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Ann Thorac Surg 2002;74:588-590
© 2002 The Society of Thoracic Surgeons

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Case report

Floating nonocclusive thrombus in the ascending aorta

^a Department of Cardiothoracic and Vascular Surgery, Deutsches Herzzentrum Berlin, Berlin, Germany

Accepted for publication March 14, 2002.

* Address reprint requests to Dr Sodian, Department of Cardiothoracic and Vascular Surgery, German Heart Institute Berlin, Augustenburger Platz 1, 13353 Berlin, Germany
e-mail: sodian{at}dhzb.de

	Abstract

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We report the case of a 55-year-old woman seen with signs of angina pectoris and dyspnea. Transesophageal echocardiography showed a floating thrombus distal to the right coronary ostium. At operation, we found a highly mobile thrombus attached to an atherosclerotic plaque distal to the right coronary ostium. The atherosclerotic lesion and the pedunculated thrombotic mass were removed without resection of the adjacent aortic wall. In our judgment, a floating mass in the ascending aorta represents an emergency and should be removed before major thromboembolic complications occur.

	Introduction

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Floating structures in the ascending aorta are rarely reported. When they occur, severe central and peripheral thromboembolic complications can result [1]. We report the case of a 55-year-old woman with a floating thrombus distal to the right coronary ostium causing angina pectoris and dyspnea. Systemic thromboembolic complications and even coronary occlusion leading to infarction and ultimately death have been reported by other investigators [2]. In our patient, the exact cause of the floating mass attached to an atherosclerotic plaque at the sinus of Valsalva was unknown. The pedunculated thrombus was removed surgically, and the patient had an uneventful postoperative course with no clinically relevant thromboembolic complications. The finding of a floating structure in the aorta is rare and in our judgment should be treated urgently by surgical intervention to avoid major thromboembolic complications.

A 55-year-old woman was seen with angina pectoris and dyspnea. She had a history of transient ischemic attacks but no cardiovascular pathological conditions and no hormonal treatment. She had no family history of arterial or venous thromboembolic events. At the time of admission, blood pressure was normal and heart rate, 90 beats per minute. The electrocardiogram showed ST segment depression in leads V₂ through V₅ and no evidence of cardiac arrhythmia. The chest roentgenogram was free from pathological findings. Blood chemistry studies showed an increase in creatine kinase levels (33 U/L) and an elevated blood plasma level of troponin I (13.1 ng/mL). Hemostatic variables were increased (prothrombin time 62%; partial thromboplastin time, 62.7 seconds; antithrombin III, 59%), but there were no signs of a hypercoagulable disorder. We excluded HIT type II (HIPA and Enzyme-linked immunosorbent assay) with a median platelet count of 150 x 10³/µL preoperatively and postoperatively.

Transthoracic echocardiography showed an unidentified floating mass in the ascending aorta but no intracardiac thrombus or pathological findings indicative of thrombus. Transesophageal echocardiography confirmed the presence of a pedunculated free-floating thrombus measuring 3 x 1 cm distal to the right coronary ostium without evidence of an aortic dissection; the inner diameter of the ascending aorta measured 3.4 cm. The thrombus was attached to the sinus of Valsalva and was floating in the direction of blood flow (Fig 1). Transesophageal echocardiography demonstrated a tricuspid aortic valve without any evidence of aortic regurgitation or stenosis.

View larger version (136K): [in this window] [in a new window]   Fig 1. Long-axis echocardiogram showing pedunculated thrombus (arrow) in ascending aorta with aortic valve in closed position.

View larger version (110K): [in this window] [in a new window]   Fig 2. The thrombus is attached to the sinus of Valsalva close to the right coronary ostium.

	Comment

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The formation of thrombus is due to many factors and is related to a combination of regional myocardial akinesis or dyskinesis, abnormal endocardial or vascular surfaces, and aberrant blood flow dynamics associated with arrhythmia. Most frequently the source of the thrombus is located in the cardiac chambers, and patients with prosthetic heart valves have a high risk of thromboembolic events [3]. Reports concerning a floating thrombus in the ascending aorta are rare. When such a thrombus has occurred, it has been associated with major complications such as massive myocardial infarction and peripheral emboli [4]. Some authors [5] hypothesized that atherosclerotic plaques and a hypercoagulable condition might cause a thrombus in the ascending aorta. In our patient, we could find no hypercoaguable or systemic disorder that could cause unusual thrombosis but only an atherosclerotic plaque, which could lead to endothelial injury and resulting thrombus formation [6]. However, the exact mechanisms of giant thrombus in a high-flow environment such as the ascending aorta are not fully known. In most of the reported cases, fatal complications developed, and surgical intervention was undertaken after myocardial infarction, coronary occlusion, or peripheral or central emboli had already occurred [1, 4]. An important feature in our report is that we removed the floating structure in an emergency procedure before any of these events happened.

Although other investigators [7] reported successful thrombolytic treatment of an aortic arch thrombus in a patient, we consider the risk of thromboembolism to be high and therefore decided to remove the mass surgically. The surgical intervention was easily performed and uneventful. Whereas surgical resection of an atheromatous lesion has been reported to be successful in patients with plaque-related thrombus in the aortic arch, we decided not to excise the plaque because it was located very close to the right coronary ostium. Excision of a small button of the aortic wall surrounding the pedunculated thrombus and local patch graft replacement close to the coronary ostium may even increase the risk of perioperative thromboembolic and ischemic complications. In addition, to avoid destroying the complex anatomical architecture of the sinus of Valsalva and the coronary ostium, we decided not to resect part of the aortic wall and carefully removed only the thrombus and the underlying adherent plaque. Bearing in mind that the remaining atherosclerotic plaque or other plaques might increase the risk of recurrent thrombus formation, we initiated long-term anticoagulant therapy with warfarin sodium (international normalized ratio, 2.0 ± 0.2). However, appropriate treatment of a floating thrombus in the ascending aorta or aortic arch originating from an atheromatous lesion remains uncertain and depends on the exact location of the atherosclerotic plaques.

In our case, the decision in favor of surgical intervention and against resection of the attached aortic wall was based on the transesophageal echocardiographic examination. Transesophageal echocardiography provided almost all the information necessary for the surgical treatment of the floating mass—morphology, mobility, dimensions, and exact localization. Therefore, the evaluation of patients with unexplained disorders of the ascending or descending aorta or the presence of myocardial ischemia with normal coronary arteries should include transesophageal echocardiography.

In conclusion, our report demonstrates an unusual cause of angina pectoris and dyspnea found by transesophageal echocardiography. We prefer surgical removal of a floating thrombus to avoid fatal thromboembolic complications in patients with this pathological finding. The decision whether or not to resect the atheromatous aortic wall should be made on an individual basis depending on the localization, morphology, and size of the thrombus and the attached aortic wall.

	References

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1. Farah M.G., Hawawini H. Thrombus of the ascending aorta as a source of cerebral embolism. Chest 1993;104:1604-1605.[Abstract/Free Full Text]
2. Dunkman W.B., Johnson G.R., Carson P.E., Bhat G., Farrell L., Cohn J.N. Incidence of thromboembolic events in congestive heart failure. The V-HeFT VA Cooperative Studies Group. Circulation 1993;87(6 Suppl):94-101.[Abstract/Free Full Text]
3. Nader R.G., Barr F., Rubin R., Hirshfeld J.W., Jr, Eisen H.J., Laposata E. Aortic degenerative changes and thrombus formation: an unusual cause of massive myocardial infarction with normal coronary arteries. Am J Med 1989;86:718-722.[Medline]
4. Bruno P., Massetti M., Babatasi G., Khayat A. Catastrophic consequences of a free floating thrombus in ascending aorta. Eur J Cardio-thorac Surg 2001;19:99-101.[Abstract/Free Full Text]
5. Fuster V., Badimon J.J., Chesebro J.H. Atherothrombosis: mechanisms and clinical therapeutic approaches. Vasc Med 1998;3:231-239.[Abstract/Free Full Text]
6. Amarenco P., Cohen A., Tzourio C., et al. Atherosclerotic disease of the aortic arch and the risk of ischemic stroke. N Engl J Med 1994;331:1474-1479.[Medline]
7. Hausmann D., Gulba D., Bargheer K., Niedermeyer J., Comess K.A., Daniel W.G. Successful thrombolysis of an aortic-arch thrombus in a patient after mesenteric embolism. N Engl J Med 1992;327:500-501.[Medline]

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