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Eur J Cardiothorac Surg 2001;20:880-882
© 2001 Elsevier Science NL
Case report |
a Second Medical Department, Krankenanstalt Rudolfstiftung, Vienna, Austria
b Radiological Department, Krankenanstalt Rudolfstiftung, Vienna, Austria
c Second Neurological Department, Neurological Hospital Rosenhügel, Vienna, Austria
Received 25 June 2001; received in revised form 6 July 2001; accepted 8 July 2001.
Corresponding author. Steingasse 31/18, A-1030 Vienna, Austria. Tel./fax: +43-1-713-9870
e-mail: claudia.stoellberger{at}chello.at
| Abstract |
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Key Words: Aorta Thrombus Transesophageal echocardiography Cardiac magnetic resonance imaging
| 1. Introduction |
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| 2. Case report |
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Eight years before, she had undergone a surgical subclavia-carotis-transposition after an embolic event of the left upper extremity due to a left subclavian artery origin stenosis. Angiography, performed at that time, did not show any atherosclerosis. Since then the patient was on oral anticoagulant therapy with phenprocoumon. She had a low compliance and, whenever tested by her general practitioner, international normalized ratio (INR) values were only between 1.2 to 1.6. Because of chronic obstructive lung disease, she had been treated with oral glucocorticoids over the last 3 years. Except for smoking, she had no vascular risk factors. The actual symptoms were explained with only clinically suspected emboli to the lower limbs and a left renal infarction, confirmed by computed tomography. Anticardiolipin antibodies, antithrombin III, protein C, protein S, fibrinogen, platelet count, evaluation for vasculitis and serologic tests for syphilis were normal. Transesophageal echocardiography (TEE) detected in the descending aorta a 10-cm long floating, highly mobile thrombus with a diameter of 1520 mm. The aortic wall was free of any atheroma. Neither TEE, computed tomography nor magnetic resonance imaging (MRI) detected any calcifications or thickening of the aortic wall. Cardiac MRI revealed the only insertion site of the thrombus in the left subclavian artery stump (Fig. 1) . Because of obesity and lung disease, the risk of surgery was considered too high. Thrombolysis was rejected because of the size of the thrombus and concern that it might re-embolize. Thus, the patient underwent intravenous heparinization over 3 weeks with prothrombin time test (PTT) values between 80 and 100 s (baseline PTT 23.7 s), followed by oral anticoagulation with INR values between 3.0 and 4.0. No further clinically apparent embolic event occurred. Because TEE, performed after 4 weeks, showed regression of the thrombus to a length of 4 cm she was dismissed from the hospital. Cardiac MRI after another 6 weeks showed complete resolution of the aortic thrombus. Only in the subclavian artery stump a small thrombus was visible (Fig. 1). After dismissal, the patient's compliance improved and it was possible to achieve and maintain her INR values between 3.0 and 4.0. During a further follow-up period of 30 months, no events occurred suggestive of embolism, nor did echocardiographic and MRI examinations show any recurrence of thrombus formation.
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| 3. Discussion |
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The ideal treatment of mobile aortic thrombi without atheromatosis has not been ascertained. Surgical removal, either by aortotomy with endarterectomy, thrombectomy or balloon embolectomy, and thrombolysis are the proposed therapies [13,710]. Surgical as well as thrombolytic therapy carries associated risks. Anticoagulant therapy could at least avoid the surgical risk but implies the risk of recurrent, potentially life-threatening embolization [8,9]. Resolution of small mobile aortic thrombi, sized 0.53 cm, under anticoagulant therapy has been documented by TEE and computed tomography [2,8,9]. In two further cases with large aortic thrombi, sized 10 cm and 15 cm, anticoagulant therapy has been performed without embolic events [4]. Whether in our case the resolution of the thrombus was due to anticoagulant therapy, to silent re-embolization or spontaneous fibrinolysis could not be definitively decided, but we assume that the anticoagulant therapy permitted the endogenous fibrinolytic system to dissolve the thrombus. Intravenous heparinization in our patient necessitated a prolonged hospitalization of 4 weeks. Only after that period, when TEE showed a significant decrease in the size of the thrombus, a change to oral anticoagulation and dismissal of the patient deemed justified.
Since large, mobile aortic thrombi without aortic atheromatosis resolve during strong and well-controlled anticoagulant therapy, this case may provide impetus to use anticoagulant therapy for similar situations. However, anticoagulation in a patient with mobile aortic thrombi should only be performed in hospitals equipped with vascular surgery. Special care should be taken to maintain the level of anticoagulation in the target range, to observe the patient closely for possible embolic events, and to hospitalize the patient until significant reduction in the size of the thrombus can be documented.
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