Gen Thorac Cardiovasc Surg DOI 10.1007/s11748-014-0511-x
CASE REPORT
Plural large floating thrombi in the ascending aorta Hisao Harada • Takeshi Soeda • Yuhei Saitoh Takahiro Nakahara
•
Received: 20 June 2014 / Accepted: 11 December 2014 Ó The Japanese Association for Thoracic Surgery 2014
Abstract Floating thrombi in the ascending aorta are a very rare finding in non-aneurysmal, mildly atherosclerotic or normal aortas. We report a case of floating thrombi in a 66-year-old man who was admitted to the hospital with acute chest pain and dyspnea. Enhanced computed tomography showed two large floating thrombi in the ascending aorta, type B aortic dissection, deep venous thrombosis, and pulmonary embolism. A temporary inferior vena cava filter was inserted and the subject underwent an emergency surgical intervention to remove both masses. His postoperative course was uneventful; the etiology of the thrombi is unknown. Lifelong anticoagulation therapy was started and the subject has been stable without recurrence for the last 2 years. Keywords Ascending aorta Thrombus Aortic dissection Pulmonary embolism
Introduction An ascending aortic thrombus is a rare event [1]. We report a particularly rare case in which plural pedunculated freefloating thrombi of unknown cause attached to the anterior wall of the ascending aorta. There are very few reports in the literature describing plural thrombosis in the ascending aorta.
H. Harada (&) T. Soeda Y. Saitoh T. Nakahara Department of Cardiovascular Surgery, Matsue Red Cross Hospital, 200 Horomachi, Matsue, Shimane 690-8506, Japan e-mail: [email protected]
Case report A 66-year-old man was taken to the hospital by ambulance due to the onset of acute chest pain and dyspnea. He gradually experienced symptomatic relief at the hospital. He had no edema of the lower extremities. His medical history included documented hypertension, type 2 diabetes mellitus treated with oral medication, and rheumatoid arthritis for 15 years. Adrenal corticosteroids had not been administered over the last year. He had quit smoking for about 3 years, before which he had been a two-pack-a-day smoker for 40 years. A year previous to this incident, he had presented with a left renal infarction, which was managed conservatively without pharmacologic intervention because of his refusal to undergo additional investigation. Other embolic events were not known. At the present admission, an enhanced computed tomography (CT) was performed, which revealed a type B acute aortic dissection (the non-communicating type), an acute pulmonary embolism (PE) with left deep venous thrombosis (DVT), and two masses, 5 and 3 cm in length, respectively, which were attached to the anterior wall of the ascending aorta (Fig. 1a–d). The ascending aorta was 36 mm in diameter with no aneurysmal change. CT scans of the thorax/abdomen/pelvis regions revealed no evidence of malignancy. The patient had no familial history of thromboembolic events. A laboratory workup for coagulation disorders, such as anti-phospholipid syndrome, protein S, protein C, and antithrombin III deficiency was negative. The transthoracic echocardiographic study did not reveal any anomaly. The aortic valve was tricuspid without evidence of valvulopathy. Trans-aortic valve flow velocity was 0.8 m/s. The LV wall motion and the left atrial size
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Fig. 1 a Computed tomography (CT) shows two large thrombi in the ascending aorta (arrow); asterisk denotes aortic dissection; white circles denote bilateral pulmonary embolism. b Thrombi attachments to the anterior wall of the ascending aorta can be seen. c, d Pedunculated formations of thrombi can be seen on CT
angiography; (left) from a frontal view; (right) from a lateral view. The red color indicates the attachment portion. e The sizes of removed aortic thrombi; 47 9 28 9 22 mm, 32 9 18 9 13 mm. f Pathological examination revealed organized fibrin masses. These are ‘‘lines of Zahn’’ (asterisk)
were normal. The LV ejection fraction was 69.5 %. Preoperative transesophageal echocardiography confirmed that the left atrial appendage was normal with no thrombus. No patent foramen ovale was detected on the color Doppler echocardiogram. The patient underwent emergency surgery on the admission day to avert an embolic event, particularly brain embolization. Prior to the surgical intervention, he had a temporary inferior vena cava (IVC) filter inserted as a prophylactic measure to prevent additional pulmonary embolisms. Anticoagulation therapy was not indicated preoperatively. The surgery was performed via a median sternotomy and conducted using a cardiopulmonary bypass with moderate hypothermia (25 °C) which was initiated
between the right atrium and the right femoral artery. We performed intraoperative epiaortic echocardiography. As it turned out, there were few atheromatous changes in the ascending aortic wall which might cause debris under aortic cross clamping. However, one mass protruded forward into the aortic arch so we had to withdraw the mass so as not to break it. We performed hypothermic circulatory arrest for 2 min to withdraw the mass and clamp the ascending aorta at the upper end. The masses were removed along with the aortic wall, because malignancy could not be ruled out by appearance alone. The masses were yellowish-white nodular tumors, with a rubber-like hardness that were removed from the intima with relatively little effort (Fig. 1e). The intima of the aorta appeared almost normal, except for the slightly
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discolored area of insertion, and lacked any evidence of tears or ulcerations. The ascending aorta was replaced with a synthetic graft. Histologic examination of the masses revealed old thrombi composed of a fibrous material with erythrocytes, leucocytes, and histiocytes, which were organized partly along the periphery. These are ‘‘lines of Zahn’’ which are the alternating pale pink bands of platelets with fibrin and red bands of erythrocytes. A histopathological evaluation of the aortic wall revealed mild atherosclerosis on the intima and secondary mild capillary invasion into media without any evidence of other arterial wall disease. The postoperative course was uneventful and the IVC filter was removed on postoperative day 14. Brain magnetic resonance imaging showed no findings of cerebral infarction upon postoperative examination. The subject commenced lifelong oral anticoagulation therapy. The patient has been doing well over the past 2 years post-surgery without evidence of recurrent aortic thrombi in follow-up enhanced computed tomography scans.
Discussion An aortic free-floating thrombus is a very rare finding because the aorta is a high-flow vascular region that normally precludes clot formation. In most cases, a patient is taken to a doctor because of peripheral arterial emboli [2–6]. In the present case, the subject had a left renal infarction a year ago, but it was not further scrutinized with enhanced CT. Despite that, he refused further exploration following renal embolism. His home doctor, if any, could have examined him mindfully with transthoracic echocardiography and found the thrombus in the ascending aorta. This time, he complained of symptoms of type B aortic dissection, DVT, and PE, which led to the present discovery. In general, intra-aortic thrombi are associated with aneurysms, aortic dissection, trauma, or complicated atherosclerotic plaques. Uncommonly, they are also due to blood predisposition or disease; anti-phospholipid syndrome [2], heparin-induced thrombocytopenia (HIT) [7], polycythemia, and thrombocytosis. However, an aortic mural thrombus in a non-aneurysmal mildly atherosclerotic or normal aorta is a very rare clinical entity [1, 3]. Therefore, with respect to the primary management for this unusual problem, many physicians are at a loss which to choose [4, 8]. Fayad et al. [1] reported that literature about aortic mural thrombi in a non-aneurysmal mildly atherosclerotic or normal aorta was found in 200 patients from 98 documented articles. The descending thoracic aorta was the most common location of the thrombus (38 %), followed by the arch of the aorta (36 %), the abdominal aorta
(14 %), and finally the ascending aorta (n = 23; 12 %). Of the ascending aorta cases, 22 were floating, one was sessile, and there were no plural mural thrombi cases. Admitting a thrombus in the ascending aorta is extremely rare. For coronary arteries and aortic arch branches that are in close proximity to each other, if the embolism occurs, the risk of sequelae or death due to myocardial infarction and stroke is higher. In the present case, there were two huge thrombi in the ascending aorta. As to the cause, we doubt the association between aortic dissection, DVT, or PE at first glance [6]. We have subsequently determined that there is no direct association. We thought the symptoms at onset were caused by acute PE in view of the nature of the pain. Although the exact time of the onset of the aortic dissection is unknown, it is presumed that the aortic dissection was in the acute phase upon admission, because morphological changes of false lumen were subsequently radical, and had regressed almost completely at the time of discharge. DVT/PE had also disappeared on enhanced CT after 3 months. On the other hand, we considered that the intra-aortic thrombi were in a relatively chronic phase, because of the pathological findings of the thrombi and mild color changes limited to the aortic attachment portion. Although the subject has several risk factors, collagen disease, diabetes mellitus, and smoking history in the past, mechanisms leading to the thrombus formation in the ascending aortic tract remain obscure. Except for the report of drastic hypercoagulable state by HIT [7], there is no report so far, of plural thrombi in the ascending aorta. Both anticoagulation therapy (including thrombolysis) and aortic surgery are commonly used as primary treatment [2–5, 8], but there is no consensus. The results of the literature described above [1] showed that mortality rates were similar between groups; however, patients who received anticoagulation medication as primary therapy tended to have more complications such as stroke, limb loss, and bowel resection. Aortic thrombi persist or recur in 26.4 % of the anticoagulation group and in 5.7 % of the surgery group, and a quarter of the anticoagulation group underwent a secondary aortic procedure. In view of the aforementioned, also in the normal or mild diseased aorta, we are in favor of prioritizing a surgical intervention. In this case, due to two great thrombi in the ascending aorta and considering the risk of embolism, we decided to perform an emergency surgery. It is controversial to replace the aorta with a synthetic graft, because of the possibility of tumors such as sarcoma [9]; however, we decided to proceed. Even if the thrombi were surgically removed, there is a significant risk of recurrence [1], so we consider it necessary to prescribe lifelong anticoagulation treatment due to the subject’s remaining risk factors.
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Conclusion We reported an extremely rare case of plural large floating thrombi in the ascending aorta. The absence of recurrence at the 2-year follow-up confirmed the appropriateness of our therapeutic strategy.
Conflict of interest
None declared.
References 1. Fayad ZY, Semaan E, Fahoum B, Briggs M, Tortolani A, D’Ayala M. Aortic mural thrombus in the normal or minimally atherosclerotic aorta. Ann Vasc Surg. 2013;27:282–90. 2. Humbert VH Jr, Tuna IC, Harrison MR, Curtis DB, Webster SA. Aortic tumour in primary anti-phospholipid syndrome. Lancet. 2003;361:1676. 3. Mandegar MH, Roshanali F, Kocharian A. Complicated course consequences of a floating thrombus in ascending aorta. Eur J Echocardiogr. 2008;9:846–8.
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4. Chatterjee S, Eagle SS, Adler DH, Byrne JG. Incidental discovery of an ascending aortic thrombus: should this patient undergo surgical intervention? J Thorac Cardiovasc Surg. 2010;140:e14–6. 5. Hausmann D, Gulba D, Bargheer K, Niedermeyer J, Comess KA, Daniel WG. Successful thrombolysis of an aortic-arch thrombus in a patient after mesenteric embolism. N Engl J Med. 1992;327:500–1. 6. Nakajima M, Tsuchiya K, Honda Y, Koshiyama H, Kobayashi T. Acute pulmonary embolism after cerebral infarction associated with a mobile thrombus in the ascending aorta. Gen Thorac Cardiovasc Surg. 2009;57:654–6. 7. Koster A, Amin-Parsa M, Kaufmann M, Meyer-Jark T, Rudloff M, Diekmann J, et al. Fulminate heparin-induced thrombocytopenia and surgery with deep hypothermic circulatory arrest using bivalirudin. Ann Thorac Surg. 2013;95:1079–81. 8. Ito H, Takahashi K, Sasaki H, Akiho H, Katahira Y, Saito H, et al. Large thrombus in the ascending aorta successfully treated by thrombolysis—an unusual cause of acute massive myocardial infarction. Jpn Circ J. 2001;65:572–4. 9. Rhee MY, Myong NH, Park YB. Primary intimal sarcoma of the aorta: role of transesophageal echocardiography. Circ J. 2002;66:111–3.
CASE REPORT
Plural large floating thrombi in the ascending aorta Hisao Harada • Takeshi Soeda • Yuhei Saitoh Takahiro Nakahara
•
Received: 20 June 2014 / Accepted: 11 December 2014 Ó The Japanese Association for Thoracic Surgery 2014
Abstract Floating thrombi in the ascending aorta are a very rare finding in non-aneurysmal, mildly atherosclerotic or normal aortas. We report a case of floating thrombi in a 66-year-old man who was admitted to the hospital with acute chest pain and dyspnea. Enhanced computed tomography showed two large floating thrombi in the ascending aorta, type B aortic dissection, deep venous thrombosis, and pulmonary embolism. A temporary inferior vena cava filter was inserted and the subject underwent an emergency surgical intervention to remove both masses. His postoperative course was uneventful; the etiology of the thrombi is unknown. Lifelong anticoagulation therapy was started and the subject has been stable without recurrence for the last 2 years. Keywords Ascending aorta Thrombus Aortic dissection Pulmonary embolism
Introduction An ascending aortic thrombus is a rare event [1]. We report a particularly rare case in which plural pedunculated freefloating thrombi of unknown cause attached to the anterior wall of the ascending aorta. There are very few reports in the literature describing plural thrombosis in the ascending aorta.
H. Harada (&) T. Soeda Y. Saitoh T. Nakahara Department of Cardiovascular Surgery, Matsue Red Cross Hospital, 200 Horomachi, Matsue, Shimane 690-8506, Japan e-mail: [email protected]
Case report A 66-year-old man was taken to the hospital by ambulance due to the onset of acute chest pain and dyspnea. He gradually experienced symptomatic relief at the hospital. He had no edema of the lower extremities. His medical history included documented hypertension, type 2 diabetes mellitus treated with oral medication, and rheumatoid arthritis for 15 years. Adrenal corticosteroids had not been administered over the last year. He had quit smoking for about 3 years, before which he had been a two-pack-a-day smoker for 40 years. A year previous to this incident, he had presented with a left renal infarction, which was managed conservatively without pharmacologic intervention because of his refusal to undergo additional investigation. Other embolic events were not known. At the present admission, an enhanced computed tomography (CT) was performed, which revealed a type B acute aortic dissection (the non-communicating type), an acute pulmonary embolism (PE) with left deep venous thrombosis (DVT), and two masses, 5 and 3 cm in length, respectively, which were attached to the anterior wall of the ascending aorta (Fig. 1a–d). The ascending aorta was 36 mm in diameter with no aneurysmal change. CT scans of the thorax/abdomen/pelvis regions revealed no evidence of malignancy. The patient had no familial history of thromboembolic events. A laboratory workup for coagulation disorders, such as anti-phospholipid syndrome, protein S, protein C, and antithrombin III deficiency was negative. The transthoracic echocardiographic study did not reveal any anomaly. The aortic valve was tricuspid without evidence of valvulopathy. Trans-aortic valve flow velocity was 0.8 m/s. The LV wall motion and the left atrial size
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Gen Thorac Cardiovasc Surg
Fig. 1 a Computed tomography (CT) shows two large thrombi in the ascending aorta (arrow); asterisk denotes aortic dissection; white circles denote bilateral pulmonary embolism. b Thrombi attachments to the anterior wall of the ascending aorta can be seen. c, d Pedunculated formations of thrombi can be seen on CT
angiography; (left) from a frontal view; (right) from a lateral view. The red color indicates the attachment portion. e The sizes of removed aortic thrombi; 47 9 28 9 22 mm, 32 9 18 9 13 mm. f Pathological examination revealed organized fibrin masses. These are ‘‘lines of Zahn’’ (asterisk)
were normal. The LV ejection fraction was 69.5 %. Preoperative transesophageal echocardiography confirmed that the left atrial appendage was normal with no thrombus. No patent foramen ovale was detected on the color Doppler echocardiogram. The patient underwent emergency surgery on the admission day to avert an embolic event, particularly brain embolization. Prior to the surgical intervention, he had a temporary inferior vena cava (IVC) filter inserted as a prophylactic measure to prevent additional pulmonary embolisms. Anticoagulation therapy was not indicated preoperatively. The surgery was performed via a median sternotomy and conducted using a cardiopulmonary bypass with moderate hypothermia (25 °C) which was initiated
between the right atrium and the right femoral artery. We performed intraoperative epiaortic echocardiography. As it turned out, there were few atheromatous changes in the ascending aortic wall which might cause debris under aortic cross clamping. However, one mass protruded forward into the aortic arch so we had to withdraw the mass so as not to break it. We performed hypothermic circulatory arrest for 2 min to withdraw the mass and clamp the ascending aorta at the upper end. The masses were removed along with the aortic wall, because malignancy could not be ruled out by appearance alone. The masses were yellowish-white nodular tumors, with a rubber-like hardness that were removed from the intima with relatively little effort (Fig. 1e). The intima of the aorta appeared almost normal, except for the slightly
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Gen Thorac Cardiovasc Surg
discolored area of insertion, and lacked any evidence of tears or ulcerations. The ascending aorta was replaced with a synthetic graft. Histologic examination of the masses revealed old thrombi composed of a fibrous material with erythrocytes, leucocytes, and histiocytes, which were organized partly along the periphery. These are ‘‘lines of Zahn’’ which are the alternating pale pink bands of platelets with fibrin and red bands of erythrocytes. A histopathological evaluation of the aortic wall revealed mild atherosclerosis on the intima and secondary mild capillary invasion into media without any evidence of other arterial wall disease. The postoperative course was uneventful and the IVC filter was removed on postoperative day 14. Brain magnetic resonance imaging showed no findings of cerebral infarction upon postoperative examination. The subject commenced lifelong oral anticoagulation therapy. The patient has been doing well over the past 2 years post-surgery without evidence of recurrent aortic thrombi in follow-up enhanced computed tomography scans.
Discussion An aortic free-floating thrombus is a very rare finding because the aorta is a high-flow vascular region that normally precludes clot formation. In most cases, a patient is taken to a doctor because of peripheral arterial emboli [2–6]. In the present case, the subject had a left renal infarction a year ago, but it was not further scrutinized with enhanced CT. Despite that, he refused further exploration following renal embolism. His home doctor, if any, could have examined him mindfully with transthoracic echocardiography and found the thrombus in the ascending aorta. This time, he complained of symptoms of type B aortic dissection, DVT, and PE, which led to the present discovery. In general, intra-aortic thrombi are associated with aneurysms, aortic dissection, trauma, or complicated atherosclerotic plaques. Uncommonly, they are also due to blood predisposition or disease; anti-phospholipid syndrome [2], heparin-induced thrombocytopenia (HIT) [7], polycythemia, and thrombocytosis. However, an aortic mural thrombus in a non-aneurysmal mildly atherosclerotic or normal aorta is a very rare clinical entity [1, 3]. Therefore, with respect to the primary management for this unusual problem, many physicians are at a loss which to choose [4, 8]. Fayad et al. [1] reported that literature about aortic mural thrombi in a non-aneurysmal mildly atherosclerotic or normal aorta was found in 200 patients from 98 documented articles. The descending thoracic aorta was the most common location of the thrombus (38 %), followed by the arch of the aorta (36 %), the abdominal aorta
(14 %), and finally the ascending aorta (n = 23; 12 %). Of the ascending aorta cases, 22 were floating, one was sessile, and there were no plural mural thrombi cases. Admitting a thrombus in the ascending aorta is extremely rare. For coronary arteries and aortic arch branches that are in close proximity to each other, if the embolism occurs, the risk of sequelae or death due to myocardial infarction and stroke is higher. In the present case, there were two huge thrombi in the ascending aorta. As to the cause, we doubt the association between aortic dissection, DVT, or PE at first glance [6]. We have subsequently determined that there is no direct association. We thought the symptoms at onset were caused by acute PE in view of the nature of the pain. Although the exact time of the onset of the aortic dissection is unknown, it is presumed that the aortic dissection was in the acute phase upon admission, because morphological changes of false lumen were subsequently radical, and had regressed almost completely at the time of discharge. DVT/PE had also disappeared on enhanced CT after 3 months. On the other hand, we considered that the intra-aortic thrombi were in a relatively chronic phase, because of the pathological findings of the thrombi and mild color changes limited to the aortic attachment portion. Although the subject has several risk factors, collagen disease, diabetes mellitus, and smoking history in the past, mechanisms leading to the thrombus formation in the ascending aortic tract remain obscure. Except for the report of drastic hypercoagulable state by HIT [7], there is no report so far, of plural thrombi in the ascending aorta. Both anticoagulation therapy (including thrombolysis) and aortic surgery are commonly used as primary treatment [2–5, 8], but there is no consensus. The results of the literature described above [1] showed that mortality rates were similar between groups; however, patients who received anticoagulation medication as primary therapy tended to have more complications such as stroke, limb loss, and bowel resection. Aortic thrombi persist or recur in 26.4 % of the anticoagulation group and in 5.7 % of the surgery group, and a quarter of the anticoagulation group underwent a secondary aortic procedure. In view of the aforementioned, also in the normal or mild diseased aorta, we are in favor of prioritizing a surgical intervention. In this case, due to two great thrombi in the ascending aorta and considering the risk of embolism, we decided to perform an emergency surgery. It is controversial to replace the aorta with a synthetic graft, because of the possibility of tumors such as sarcoma [9]; however, we decided to proceed. Even if the thrombi were surgically removed, there is a significant risk of recurrence [1], so we consider it necessary to prescribe lifelong anticoagulation treatment due to the subject’s remaining risk factors.
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Conclusion We reported an extremely rare case of plural large floating thrombi in the ascending aorta. The absence of recurrence at the 2-year follow-up confirmed the appropriateness of our therapeutic strategy.
Conflict of interest
None declared.
References 1. Fayad ZY, Semaan E, Fahoum B, Briggs M, Tortolani A, D’Ayala M. Aortic mural thrombus in the normal or minimally atherosclerotic aorta. Ann Vasc Surg. 2013;27:282–90. 2. Humbert VH Jr, Tuna IC, Harrison MR, Curtis DB, Webster SA. Aortic tumour in primary anti-phospholipid syndrome. Lancet. 2003;361:1676. 3. Mandegar MH, Roshanali F, Kocharian A. Complicated course consequences of a floating thrombus in ascending aorta. Eur J Echocardiogr. 2008;9:846–8.
123
4. Chatterjee S, Eagle SS, Adler DH, Byrne JG. Incidental discovery of an ascending aortic thrombus: should this patient undergo surgical intervention? J Thorac Cardiovasc Surg. 2010;140:e14–6. 5. Hausmann D, Gulba D, Bargheer K, Niedermeyer J, Comess KA, Daniel WG. Successful thrombolysis of an aortic-arch thrombus in a patient after mesenteric embolism. N Engl J Med. 1992;327:500–1. 6. Nakajima M, Tsuchiya K, Honda Y, Koshiyama H, Kobayashi T. Acute pulmonary embolism after cerebral infarction associated with a mobile thrombus in the ascending aorta. Gen Thorac Cardiovasc Surg. 2009;57:654–6. 7. Koster A, Amin-Parsa M, Kaufmann M, Meyer-Jark T, Rudloff M, Diekmann J, et al. Fulminate heparin-induced thrombocytopenia and surgery with deep hypothermic circulatory arrest using bivalirudin. Ann Thorac Surg. 2013;95:1079–81. 8. Ito H, Takahashi K, Sasaki H, Akiho H, Katahira Y, Saito H, et al. Large thrombus in the ascending aorta successfully treated by thrombolysis—an unusual cause of acute massive myocardial infarction. Jpn Circ J. 2001;65:572–4. 9. Rhee MY, Myong NH, Park YB. Primary intimal sarcoma of the aorta: role of transesophageal echocardiography. Circ J. 2002;66:111–3.
