Eur J Cardiothorac Surg 2001;19:99-101
© 2001 Elsevier Science NL
Catastrophic consequences of a free floating thrombus in ascending aorta
Piergiorgio Bruno,
Massimo Massetti,
Gerard Babatasi,
Andre Khayat
Thoracic and Cardiovascular Surgery Department, University Hospital Caen, 14033-Caen, France
Received 11 February 2000;
received in revised form 2 October 2000;
accepted 19 October 2000.
Corresponding author. Tel.: +33-2-31066-4457; fax: +33-2-3106-4986
e-mail: massetti-m{at}chu-caen.fr
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Abstract
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Floating masses in ascending aorta are an uncommon source of embolism. We report the case of a 46-year-old woman, smoker, on synthetic progestagen, with no previous history of thrombotic events, who was admitted to our emergency department for an acute anterior myocardial infarction. Coronary angiogram showed occlusion of left main coronary trunk. Recanalization of the artery was obtained. Ascending aorta angiogram revealed a free floating mass attached to the aortic wall without evidence of aortic dissection. Transesophageal echocardiography confirmed the presence of a pedunculated mobile mass attached to the aortic wall superior to the left coronary ostium. The patient underwent urgent surgery. Intraoperatively a floating thrombus was localized in the posterior wall of ascending aorta. At macroscopical examination aortic wall and leaflets were normal. Post-operative low cardiac output refractory to inotropic drugs and intraaortic balloon counterpulsation required a circulatory assist device. Consequences for the patient were catastrophic in terms of outcome.
Key Words: Ascending aorta • Free floating thrombus • Myocardial infarction • Cardiac surgery
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Introduction
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Left main coronary artery occlusion is a rare finding and usually gives rise to cardiogenic shock. We report a case of massive myocardial infarction caused by a pedinculated free-floating thrombus in the ascending aorta. Most frequently emboli originate from cardiac chambers or aortic atherosclerotic plaques. Floating thrombi is a rare finding and an uncommon source of systemic embolism or myocardial infarction. The aethiology of the thrombus was unknown and it was attached to a normal aortic wall. The thrombus was surgically removed. Post-operative course was characterized by severe complications leading to the patients death.
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Case report
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A 46-year-old woman was admitted to our emergency department for a massive acute anterior myocardial infarction. In her past medical history there were no cardiovascular pathologies and thrombotic events. She was a smoker and was taking synthetic progestagen.
At admission she presented cardiogenic shock blood systolic pressure of 70 mmHg, a heart rate of 120 beats/min, the electrocardiogram showed marked anterolateral ST-segment depression with T wave inversion and the chest radiogram documented pulmonary oedema. She had no neurological deficits, or signs of peripheral embolization. After the insertion of an intra-aortic balloon pumping coronary angiogram was performed it showed a complete obstruction of the left main coronary trunk. Recanalization of the artery was immediately obtained by transcatheter aspiration and thrombolytic therapy. Ascending aorta angiogram revealed a free floating mass attached to the posterior aortic wall (Fig. 1) without any evidence of aortic dissection. Transesophageal echocardiography confirmed the presence of a large and mobile mass attached at its tip to the wall of ascending aorta (Fig. 2) about 3 cm superior to the level of the left aortic cusp. The aortic valve was tricuspid and normal; the four cardiac chambers and the ascending aorta were of normal dimensions. She had no family history of arterial or venous thrombotic events. She presented normal haemostatic parameters (Fibrinogen 4 g/l; Prothrombin time 85%; Antithrombin III 90%; Factor V 70%). Urgent surgery was planned. The operation was conducted using cardiopulmonary bypass. After aortic crossclamping a transverse aortotomy was performed, cold cristalloid cardioplegic solution was injected selectively to both coronary ostia. A floating mass, 3.5x1.5 cm, was localized in the posterior wall of the ascending aorta (Fig. 1). It was attached about2 cm superior of the left coronary ostium. The aortic wall and leaflets appeared normal without any atherosclerotic changes. This mass was removed with a small button of the aortic wall surrounding its pedicle. The aortic wall histologic examination demonstrated layers of foam cells in a thin intima, with initial visible extracellular lipid droplets. Histologic examination of the mass revealed a fresh thrombus composed of a fibrinous material and platelets.
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Fig. 1. Coronary Angiogram: left main trunk occlusion; Angiography of ascending aorta: free floating thrombus.
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Fig. 2. Echocardiography, longitudinal axis view: 3 cm mass floating in the ascending aorta and attached to the posterior aortic wall.
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In the post-operative hours there was a deterioration of hemodynamic performance leading to a refractory low cardiac output. Indication was given for a left mechanical assist device. A pulsatile paracorporeal artificial ventricle (Medos VAD, Medos Medizintechnik GmbH, Germany) was implanted. Bleeding complications required two surgical re-explorations. Acute renal failure needed repeated hemodialysis until recovery of subnormal renal function. Late postoperative period was characterised by stable haemodynamic, normalisation of respiratory function until leucopenia of unknown aetiology was responsible of a fulminant generalized Cytomegalovirus sepsis. Death occurred on 50th post-operative day.
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Discussion
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Atrial fibrillation, myocardial infarction, rheumatic and bacterial endocarditis, ventricular aneurysms, and prosthetic valves are potential cardiac causes of embolism. On the other hand, the most frequent non cardiac sources are mural thrombi within proximal aneurysms, ulcerated atherosceloritic plaques and paradoxical emboli originating from the venous side of the circulation. Floating masses in the ascending aorta are uncommon source of embolism [1–3]. The most frequent cause is atherosclerosis of the ascending aorta and mobile thrombi or atherosclerotic debris located on atherosclerotic plaques [4]. In contrast, a floating thrombus with no macroscopical evidence of ascending aortic pathology has been very rarely reported [3–6]. Thrombus formation has been speculated to be caused by a hypercoagulable state. In the majority of unexplained thrombotic events, clotting abnormalities could not be detected despite the multiple current testing methods [7]. The diagnosis of hypercoagulable disorder in our patient was excluded by the negative complete coagulation profile and the lack of previously unexplained arterial or venous thromboses in herself and her family members. Moreover, the lack of atherosclerotic risk factors, except smoking and oral contraception treatment with progestogen [8,9] in the presence of a normal coagulation profile, and the innocent histologic aspect of the ascending aorta wall have raised the question of unknown mechanism in thrombus formation.
As far as we are concerned the very rare and most interesting feature of our report is the mechanism of left coronary ostium occlusion by the thrombus. The occlusion was strictly correlated to the thrombus localization and shape. The length of the pedunculated thrombus, the site of implantation on the intima of the aorta and the diastolic perfusion of the coronary arteries system could have been, in our opinion, the factors responsible of the dynamics leading to the massive myocardial infarction. However in the presence of acute myocardial infarction with normal coronary arteries suspicion of coronary embolization plays an important role in diagnosis making. In the treatment of this pathology, thrombi localized in the ascending aorta, surgery should always be considered [1,3,5,10].
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Abstract
Introduction
