802
Brief Communications
American
4. Vignola PA, Aonuma K, Swaye PS, Rozanski JJ, Blankstein RL, Benson J, Gosselin AJ, Lister JW. Lymphocytic myocarditis presenting as unexplained ventricular arrhythmias: diagnosis with endomyocardial biopsy and response to immunosuppression. J Am Co11 Cardiol 198&4:812-g. 5. James TN, MacLean WA. Paroxysmal ventricular arrhythmias and familial sudden death associated with neural lesions in the heart. Chest 1980;78:24-30. 6. Emmons PR, Blume WT, DuShane JW. Cardiac monitoring and demand pacemaker in Guillain-Barre syndrome. Arch Neurol 19’75;32:59-61. 7. Greenland P, Griggs RC. Arrhythmic complications in the Guillain-Barre syndrome. Arch Intern Med 1980;140:1053-5. 8. Lichtenfeld P. Autonomic dysfunction in the Guillain-Barrit syndrome. Am J Med 1971;50:772-80. 9. Haymaker W, Kernohan JW. The Landry-Guillain-Barre syndrome: clinicopathologic report of 50 fatal cases and critique of literature. Medicine 1949;28:59-141. 10. Kahn JK, Sisson JC, Vinik AI. QT interval prolongation and sudden cardiac death in diabetic autonomic neuropathy. J Clin Endocrinol Metab 1987;64:751-4.
Right atrial mobile thrombus: Improved visualization by transesophageal echocardiography Tomasz J. Pasierski, MD, Mary E. Alton, MD, Douglas B. Van Fossen, MD, and Anthony C. Pearson, MD. Columbus, Ohio
Right atria1 mobile thrombus is an infrequent but nevertheless life-threatening disease diagnosed by two-dimensional echocardiography. In the last decade, many cases of right atria1 mobile thrombi have been reported but the etiology of this disease remains still not well understood.1-4 In the majority of reports, right atrial mobile thrombus has been associated with severe pulmonary embolism and high morbidity.1-4 Mobile right atria1 thrombi are thought to originate in peripheral veins and subsequently migrate to the right atrium, where they become entrapped. The site of entrapment may be a persistent foramen ovale, the eustachian valve, or a Chiari network. Previous reports have not established whether thrombus may stay within the right atrium without any attachment to cardiac structures. Transesophageal echocardiography is far superior to surface echocardiography in visualizing the interatrial septum and right atria1 structures.5 In this report we describe the first right atria1 mobile thrombus clearly shown by transesophageal echocardiography to have no atria1 attachment point. A 56-year-old white man with a remote history of myo-
From the Ohio State Reprint Means 414134512
Department University
requests: Hall, 1654
of Internal Hospitals.
Anthony Upham
Medicine,
Division
of Cardiology,
C. Pearson, MD, Division of Cardiology, Drive, Columbus, OH 43210-1228.
The 657
March 1992 Heart Journal
cardial infarction in 1983 and chronic obstructive lung disease was admitted to a local hospital because of progressive dyspnea on exertion, prominent weight gain, leg edema, and syncope. Echocardiographic examination, despite its poor technical quality, revealed a right atria1 mass that appeared to be attached to the interatrial septum. The patient was transferred to The Ohio State University Hospitals for further evaluation. On admission, the patient was dyspneic and tachypneic with visible cyanosis. Physical examination was significant for blood pressure of 120/90 mm Hg, a heart rate of 60 beats/min with irregular rhythm, jugular venous distention, expiratory wheezes, and a grade 2/6 apical systolic murmur. The liver was mildly enlarged and there was edema to the level of the mid thigh. The electrocardiogram showed multiple premature supraventricular beats, along with evidence of an old anterolateral myocardial infarction. His medical regimen consisted of digoxin, furosemide, and intravenous heparin. A surface echocardiogram confirmed the presence of a mobile right atria1 mass apparently attached to the interatrial septum that could have been either myxoma or thrombus (Fig. 1). Transesophageal echocardiography was ordered to better define the right atria1 mass. An extremely mobile, elongated, serpiginous mass that nearly filled the entire right atria1 cavity was found (Fig. 2). The inferior and superior vena cava, as well as the interatrial septum, were well visualized but no attachment point of the right atria1 mass was identified. Left ventricular systolic function was depressed (ejection fraction calculated to be 20 70) and anteroapical akinesis along with moderate mitral regurgitation was found. The risk of surgical removal of the thrombus was considered too high because of poor left ventricular function. He was continued on a regimen of intravenous heparin and was started on oral warfarin sodium. During further observation, the patient’s dyspnea diminished and syncope did not recur. A left ventriculogram and coronary angiogram were obtained and showed an ejection fraction of 18% and an occluded left anterior descending coronary artery. No echocardiographic follow-up was performed. The patient died suddenly 2 days later. During attempted resuscitation, he was initially asystolic. Despite mechanical ventilation, adequate oxygenation was never obtained and the blood pressure was unmeasurable. At autopsy a large organized thrombus nearly occluding the right pulmonary artery was found. In the left pulmonary artery a thromboembolus that appeared acute was present. Multiple emboli were found in the peripheral pulmonary artery branches. The most important differential diagnosis for right atria1 thrombus is atria1 myxoma, and visualization of a septal attachment of a right atria1 mass of unknown etiology is of critical importance.6 Transesophageal echocardiography allows for excellent visualization of the entire interatrial septum, contributing to the diagnosis of the character of right atria1 masses. It also allows excellent visualization of the superior vena cava, inferior vena cava eustachian valve, and Chiari network, which may be sites of thrombus entrapment. In this case transesophageal echocardiography demonstrated that thrombus may stay within the right atrium without any attachments. The factors favoring this
Volume Number
123
Brief Communications
3
Fig.
1.
Transthoracic
study. Right atrial
mass (arrows);
RA, right atrium;
RV, right ventricle;
803
LV, left
ventricle.
Fig.
2. Transesophageal
study. Right
atria1 mass (arrows);
“unattached” state may have been reduced cardiac output as a result of severe left ventricular dysfunction and lack of organized atria1 contraction. It is possible that improvement of forward cardiac flow during treatment of the heart failure contributed to the clot’s eventually moving from the right atrium to the pulmonary artery. Although the freefloating right atria1 thrombus in this case was rapidly lethal, the prognostic meaning of thrombus anchorage requires larger series and further study. REFERENCES
1. Starkey IR, de Bono DP. Echocardiographic identification of right-sided cardiac intracavitary thromboembolus in massive pulmonary embolism. Circulation 1982;66:1322-6.
RA, right atrium;
Ao, ascending
aorta.
2. Felner JM, Churchwell AL, Murphy DA. Right atria1 thromboemboli: clinical echocardiographic and pathophysiological manifestations. J Am Co11 Cardiol 1984&1041-51. 3. Torbicki A, Pasierski T, Uchman B, Miskiewicz Z. Right atria1 mobile thrombi: two-dimensional echocardiographic diagnosis and clinical outcome. Cor Vasa 1987;29:293-303. 4. The European Cooperative Study on the clinical significance of right heart thrombi. G. Kronik for the Euronean Working Group on Echocardiography. Eur Heart J 1989;lO: 1046-59. 5. Seward JB, Khenheria BK, Oh KJ, et al. Transesophageal echocardiography: technique, anatomic correlations, implementation and clinical applications. Mayo Clin Proc 1988; 63:649-80. 6. Panidis IP, Kotler MN, Mintz GS, Ross J. Clinical and echocardiographic features of right atria1 masses. AM HEART J 1984;107:745-58.
Brief Communications
American
4. Vignola PA, Aonuma K, Swaye PS, Rozanski JJ, Blankstein RL, Benson J, Gosselin AJ, Lister JW. Lymphocytic myocarditis presenting as unexplained ventricular arrhythmias: diagnosis with endomyocardial biopsy and response to immunosuppression. J Am Co11 Cardiol 198&4:812-g. 5. James TN, MacLean WA. Paroxysmal ventricular arrhythmias and familial sudden death associated with neural lesions in the heart. Chest 1980;78:24-30. 6. Emmons PR, Blume WT, DuShane JW. Cardiac monitoring and demand pacemaker in Guillain-Barre syndrome. Arch Neurol 19’75;32:59-61. 7. Greenland P, Griggs RC. Arrhythmic complications in the Guillain-Barre syndrome. Arch Intern Med 1980;140:1053-5. 8. Lichtenfeld P. Autonomic dysfunction in the Guillain-Barrit syndrome. Am J Med 1971;50:772-80. 9. Haymaker W, Kernohan JW. The Landry-Guillain-Barre syndrome: clinicopathologic report of 50 fatal cases and critique of literature. Medicine 1949;28:59-141. 10. Kahn JK, Sisson JC, Vinik AI. QT interval prolongation and sudden cardiac death in diabetic autonomic neuropathy. J Clin Endocrinol Metab 1987;64:751-4.
Right atrial mobile thrombus: Improved visualization by transesophageal echocardiography Tomasz J. Pasierski, MD, Mary E. Alton, MD, Douglas B. Van Fossen, MD, and Anthony C. Pearson, MD. Columbus, Ohio
Right atria1 mobile thrombus is an infrequent but nevertheless life-threatening disease diagnosed by two-dimensional echocardiography. In the last decade, many cases of right atria1 mobile thrombi have been reported but the etiology of this disease remains still not well understood.1-4 In the majority of reports, right atrial mobile thrombus has been associated with severe pulmonary embolism and high morbidity.1-4 Mobile right atria1 thrombi are thought to originate in peripheral veins and subsequently migrate to the right atrium, where they become entrapped. The site of entrapment may be a persistent foramen ovale, the eustachian valve, or a Chiari network. Previous reports have not established whether thrombus may stay within the right atrium without any attachment to cardiac structures. Transesophageal echocardiography is far superior to surface echocardiography in visualizing the interatrial septum and right atria1 structures.5 In this report we describe the first right atria1 mobile thrombus clearly shown by transesophageal echocardiography to have no atria1 attachment point. A 56-year-old white man with a remote history of myo-
From the Ohio State Reprint Means 414134512
Department University
requests: Hall, 1654
of Internal Hospitals.
Anthony Upham
Medicine,
Division
of Cardiology,
C. Pearson, MD, Division of Cardiology, Drive, Columbus, OH 43210-1228.
The 657
March 1992 Heart Journal
cardial infarction in 1983 and chronic obstructive lung disease was admitted to a local hospital because of progressive dyspnea on exertion, prominent weight gain, leg edema, and syncope. Echocardiographic examination, despite its poor technical quality, revealed a right atria1 mass that appeared to be attached to the interatrial septum. The patient was transferred to The Ohio State University Hospitals for further evaluation. On admission, the patient was dyspneic and tachypneic with visible cyanosis. Physical examination was significant for blood pressure of 120/90 mm Hg, a heart rate of 60 beats/min with irregular rhythm, jugular venous distention, expiratory wheezes, and a grade 2/6 apical systolic murmur. The liver was mildly enlarged and there was edema to the level of the mid thigh. The electrocardiogram showed multiple premature supraventricular beats, along with evidence of an old anterolateral myocardial infarction. His medical regimen consisted of digoxin, furosemide, and intravenous heparin. A surface echocardiogram confirmed the presence of a mobile right atria1 mass apparently attached to the interatrial septum that could have been either myxoma or thrombus (Fig. 1). Transesophageal echocardiography was ordered to better define the right atria1 mass. An extremely mobile, elongated, serpiginous mass that nearly filled the entire right atria1 cavity was found (Fig. 2). The inferior and superior vena cava, as well as the interatrial septum, were well visualized but no attachment point of the right atria1 mass was identified. Left ventricular systolic function was depressed (ejection fraction calculated to be 20 70) and anteroapical akinesis along with moderate mitral regurgitation was found. The risk of surgical removal of the thrombus was considered too high because of poor left ventricular function. He was continued on a regimen of intravenous heparin and was started on oral warfarin sodium. During further observation, the patient’s dyspnea diminished and syncope did not recur. A left ventriculogram and coronary angiogram were obtained and showed an ejection fraction of 18% and an occluded left anterior descending coronary artery. No echocardiographic follow-up was performed. The patient died suddenly 2 days later. During attempted resuscitation, he was initially asystolic. Despite mechanical ventilation, adequate oxygenation was never obtained and the blood pressure was unmeasurable. At autopsy a large organized thrombus nearly occluding the right pulmonary artery was found. In the left pulmonary artery a thromboembolus that appeared acute was present. Multiple emboli were found in the peripheral pulmonary artery branches. The most important differential diagnosis for right atria1 thrombus is atria1 myxoma, and visualization of a septal attachment of a right atria1 mass of unknown etiology is of critical importance.6 Transesophageal echocardiography allows for excellent visualization of the entire interatrial septum, contributing to the diagnosis of the character of right atria1 masses. It also allows excellent visualization of the superior vena cava, inferior vena cava eustachian valve, and Chiari network, which may be sites of thrombus entrapment. In this case transesophageal echocardiography demonstrated that thrombus may stay within the right atrium without any attachments. The factors favoring this
Volume Number
123
Brief Communications
3
Fig.
1.
Transthoracic
study. Right atrial
mass (arrows);
RA, right atrium;
RV, right ventricle;
803
LV, left
ventricle.
Fig.
2. Transesophageal
study. Right
atria1 mass (arrows);
“unattached” state may have been reduced cardiac output as a result of severe left ventricular dysfunction and lack of organized atria1 contraction. It is possible that improvement of forward cardiac flow during treatment of the heart failure contributed to the clot’s eventually moving from the right atrium to the pulmonary artery. Although the freefloating right atria1 thrombus in this case was rapidly lethal, the prognostic meaning of thrombus anchorage requires larger series and further study. REFERENCES
1. Starkey IR, de Bono DP. Echocardiographic identification of right-sided cardiac intracavitary thromboembolus in massive pulmonary embolism. Circulation 1982;66:1322-6.
RA, right atrium;
Ao, ascending
aorta.
2. Felner JM, Churchwell AL, Murphy DA. Right atria1 thromboemboli: clinical echocardiographic and pathophysiological manifestations. J Am Co11 Cardiol 1984&1041-51. 3. Torbicki A, Pasierski T, Uchman B, Miskiewicz Z. Right atria1 mobile thrombi: two-dimensional echocardiographic diagnosis and clinical outcome. Cor Vasa 1987;29:293-303. 4. The European Cooperative Study on the clinical significance of right heart thrombi. G. Kronik for the Euronean Working Group on Echocardiography. Eur Heart J 1989;lO: 1046-59. 5. Seward JB, Khenheria BK, Oh KJ, et al. Transesophageal echocardiography: technique, anatomic correlations, implementation and clinical applications. Mayo Clin Proc 1988; 63:649-80. 6. Panidis IP, Kotler MN, Mintz GS, Ross J. Clinical and echocardiographic features of right atria1 masses. AM HEART J 1984;107:745-58.
