Interact CardioVasc Thorac Surg 2009;9:899-900. doi:10.1510/icvts.2009.212241
© 2009 European Association of Cardio-Thoracic Surgery
Case report - Vascular thoracic |
Aortogenic cerebrovascular accident
Shin-ichi Ohki,
Insu Kubota,
Kei Aizawa and
Yoshio Misawa*
Division of Cardiovascular Surgery, Jichi Medical University, 3311-1 Yakushiji, Shimotsuke, Tochigi, 329-0498, Japan
Received 19 May 2009;
received in revised form 17 July 2009;
accepted 19 July 2009
*Corresponding author. Tel.: +81-285-58-7368; fax: +81-285-44-6271.
E-mail address: tcvmisa{at}jichi.ac.jp (Y. Misawa).
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Abstract
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A 59-year-old man was transferred to our hospital because of mural thrombus in the ascending aorta. He had suffered some neurological dysfunctions such as transient dysorientation. Electrocardiogram showed normal sinus rhythm without premature beats. Trans-thoracic echocardiogram and three-dimensional CT showed a mobile mural mass sticking to the ascending aortic wall. No coagulopathy was detected in the patient. The mural masses were thought to be a possible cause of the repeated cerebro-vascular symptoms. Under cardiopulmonary bypass and cardiac arrest, the masses were removed including the mass sticking to the aortic wall. Postoperative pathological findings showed the masses were organizing thrombi that had originated from the atherosclerotic aortic wall. Postoperative course was uneventful, and the patient was doing well one year after the operation without neurological dysfunction.
Key Words: Aortic thrombus; Atherosclerosis; Cerebral infarction
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1. Introduction
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Mural thrombosis can occur at the site of an atherosclerotic lesion on any aortic wall, with a potential risk of cerebrovascular accidents [1, 2]. We experienced a case with mural thrombi in the ascending aorta that might have caused repeated cerebro-vascular symptoms.
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2. Patient
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A 59-year-old man was transferred to our hospital because of mural thrombus in the ascending aorta. For one month previous, he had suffered recurrent neurological dysfunctions such as transient dysorientation, forgetfulness, dysphasia, and right hemiparesis. He had not been under steroid therapy. He had not experienced episodes of chest traumas. Administration of antiplatelet agents was started on his original admission and all dysfunctions had almost subsided when he was admitted to our hospital. Electrocardiogram showed normal sinus rhythm without premature beats. Trans-thoracic echocardiogram showed a mobile mural mass sticking to the ascending aortic wall without intra-cardiac abnormalities (Video 1). Three-dimensional CT-scan revealed two protruding thrombi in the ascending aorta (Fig. 1). The mural masses were thought to be a cause of the repeated cerebro-vascular symptoms, and mass resection was scheduled. Studies of plasminogen activity, D-dimer, proteic C activity, lupus anticoagulant factor, anticardiolipin antibody, and homocysteine did not reveal coagulopathy.
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Video 1. Trans-thoracic echocardiogram showed a mobile mural mass sticking to the posterior wall of the ascending aortic wall.
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Fig. 1. Three-dimensional CT of the thoracic aorta. Two floating masses sticking to the ascending aortic wall were recognized.
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Because of recurrent cerebral thromboembolic events and taking the possibility of neoplasma in the ascending aorta into account, surgical resection of the masses was scheduled. Epiaortic echocardiographic examination revealed the masses recognized preoperatively sticking to the anterior wall of the ascending aorta. The right femoral artery was cannulated for the arterial return. Under cardiopulmonary bypass and aortic cross-clamping cardiac arrest with a moderate hypothermic condition, the ascending aorta was opened. The masses were removed including the mass sticking to the aortic wall (Fig. 2). Postoperative pathological findings showed the masses were organizing thrombi that had originated from the atherosclerotic aortic wall. Antiplatelet therapy was maintained after the operation. Postoperative course was uneventful, and the patient was doing well one year after the operation without neurological dysfunction
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Fig. 2. Resected masses. Specimens were organizing thrombi originating from the atherosclerotic aortic wall.
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3. Comment
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Intra-aortic thrombi can cause systemic emboli like intra-cardiac thrombi. However, aortogenic cerebro-vascular accidents are rare. When thrombi are silent, surgical treatment might be controversial. Our patient experienced repeated neurological episodes, and no other causes of cerebro-vascular accidents were detected.
Systemic emboli have been reported to originate from the aorta. Ryu and colleagues also reported a case with primary antiphospholipid syndrome presenting a floating thrombus in the ascending aorta. They revealed that the intima at the base of the thrombus appeared relatively normal after thrombus removal [3].
Bertrand reported a case of acute myocardial infarction with a large moving filling defect unexpectedly found in the ascending aorta just above the right coronary ostium [4]. A segment with the appending thrombus on an ulceration of the aorta was surgically removed.
Atheromatous change per se can cause systemic emboli. Doufekias reviewed aortogenic brain embolisms, and found a higher risk of thromboembolism in patients with complex aortic atheromas  4 mm or containing ulceration or mobile components in atrial fibrillation than in those without [5]. The author recommended early systemic anticoagulation if there were mobile atheroma.
Our patient had multiple neurological episodes, and multiple thrombi were recognized on the ascending aortic wall. Symptomatic patients with thrombi on the aortic wall need to be surgically treated. Thus, we chose open surgical treatment with pre and postoperative antiplatelet therapy. Pathological examination revealed that the thrombi were originating from the atherosclerotic lesions. However, three-dimensional CT showed that the aortic intima looked very smooth except for the lesions and there was no shaggy intimal surface. The patient has no history of chest traumas or cardiac catheterization studies. Thus, we cannot conclude what was the cause of these sporadic atherosclerotic lesions.
In conclusion, intra-aortic thrombus has a potential risk of causing a cerebro-vascular accident. The thrombi in our case were successfully removed under cardiopulmonary bypass; demonstrating that open surgical treatment is an option for treatment for symptomatic intra-aortic thrombi.
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References
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- Kronzon I, Tunick PA. Aortic atherosclerotic disease and stroke. Circulation 2006;114:63–75.[Free Full Text]
- Meissner I, Khandheria BK, Sheps SG, Schwartz GL, Wiebers DO, Whisnant JP, Covalt JL, Petterson TM, Christianson TJ, Agmon Y. Atherosclerosis of the aorta: risk factor, risk marker, or innocent bystander?: a prospective population-based transesophageal echocardiography study. J Am Coll Cardiol 2004;44:1018–1024.[Abstract/Free Full Text]
- Ryu YG, Chung CH, Choo SJ, Kim YS, Song JK. A case of antiphospholipid syndrome presenting a floaing thrombus in the ascending aorta. Thorac Cardiovasc Surg 2009;137:500–502.[CrossRef]
- Bertrand OF, Trahan S, Rodés-Cabau J, Dumont E. Appending thrombus on ulceration of the ascending aorta: a rare cause of acute ST-elevation myocardial infarction. Circulation 2009 Mar 10;119:e227–e229.[Free Full Text]
- Doufekias E, Segal AZ, Kizer JR. Cardiogenic and aortogenic brain embolism. J Am Coll Cardiol 2008;51:1049–1059.[Abstract/Free Full Text]
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Abstract
1. Introduction