity of early diastole was decreased in this 43‐year‐old woman (D).

Figure 49‐6 A. A four‐chamber steady‐state free precession image of Case 1 with cardiac amyloidosis shows diffuse thickening of the myocardium and moderate atrial enlargement. B. A four‐chamber view from a postgadolinium delayed enhancement image shows widespread enhancement in the right and left ventricular myocardium involving both the subendocardial and entire myocardium of the LV from basal to apical regions, and RV wall. C. Two‐chamber steady‐state free precession image of shows diffuse thickening of myocardium and moderate left atrial enlargement. D. Two‐chamber long‐axis views from postgadolinium delayed enhancement images show widespread enhancement in the left ventricular myocardium.

Chapter 50

Figure 50‐1 Electrcardiogram: Sinus rhythm with a right bundle branch block pattern and old anterior myocardial infarction (V4‐6 QS pattern).

Figure 50‐2 Echocardiography: A.An apical four‐chamber view showed the apical aneurysm and left ventricle hypertrophy, most pronounced at mid‐ventricular, the left ventricular outflow tract was normal. B. The apical three‐chamber view at early diastole showed left ventricle hypertrophy, but the apical wall was thin. C.The apical three‐chamber view at early systole showed mitral regurgitation and normal blood flow in the left ventricular outflow tract. D. The apical three‐chamber view at the end systole showed mid‐ventricular hypertrophy causing LV obstruction and apical aneurysm.

Figure 50‐3 The cardiovascular magnetic resonance four‐chamber, two‐chamber and short axis of mid‐ventricular level views showed late gadolinium enhancement involving the interventricular septum, anterior, posterior, and apical wall (A, B, C. white arrows) consistent with fibrosis (D) The cardiovascular magnetic resonance four‐chamber view demonstrates LV hypertrophy with mid‐ventricular obstruction and an apical aneurysm.

Notes:

LA, left atrium; IVS, ventricular septum, LV, left ventricle; RV right ventricle; RA, right ventricle.

Chapter 51

Figure 51‐1 The initial ECG showed frequent premature ventricular complexes (A). The second ECG, after a few minutes, showed ventricular tachycardia (B). Direct‐current cardioversion (DCCV) was delivered and the rhythm was reverted instantly back to sinus. T‐wave inversions were seen from leads V1 to V3 (C).

Figure 51‐2 Transthoracic echocardiography four‐chamber (A), parasternal long (B), short (C) and subcostal four‐chamber (D) views showed a mildly dilated right ventricle.

Figure 51‐3 Cardiac magnetic resonance imaging four‐chamber view showed a dilated right ventricle (A and B) with focal aneurysm (C, arrow) at the right ventricle and fatty infiltration in the myocardium (D, arrow).

Chapter 52

Figure 52‐1 An electrocardiogram showed Wolff–Parkinson–White syndrome with very high voltage of the left ventricle (SV1 + RV5 = 13.2 mV) and inverted T‐wave.

Figure 52‐2 Electron microscopic examination revealed some autophagic vacuoles containing glycogen particles.

Figure 52‐3 The transthoracic echocardiography parasternal short (A) and long‐axis (B), apical four‐chamber (C) and three‐chamber (D) views showed severe LV concentric hypertrophy.

Figure 52‐4 Cardiac magnetic resonance imaging (MRI): The MRI short‐axis view showed severe LV hypertrophy (A, during diastole; B, during systole). Gadolinium‐DTPA delayed‐enhancement magnetic resonance imaging identified abnormal enhancement at the left ventricular apex (arrows) (C).

Chapter 53

Figure 53‐1 Parasternal long‐axis (A), short‐axis (B) and apical four‐chamber (C) views revealed thickness of left ventricular walls and right ventricular free wall was significantly increased, and the myocardium was apparently echogenic.

Figure 53‐2 Magmatic resonance imaging showed abnormal delayed enhancement signal within the myocardium (A, B, C) and pericardial effusion (C, D, E, F).

Figure 53‐3 Endomyocardial biopsy. Microscopically, myocardial disarray and eosinophilic infiltrate (arrows) can be seen in the myocardial interstitial focal area, which was in line with eosinophils endocarditis and myocarditis.

Figure 53‐4 The left ventricular systolic function estimated by the longitudinal strain of speckle tracking was significantly reduced during acute myocarditis (A), and completely recovered after therapy (B).

Chapter 54

Figure 54‐1 Ventriculography found numerous trabeculations and recesses with honeycomb‐like appearance during diastole (A) and systole (B).

Figure 54‐2 Transthoracic echocardiogram. A. Parasternal short‐axis view shows excessively prominent trabeculations with sinusoids (arrows). B. Parasternal short‐axis view with color Doppler showed excessively prominent trabeculations with blood filling in the sinusoids (arrows). C. An apical four‐chamber view indicated a thickened lateral wall with prominent trabeculations and the apical aneurysm at the end of systole (arrow). D. Apical two‐chamber view indicated the apical aneurysm at the end of diastole (arrow).

Figure 54‐3 A. Magnetic resonance imaging (MRI) showed acquisition with ECG gating, in cine Fiesta sequence (SSFP). At end diastole in the short‐axis view, the increase in subendocardial LV trabeculation in the medial, anterior, and inferior segments was noted. The maximum myocardial ratio of noncompacted (N/C) to compacted thickness was 3 (mean ratio = 2.4). B. Magnetic resonance imaging image acquisition with ECG‐gating. Delayed enhancement at end‐diastole in a four‐chamber view showed the present of delayed myocardial enhancement (arrows), compatible with myocardial necrosis / fibrosis. C. Computed tomography an axial plane showed the apical aneurysm (arrow). D. Computed tomography three‐dimensional reconstruction image showed the apical aneurysm (arrow).

Chapter 55

Figure 55‐1 Transthoracic echocardiography. A large pseudoaneurysm was seen arising from the right side of the ascending aorta (AO) in parasternal short axis view (left). There was a blood flow communication between pseudoaneurysm and RA as well as aorta (arrows at middle and right).

Notes

: AO, aorta; *, pseudoaneurysm; RVOT, right ventricular outflow tract; RA, right atrium; PA, pulmonary artery.

Figure 55‐2 Computed tomography angiogram confirmed the pseudoaneurysm was arising from ascending aorta and communicated with right atrium (arrows).

Notes

: AO, aorta; *, pseudoaneurysm; RA, right atrium; PA, pulmonary artery; RV, right ventricle; LV, left ventricle.

Chapter 56

Figure 56‐1 Echocardiography: A. Parasternal short‐axis view showed bicuspid aortic valve. B. Parasternal short‐axis view showed anterior aortic valve aneurysm. C. Parasternal long‐axis view showed an aneurysm of bicuspid aortic anterior valve (arrow). D. Apical five‐chamber view showed an aneurysm of the bicuspid aortic anterior valve (arrow). E and F. Color Doppler echocardiography demonstrated aortic insufficiency was partially from the perforation of the aneurysm.

Figure 56‐2 Echocardiography: A. An apical four‐chamber showed anterior mitral valve with vegetation (*) and aneurysm (arrow). B. An apical three‐chamber showed anterior mitral valve with vegetation (*) and aneurysm (arrow). C. A transesophageal color Doppler showed blood flow flowing through an aneurysm perforation into the left atrium (arrow). D. A transesophageal echocardiography four‐chamber view showed an aneurysm (arrow) of mitral anterior valve toward the left atrium. E. Surgery field showed the mitral valve aneurysm. F. The gross picture of mitral valve aneurysm.

Chapter 57