Although cardiac tumors can often be seen on transthoracic echocardiography (TTE), their location, size, and relation to surrounding structures are better defined by transesophageal echocardiography (TEE).
The most common primary cardiac tumor is the myxoma. This tumor rarely metastasizes, but it can cause obstruction and frequently embolize, making its immediate removal mandatory. These tumors can also cause regurgitation by interfering with valve function, and they can cause a variety of constitutional symptoms. Myxomas are usually solitary and are located most commonly in the left atrium. However, because they can occur in any chamber and may be multiple, a careful transesophageal echocardiographic investigation of all the cardiac chambers should be conducted preoperatively to be certain that all tumors have been detected and are removed. Myxomas characteristically have cystic spaces caused by hemorrhages and areas of calcification. The base of the tumor may be either broad or narrow, and a careful search should be made for the attachment point. In one patient we studied there was massive calcification that involved the left atrial free wall and protruded into the left atrial cavity, mimicking a myxoma. Heavy mitral annular calcification may also produce a confusing picture, especially if some areas are soft and mobile. Lipomas are characteristically more refractile than a noncalcified myxoma, which may help in distinguishing between them. Tumors such as a leiomyoma or leiomyosarcoma may arise from the wall of a blood vessel and cause obstruction to blood flow. Fibroelastomas often present as irregular mobile masses on valves or chamber walls, emanating from narrow stalks. Because of their embolic potential they should be surgically removed. Large mobile vegetations attached to valves may mimic fibroelastoma or a small myxoma on a valve, but the associated clinical picture, which is suggestive of infective endocarditis, helps in differentiating between them. They must be distinguished from Lambl's excrescences, which are a normal finding in many adults. These are filamentous mobile avascular structures that generally arise at the line of closure of valves and are common in adults. Fibroelastomas are not as thin as Lambl's excrescences and, unlike Lambl's excrescences, they do not arise from the line of closure, but from elsewhere on the valve. Myxomatous thickening or nodules involving the mitral valve may also simulate a small tumor.
Thrombus can mimic a tumor, and the distinction often cannot be made by echocardiography. As with tumors, identifying the point of attachment is important in surgical planning. Although low-flow velocities are often present (and are, indeed, causative) when a thrombus is found, this may not always be the case, and thrombi can occur in the absence of an identifiable precipitating factor. TEE is more sensitive than TTE for the detection of thrombi, particularly in the atrial appendages. Thrombi are generally broad based, rather than pedunculated, and are hyperechoic relative to the myocardium except that there tends to be an echolucent interface between the thrombus and the atrium. This echolucent interface may be used to try to differentiate the thrombus from the tumor, but from a practical point of view, echocardiographic differentiation of the tumor from the thrombus is frequently not feasible.
Thrombi originating in the heart are most often, but not invariably, associated with low-flow regions. In the left ventricle, thrombi commonly attach to hypokinetic or akinetic wall regions, ventricular aneurysms, or occur in the setting of cardiomyopathy.
In the left atrium, thrombus can occur anywhere, but most commonly arises in the left atrial appendage, which is far better imaged with TEE than with TTE. On TEE, the left atrial appendage thrombus must be differentiated from the pectinate muscles and from septa between multiple lobes that not infrequently make up the left atrial appendage. Spontaneous contrast, which occurs characteristically with slow flow, is caused by red blood cell aggregation and is a risk factor for the development of thrombus.
When thrombi originate in the right atrium, indwelling catheters or pacemaker leads are frequently the cause, although migrating emboli from lower extremity veins are occasionally visualized. Interestingly, during transesophageal examination we have visualized thrombi, subsequently confirmed by both surgery and pathology, attached to the mitral valve and in the region of papillary muscles in the normally functioning left and right ventricles, with no clinically or echocardiographically discernible cause. Right-sided tumors must be differentiated from normal structures such as hypertrophied trabeculations in the right atrium or right ventricle and prominent or hypertrophied right ventricular papillary muscles. A prominent eustachian or thebesian valve and Chiari network, as well as a prominent crista terminalis visualized at the junction of the superior vena cava and the right atrium, may also be mistaken for a tumor mass. Abnormal thickening of normal structures, such as lipomatous hypertrophy of the interatrial septum or nonspecific thickening of the “Q-tip” (i.e., left atrial wall invagination or infolding separating the appendage from the left upper pulmonary vein) also may mimic tumor infiltration.
Malignant tumors of the heart are unusual but, when present, they tend to metastasize early. They can often be recognized on the basis of the fact that they deform the walls of the heart. Other tumors, such as melanoma, may produce blood-borne metastases in the heart. Mediastinal tumors such as a leiomyosarcoma may compress or invade the heart, either directly or through vascular accesses such as the pulmonary veins. Because these tumors are vascular, multiple small blood vessels may be imaged within the tumor by color Doppler, especially if the Nyquist limit is kept low. Sclerosing mediastinitis producing narrowing of the systemic and pulmonary veins at their junction with the heart may simulate an extracardiac tumor. Postoperative hematomas also must be differentiated from extracardiac tumor masses.
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FIGURE 9.1. Left atrial myxoma. A–F. A huge left atrial (LA) myxoma (M) with a broad attachment on the atrial septum (AS, arrow in B). C. An area of calcification (closed arrow) in the tumor and an echolucency caused by hemorrhage (open arrow). D. M-mode study of the tumor. E. Associated mild mitral regurgitation (MR) (arrow). F.Postoperative study after removal of the myxoma shows persistence of mild MR. LA, left atrium; LV, left ventricle; MV, mitral valve; RA, right atrium; RV, right ventricle. |
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FIGURE 9.2. Left atrial myxoma. A–D. A huge myxoma (M) is seen in the left atrium (LA) obstructing the mitral orifice in diastole (D). AO, aorta; AV, aortic valve; LAA, left atrial appendage; LV, left ventricle; MV, mitral valve; RA, right atrium. |
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FIGURE 9.3. A–K. Left atrial myxoma. A. The myxoma (M) is seen attached to the base of the atrial septum. B. Another myxoma (M) is seen attached to the lower portion of the atrial septum, with a longer stalk (arrow) than the myxoma in A. C–E. Another patient with a huge myxoma (M) that has a very broad attachment (arrows in C) to the atrial septum (AS). C,D. A calcified area (C) in the tumor. In this patient, systolic anterior motion (SAM) of the mitral valve (MV) and septal thickening and narrowing of the left ventricular outflow tract (LVOT) were also present, consistent with hypertrophic cardiomyopathy. F. Schematic of a left atrial (LA) myxoma obstructing the mitral orifice. G.Specimen of an LA myxoma attached to the LA free wall. H. Specimen of a hemorrhagic, calcified myxoma that was resected. I–K. Another patient with a large lobulated LA myxoma (arrowheads in I and J). The figure shows the myxoma after surgical removal. L–S. LA leiomyosarcoma. A large mass is seen in the LA (arrowheads in L, M in M). N. The mass (arrowheads) invading the LA from the right upper pulmonary vein (RUPV). O. A narrow flow jet (arrow) shows RUPV obstruction. P. A markedly dilated left upper pulmonary vein (LUPV) and its tributaries (arrow). Q. The leiomyosarcoma (M) is seen invading the mediastinum in the vicinity of the right pulmonary artery (PA) and the superior vena cava (SVC). R,S. Multiple blood vessels (arrowheads) within the tumor mass (T) characteristic of vascular tumors such as the leiomyosarcoma. (A and F reproduced with permission from Nanda NC, Mahan EF III. Transesophageal echocardiography. AHA Counc Clin Cardiol Newsl 1990; Summer:3–22. ) AO, aorta; AML, anterior mitral leaflet;AV, aortic valve; LA, left atrium; LV, left ventricle; MV, mitral valve; P, posterior; RA, right atrium; RPA, right pulmonary artery; RV, right ventricle; TV, tricuspid valve. |
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FIGURE 9.4. Left atrial tumor mimic. A,B. A huge nonmobile mass (arrowheads) consistent with a tumor in the left atrium (LA). It appeared to have a broad attachment to the LA free wall (B). C. Spontaneous contrast echoes in LA next to the mass, which was successfully removed. D. The suture line (arrowheads) repairing the LA wall following its resection. E. The resected mass, which was found to be a thrombus and not a tumor at pathology. No etiologic factors were identified. |
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FIGURE 9.5. Left atrial tumor. A small mass consistent with a tumor is seen at the base of the left atrium (LA) appendage in this patient, who presented with symptoms of an embolic stroke. AO, aorta; LAA, left atrial appendage. |
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FIGURE 9.6. Left atrial thrombus/calcification. A. Two large thrombi (TH) are seen in the left atrium (LA). These could be distinguished from tumor by their mobility and the presence of spontaneous contrast echoes seen in other views. B,C. In another patient, heavy calcifications (CAL, arrows) involving the LA free wall are seen protruding into the LA cavity and mimicking a tumor. The findings were verified at surgery and by pathologic examination. AO, aorta; LV, left ventricle; RA, right atrium. |
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FIGURE 9.7. Sequential echocardiographic images showing dislodgement of the left atrial appendage (LAA) thrombus (TH) (arrowhead in A) and its subsequent journey into the left atrium (LA) (B) through the mitral valve (MV) into the left ventricle (LV) (C), and then into the ascending aorta (AA) (D). No residual TH is seen in the LAA (arrowhead in E) subsequent to the peripheral embolization. AO, ascending aorta; LV, left ventricle; RVO, right ventricular outflow tract. (Reproduced with permission from Nekkanti R, Nanda, NC. Left atrial appendage thrombus in transit with peripheral embolization. Am J Geriatr Cardiol 2002;11:60–61. ) |
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FIGURE 9.8. Left atrial tumor mimic. A,B. Nonspecific thickening (arrows) of the invaginated/infolded part of the left atrium (LA) free wall “Q-tip” mimicking a tumor. LA wall infolding is a normal finding at the site where the left upper pulmonary vein (LUPV) enters into the LA and appears as a “septum” separating the LUPV from the left atrial appendage (LAA). AV, aortic valve; RVO, right ventricular outflow tract. |
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FIGURE 9.9. Mitral valve myxoma. A,B. A large tumor (arrows) attached to the atrial aspect of the anterior mitral leaflet. The multiple tiny echolucencies seen within the tumor suggest the presence of hemorrhage, often seen in myxomas. C. The resected specimen. LA, left atrium; LV, left ventricle; Mitral valve (MV) RA, right atrium; RV, right ventricle; TV, tricuspid valve; VS, ventricular septum. |
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FIGURE 9.10. Mitral valve thrombus/myxomatous degeneration. A–C. The prominent echodensity involving the posterior mitral leaflet (PML) was identified as a thrombus (TH) at surgery and on pathologic examination. B. Mild mitral regurgitation (MR) is noted. The arrowheads in (D,E, and G) show two other patients with masses involving the mitral valve (MV) that were found to be thrombi at surgery and pathology. F,H. The resected thrombi from these two patients. No predisposing factors were identified in any of the three patients shown here. I–K. A different patient with a small rounded mass (arrowheads) attached to the base of the PML. The MV showed prolapse and mild MR (arrow in K). Pathologic examination of the resected mass showed myxomatous degenerative changes and no evidence of tumor. AML, anterior mitral leaflet. |
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FIGURE 9.11. Left ventricular myxoma. A–C. A large mass (M) in the left atrium (LA) that appears to be attached to the anterior mitral leaflet (AML). D–F. Further examination showed that the mass actually arose from the left ventricle (LV) and was attached by a long stalk (S) to a papillary muscle (PM). G. In the short-axis view, two separate masses (M1 and M2) together with two separate stalks (arrows) were identified in the region of the papillary muscles. H. An M-mode study demonstrates the mass in the LA only during systole. Note a large arc-like side-lobe (SL) artifact in C. Because of the long stalk, one of the myxomas intermittently prolapsed into the LA, sometimes becoming trapped in that chamber. These tumors were successfully resected. PML, posterior mitral leaflet. (A and G reproduced with permission from Samdarshi TE, Mahan EF III, Nanda NC, et al. Transesophageal echocardiographic diagnosis of multicentric LV myxomas mimicking a left atrial tumor. J Thorac Cardiovasc Surg 1992;103:471–474. ) LA, left atrium; LV, left ventricle; M, myxoma; M1 and M2, two separate masses; MV, mitral valve; RA, right atrium; RV, right ventricle; VS, ventricular septum. |
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FIGURE 9.12. Left ventricular myxoma. A large mass (M; arrows) arising from the apex. Pathology examination demonstrated it to be a myxoma. AL, anterior mitral leaflet;PL, posterior mitral leaflet. LA, left atrium; LV, left ventricle; M, myxoma; RV, right ventricle; T, transverse plane. (Reproduced with permission from Nanda NC, Pinheiro L, Sanyal RS, et al. Transesophageal biplane echocardiographic imaging: technique, planes, and clinical usefulness. Echocardiography 1990;7:771–788. ) |
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FIGURE 9.13. Left ventricular lipoma. A. The lower arrow shows a bright, highly echogenic, and generally homogeneous mass arising from the apical portion of the ventricular septum. The mass (arrow, T) was also well seen in the two-chamber (B) and short-axis (C) views. This elderly female patient underwent angioplasty of the proximal left anterior descending coronary artery subsequent to an episode of chest pain, and the mass was discovered on a follow-up two-dimensional echocardiogram. Consequently, thrombus was considered in the differential diagnosis, along with myxoma and lipoma. There were no obvious wall motion abnormalities. The mass was surgically removed and found to be a lipoma. D. Patch repair (arrow) of the apical ventricular septum following lipoma resection. E,F. Mild turbulence (arrows) is seen in the region of the patch, but no defect is present. The resected lipoma and a myxoma removed from another patient were studied in vitro by suspending them in a water bath using the same transesophageal probe used for the in vivo study. At the same instrument settings and similar distance from the transducer surface, the lipoma (G) appeared to be significantly hyper-refractile compared to the myxoma (H), except for the areas of calcifications (C in frame I) in the myxoma. I. S indicates the string that suspended the myxoma in the water bath. This study suggests that, in the absence of calcification, a very hyperrefractile mass may be a lipoma rather than a myxoma. LA, left atrium; LV, left ventricle; M, myxoma; RA, right atrium; RV,right ventricle; T, transverse plane. (A,B, and G through I reproduced with permission from Mehta R, Nanda NC, Osman K, et al. Left ventricular lipoma by transesophageal and in vitro echocardiographic studies. Echocardiography 1995;12:283–288. ) |
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FIGURE 9.14. Left ventricular thrombus. A–C. A mass (arrowheads) attached to a papillary muscle in the left ventricle (LV) in a patient with aortic stenosis. This mass was found to be a thrombus (TH) at surgery. LA, left atrium; MV, mitral valve; RA, right atrium; RV, right ventricle. |
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FIGURE 9.15. Aortic valve fibroelastoma. A small irregular mass (arrow in B, transverse plane [T]) in C) is seen attached to the left coronary leaflet of the aortic valve (AV) by a short stalk (A). There was no clinical evidence of endocarditis or significant aortic regurgitation (AR) in this patient. The mass was resected and found to be a fibroelastoma.D. Schematic shows a fibroelastoma. LA, left atrium; LV, left ventricle; RA, right atrium; RVOT, right ventricular outflow tract. |
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FIGURE 9.16. Aortic valve mass. A–D. The mass-like lesion (T) attached to the noncoronary cusp of the aortic valve (AV) in this patient mimics a tumor but is actually a vegetation with typical clinical findings of endocarditis. Note associated severe AR (C). AO, aorta; AR, aortic regurgitation; LA, left atrium; LV, left ventricle; RA, right atrium;RV, right ventricle; RVO, right ventricular outflow. |
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FIGURE 9.17. Aortic leiomyosarcoma. A–F. A mass (arrowheads) in the descending thoracic aorta (DA). Color Doppler examination shows prominent flow signals in the unobstructed portion of the aorta (AO). This makes thrombus unlikely, because associated spontaneous contrast echoes caused by a low-flow state usually are present. Also, no dissection flap is identified. The arrows in A through C and E through H show a large echogenic mass outside the aorta, consistent with hematoma. G,H. A hematoma (arrow, arrowheads) is seen extending on both sides of the descending aorta (DA, AO), even where the tumor mass is not present. At surgery, the mass was found to be a leiomyosarcoma that involved the aortic wall, resulting in perforation that caused the hematoma. |
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FIGURE 9.18. Primary leiomyoma of the inferior vena cava. A,B. The subcostal transverse planes show the large tumor mass (T) clearly attached (S) in the inferior vena cava (IVC). B,C. The portion of the tumor protruding into the right atrium (RA) is highly echogenic, indicative of calcific involvement, whereas the IVC portion has very few highly refractile echo densities, suggesting paucity of calcific deposits. D. Longitudinal plane examination also demonstrates the tumor (T) protruding into the RA. L, liver; LA, left atrium; SVC, superior vena cava. (Reproduced with permission from Loungani RR, Nanda NC, Sanyal RS, et al. Transesophageal echocardiographic findings in primary leiomyoma of inferior vena cava. Echocardiography 1993;10:623–627. ) |
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FIGURE 9.19. Primary leiomyoma of the inferior vena cava (IVC). Surgically resected tumor from the patient shown in Figure 9.17. (Reproduced with permission from Loungani RR, Nanda NC, Sanyal RS, et al. Transesophageal echocardiographic findings in primary leiomyoma of inferior vena cava. Echocardiography 1993;10:623–627. ) |
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FIGURE 9.20. Right atrial myxoma. A,B. A large mass (M) is seen attached by a short stalk (arrow in B) to the right atrium (RA) free wall. At surgery, it was found to be a myxoma. C,D, and E. Two other patients with huge myxomas (arrowheads) in the RA. The echolucencies within the tumor represent hemorrhagic areas. CS, coronary sinus; IVC, inferior vena cava; LA, left atrium; LV, left ventricle; MV, mitral valve; RV, right ventricle; T, transverse plane; TV, tricuspid valve. |
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FIGURE 9.21. Right atrial myxoma. A. Another patient with a mass (M) in the right atrium (RA) is shown. B. The mass is attached by a broad stalk to the RA free wall near the entrance of the inferior vena cava (IVC). At surgery, it was identified as a myxoma and was successfully removed. |
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FIGURE 9.22. A–E. Right atrial thrombus. A. Multiple masses consistent with thrombus (TH) are seen in the right atrium (RA). B–D. Further examination shows them to be components of a single TH. The elongated shape of the TH suggests a possible origin in the leg veins. (D) Bulging of the atrial septum (AS) into the left atrium (LA) (arrowheads) indicates elevated RA pressure. E. A portion of the TH is seen in the LA, presumably having crossed over through a patent foramen ovale. F–L. Impending paradoxic embolus: right atrial TH wedged in the foramen ovale and extending into the LA. The multiple echo densities seen in the RA in (F) are parts of the large elongated TH seen in (G) (left panel). The right panel in (G) shows attachment of a portion of the TH to the eustachian valve (EV). H,I. The TH crosses into the LA (arrow in H). J–L. Gross specimens of the surgically resected TH. AO, aorta; LAA, left atrial appendage; LV, left ventricle; RAA, right atrial appendage; RV, right ventricle; RVO, right ventricular outflow; SVC, superior vena cava. (Courtesy of Drs. Vasu Goli [Birmingham, AL] and T. Narain Srivastava [Jackson, MS].) |
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FIGURE 9.23. Right atrial thrombus. An elongated thrombus (M) is seen in the right atrium (RA). EV, eustachian valve; IVC, inferior vena cava; RAA, right atrial appendage. |
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FIGURE 9.24. Lipomatous hypertrophy of the atrial septum. A–C. The arrows in A and C point to thickening of the atrial septum (AS) that spares the foramen ovale. This is caused by fatty infiltration of the septum and usually has no clinical sequelae. EV, eustachian valve. D,E. Massive lipomatous hypertrophy (arrowheads) affects the entire AS and occupies most of the right atrium (RA) in another patient. F. A third patient with extensive lipomatous involvement of the AS. AV, aortic valve; IVC, inferior vena cava; LA, left atrium; LV, left ventricle; RA, right atrium; RAA, right atrial appendage; RPA, right pulmonary artery; RV, right ventricle; SVC, superior vena cava. (D and E courtesy of Dr. Allan Schwadron, Dothan, AL.) |
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FIGURE 9.25. Papillary fibroelastoma of the tricuspid valve. A,B. Transverse plane four-chamber view shows the tumor (T, M) in the right atrium (RA) in the vicinity of the septal (SL) tricuspid leaflet, but the exact site of attachment of the tumor is not clear. C,D. Longitudinal plane (LP) examination clearly shows the tumor (T, M) arising from the posterior leaflet (PL). These findings were confirmed at surgery. AL, anterior tricuspid leaflet; AO, aorta; IVC, inferior vena cava; LA, left atrium; LV, left ventricle; RV, right ventricle; S, tumor stalk; TV, tricuspid valve. (Reproduced with permission from Maxted W, Nanda NC, Kim KS, et al. Transesophageal echocardiographic identification and validation of individual tricuspid valve leaflets. Echocardiography 1994;11:585–590. ) |
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FIGURE 9.26. Myxoma of the tricuspid valve. A–B. A large mass (M) is seen attached to the anterior leaflet of the tricuspid valve (TV) by a short stalk. Rounded areas of echolucency in the mass suggest hemorrhagic areas within the tumor, characteristic of a myxoma. These findings were confirmed at surgery, and the tumor was successfully removed. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle. |
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FIGURE 9.27. Metastatic melanoma involving the right ventricle. A–G. A huge tumor mass (M,T) is noted in the right ventricle (RV) reaching up to the pulmonary valve (PV). The arrows in (B) and (F) show narrowing of the systolic flow signals in the right ventricular outflow (RVO) produced by obstruction caused by the tumor. G. Color Doppler–guided pulsed Doppler demonstrates a high velocity of 2.02 m/sec in the right ventricular outflow tract (RVOT). H. Right ventricular (RV) thrombus (TH). A thrombus (arrowheads) in the RV imaged from the transgastric approach in another patient. AO, aorta; LA, left atrium; LV, left ventricle; PA, pulmonary artery; RA, right atrium; TV, tricuspid valve. |
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FIGURE 9.28. Thrombus in the pulmonary artery. A–C. Large thrombi (M, C) are noted in the superior vena cava (SVC) and the right pulmonary artery (RPA) in this patient with an infusion catheter, which acted as the nidus for the thrombus (TH). D,E. A large TH (arrowheads in D, arrow in E) is seen in the RPA in another patient. AO, aorta; ASC AO, ascending aorta; LA, left atrium; LV, left ventricle; RA, right atrium. |
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FIGURE 9.29. Thrombotic obstruction of distal left and right pulmonary arteries. A,B. The arrowhead points to a large thrombus (TH) in the distal left pulmonary artery (LPA, A) and in the distal right pulmonary artery (RPA, B). AO, aorta. (Reproduced with permission from Kang SW, Nekkanti R, Nanda NC, et al. Transesophageal echocardiographic identification of thrombus producing obstruction of left pulmonary artery descending lobar branches and bronchial artery dilatation. Echocardiography 2002;19:83–88. ) T, transverse plane. |
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FIGURE 9.30. Thrombotic obstruction of left pulmonary artery (LPA) descending lobar branches. A. The large arrowhead points to the thrombus (TH) and the small arrowhead points to an echolucent area of clot lysis. The arrow shows the extension of the TH into a descending lobar branch of the LPA. B. Turbulent flow signals with prominent flow acceleration are noted in a descending lobar branch (labeled 2). Arrow points to left pulmonary vein (LPV), and arrowhead shows the TH. C. Color Doppler guided continuous-wave Doppler interrogation (arrow) shows a high systolic velocity of 2.2 m/sec and a high diastolic velocity of 1.0 m/sec indicative of significant obstruction. (Reproduced with permission from Kang SW, Nekkanti R, Nanda NC, et al. Transesophageal echocardiographic identification of thrombus producing obstruction of left pulmonary artery descending lobar branches and bronchial artery dilatation. Echocardiography 2002;19:83–88. ) L, longitudinal plane; T, transverse plane. |
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FIGURE 9.31. A–G. Extracardiac tumor. A–C. A tumor (T) is seen posterior to the aortic root bulging into the left atrium (LA). D. Narrowing (arrows) of the left pulmonary vein (LPV) at its entrance into the LA. E. Unrestricted flow through unobstructed right lower pulmonary vein (RLPV) and right upper pulmonary vein (RUPV). F. The tumor wedged between the esophagus and the right pulmonary artery (RPA). G. Narrowing (arrow) of the superior vena cava (SVC) flow jet at its entrance into the right atrium (RA). AO, aorta; AV, aortic valve; LV, left ventricle; MPA, main pulmonary artery; PA, pulmonary artery; RV, right ventricle; RVO, right ventricular outflow. |
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FIGURE 9.32. Mediastinal metastasis from ductal carcinoma of the breast. A. A large mediastinal mass (M) compresses the right upper pulmonary vein (RUPV) and produces aliased flow signals in a 39-year-old woman. B. High-pulse-repetition-frequency Doppler interrogation demonstrates a high peak velocity of 1.5 m/sec with little phasic variation. RA, right atrium. (Reproduced with permission from Samdarshi TE, Morrow WR, Helmcke FR, et al. Assessment of pulmonary vein stenosis by transesophageal echocardiography. Am Heart J 1991;122:1495–1498. ) |
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FIGURE 9.33. Transesophageal two-dimensional echocardiographic demonstration of normal lymph nodes mimicking a mediastinal mass. A–C. The arrowhead points to lymph nodes having a nodular appearance. Inset in (C) reveals the typical venous type flow from a mediastinal vein probably from the hemiazygos/azygos system (V), interposed between the probe in the esophagus and the lymph nodes. D. Demonstrates a small mediastinal artery (A) overlying the vein. Inset in (D) illustrates the typical arterial waveform from this artery. AO, aorta. (Reproduced with permission from Nekkanti R, Nanda NC, Ahmed S, et al. Normal lymph nodes mimicking a mediastinal mass during transesophageal echocardiography. Echocardiography 2003;20:443–447. ) |
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FIGURE 9.34. Transesophageal two-dimensional echocardiographic identification of hiatal hernia. A. Arrowheads point to a few microbubbles present within the hiatal hernia (H). B. Color Doppler examination shows flow signals in the descending thoracic aorta (DA) and in the left upper pulmonary vein (LPV) but not in H. C. Note the thickened inner lining resembling normal stomach mucosa (M). The thickened mucosa results from tubular gastric glands extending down into it from the foveolae. D-F. Arrowheads point to a cloud of echoes (D,E) as well as to an increased number of microbubbles (F) in H following a 10 mL flush of agitated normal saline through an indwelling nasogastric tube.G. Normal stomach imaged in another patient using a transgastric approach shows microbubbles and a thick mucosa (M) measuring 1.3 cm in maximal thickness. (Reproduced with permission from Frans EE, Nanda NC, Patel V, et al. Transesophageal two-dimensional echocardigoraphic identification of hiatal hernia. Echocardiography 2005;22:533–535. ) |
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FIGURE 9.35. Pulmonary vein obstruction following lung transplantation. The arrows in A,C, and D show localized narrowing of the right upper pulmonary vein (RUPV) and lower pulmonary vein (RLPV) following right lung transplantation. In C, the narrowing is seen better with color Doppler than without. B. Pulsed Doppler examination shows a high velocity of 1.82 m/sec, with spectral broadening consistent with some obstruction to the flow. E. Doppler examination of the nonobstructed left upper pulmonary vein (LUPV) shows lower velocities and less spectral broadening. Mild obstruction of the right pulmonary veins in this patient resulted in increased flow through the normal left-sided pulmonary veins, producing flow velocity higher than normal and spectral broadening. This patient did not require surgical intervention and was managed conservatively. LA, left atrium; PV, pulmonary valve. |
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FIGURE 9.36. Sclerosing mediastinitis. This 43-year-old man presented with respiratory failure. A. Contrast-enhanced chest computed tomography (CT) scan at the level of the right upper lobe bronchus. There are bilateral pleural effusions. Abnormal soft tissue is noted between the right upper lobe bronchus, left main stem bronchus, and ascending aorta (AO), as well as the superior vena cava (C). This abnormal tissue also separates the ascending aorta from the superior vena cava. There is dense opacification of the azygous vein (AZ), indicating superior vena caval obstruction and collateral flow. PA, main pulmonary artery. B. Contrast-enhanced chest CT scan at the level of the aortic root. Abnormal soft tissue (m) is noted all around the left atrium (LA). This tissue extends around the interatrial septum on the right and involves the venoatrial junctions of the right and left lower lobe pulmonary veins (arrow). Note the opacification of enlarged azygous (A) and hemiazygous (H) veins resulting from collateral flow. (Reproduced with permission from Kovach TA, Nanda NC, Kim KS, et al. Transesophageal echocardiographic findings in sclerosing mediastinitis. Echocardiography 1996;13:103–108. ) |
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FIGURE 9.37. Sclerosing mediastinitis. Same patient as in Figure 9.28. A. A mass (M) surrounds the left atrium (LA), right pulmonary artery (RPA), and superior vena cava (SVC). B,C. The mass appears to infiltrate and invaginate into the LA and extends up to the base of the left atrial appendage (LAA). This resembles an intracardiac tumor. AO, aorta; AV, aortic valve; PA, pulmonary artery; RA, right atrium; RVO, right ventricular outflow. (Reproduced with permission from Kovach TA, Nanda NC, Kim KS, et al. Transesophageal echocardiographic findings in sclerosing mediastinitis. Echocardiography 1996;13:103–108. ) |
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FIGURE 9.38. Sclerosing mediastinitis. Same patient as in Figures 9.28 and 9.29. A,B. Both the right lower pulmonary vein (RLPV) and right upper pulmonary vein (RUPV) demonstrate obstruction near their entrance into the left atrium (LA). The exact sites of obstruction in the lower and upper pulmonary veins, shown by the arrow and the arrowhead, respectively, mark the transition from laminar (red) to disturbed (mosaic) flow. C. Pulsed Doppler interrogation of the mosaic flow reveals a high velocity of 2.58 m/sec, indicative of obstruction. LV, left ventricle; M, mass; RVO, right ventricular outflow; SVC, superior vena cava. (Reproduced with permission from Kovach TA, Nanda NC, Kim KS, et al. Transesophageal echocardiographic findings in sclerosing mediastinitis. Echocardiography 1996;13:103–108. ) |
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FIGURE 9.39. Sclerosing mediastinitis. Same patient as in Figures 9.28, 9.29, 9.30, 9.31, 9.32, 9.33 and 9.34. A,B. The arrow points to the site of obstruction in the superior vena cava (SVC) near its junction with the right atrium (RA). Color Doppler examination shows a thin mosaic flow jet in (B), indicative of obstruction. C. Pulsed Doppler interrogation reveals a high velocity of at least 1.61 m/sec. LA, left atrium; M, mass; RPA, right pulmonary artery. (Reproduced with permission from Kovach TA, Nanda NC, Kim KS, et al. Transesophageal echocardiographic findings in sclerosing mediastinitis. Echocardiography 1996;13:103–108. ) |
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FIGURE 9.40. Sclerosing mediastinitis. Histology of mediastinal biopsy tissue from the same patient shown in Figures 9.28, 9.29, 9.30, 9.31, 9.32, 9.33 and 9.34. A.Photomicrograph of sclerosing process impinging on mediastinal adipose tissue (Congo red, original magnification × 125). B. Photomicrograph of collagenization of blood vessel wall with narrowing of the lumen (center), a region of cellular fibrosis (above), and a region of acellular fibrosis (below) (hematoxylin and eosin, original magnification 125). (Reproduced with permission from Kovach TA, Nanda NC, Kim KS, et al. Transesophageal echocardiographic findings in sclerosing mediastinitis. Echocardiography 1996;13:103–108. ) |
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FIGURE 9.41. Hematoma following surgery. A large hematoma (H) is noted in the interatrial septum between the right atrium (RA) and left atrium (LA) in A and between the superior vena cava (SVC) (arrowheads) and the LA in B and C. This developed immediately following aortic valve (AV) replacement but did not cause any hemodynamic compromise. The patient had an uneventful course. AO, aorta; RPA, right pulmonary artery. |
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FIGURE 9.42. Hematoma following cardiac surgery. Two different patients with hematoma (H in A, arrowheads in B) that developed around the aortic root following aortic valve replacement are shown. Both had a benign course. AO, aorta; LA, left atrium; LAA, left atrial appendage; SVC, superior vena cava. |
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FIGURE 9.43. Hematoma compressing the right atrium. A huge hematoma (H) compressing the right atrium (RA) and producing tricuspid inflow obstruction (arrowheads inA,B). This developed after replacement with a porcine aortic valve that appeared to be functioning normally. Because of hemodynamic deterioration and severe hypotension, the hematoma was surgically evacuated. LA, left atrium; LV, left ventricle; MV, mitral valve; RV, right ventricle; TV, tricuspid valve. |
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