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Intraluminal Thrombus of the Ascending Aorta with Systemic Embolism Detected by Spiral CT
75
CASE REPORTS
REFERENCES 1 Resnick D, Niwayama G. Enostosis, hyperostosis and periostitis. In: Resnick D, Niwayama G, eds. Diagnosis of Bone and Joint Disorders. Philadelphia, USA: W.B. Saunders Company, 1988:4097– 4115. 2 Greenfield GB. Cardinal roentgen features. In: Greenfield GB, ed. Radiology of Bone Diseases. Philadelphia, USA: J.B. Lippincott Company, 1990:405–578.
3 Wilner D. Periosteal and proliferative disorders. In: Wilner D, ed. Radiology of Bone Tumours and Allied Disorders. Philadelphia, USA: W.B. Saunders Company, 1982:1792–1842. 4 Dickinson CJ. The aetiology of clubbing and hypertrophic osteoarthropathy. Eur J Clin Invest 1993;23:330–338. 5 Martinez-Lavin J. Pathogenesis of hypertrophic osteoarhropathy. Clin Exp Rheumatol 1992;10:49–50. 6 Pineda C. Diagnostic imaging in hypertrophic osteoarthropathy. Clin Exp Rheumatol 1992; 10:27–33.
Intraluminal Thrombus of the Ascending Aorta with Systemic Embolism Detected by Spiral CT S. D . QAN ADL I, A . S. RANGHE ARD, P. L ACOMBE Department of Radiology, University Rene´ Descartes-Paris V, Ambroise Pare´ Hospital, Boulogne, France
Aortic thrombus without aneurysm as a source of systemic embolism is a rare entity that is little documented. It is usually described in the abdominal aorta [1–3] or in the aortic arch [4– 9]. Intraluminal thrombus (IT) in the aorta is mostly attributed to atherosclerosis [1,5–7,10] or to previous heparin therapy [2,11]. We report two unusual cases of IT of the ascending aorta diagnosed by spiral computed tomography (CT) and managed by anticoagulation therapy.
approach in order to avoid potential thrombus mobilization, and because of the reported high risk of catheter-related emboli in similar conditions [12]. The mass showed the typical features of thrombus, both on CT and on ultrasound examination. In addition, CT showed a limited left renal infarction. The patient was treated with intravenous heparin IV for one week (1000 IU/h) followed by warfarin therapy. The clinical course was favourable with complete disappearance of the thrombus 3 weeks later (Fig. 1d). There has been no recurrence of thromboembolism during 15 months follow-up.
CASE REPORTS
Case 2
Case 1
A 50-year-old woman was admitted with acute ischaemia of the left leg. She had no history of ischaemic heart disease, hypertension, vasculopathy, thromboembolic disease or malignancy. She had not received heparin previously. Smoking was her only cardiovascular risk factor. Angiography showed emboli in the left tibio-fibular trunk and in the right fibular artery without severe atherosclerosis. The patient received intravenous heparin. Spiral CT of the aorta performed on the third day showed an intraluminal filling defect in the ascending aorta (Fig. 2a). No severe atherosclerosis or evidence of intimal dissection was detected. TOE, performed 3 h previously, was normal. CT findings were confirmed by DSA of the thoracic aorta (Fig. 2b) following contrast injection into the pulmonary artery. Continuing heparin therapy resulted in resolution of the thrombus, and spiral CT performed 1 week later did not reveal any filling defect. At the time of discharge the patient was asymptomatic with no recurrence of thromboembolism on 6 months follow-up.
A 62-year-old woman was admitted to the hospital for acute ischaemia of the left hand evolving over 24 h. Six weeks previously she experienced subacute ischaemia of the right leg which spontaneously resolved. Doppler ultrasound of the left arm demonstrated an occlusion of the left brachial artery at its medial third, treated by embolectomy using a Fogarty catheter. The patient had no cardiovascular risk factors. She was normotensive and the heart was in normal sinus rhythm. Electrocardiogram, chest radiography and laboratory tests including coagulation (fibrinogen, prothrombin time, platelet count, bleeding time, dimer test, protein C, protein S, antithrombin III), and immunological studies (antinuclear and anticardiolipin antibodies, lupus anticoagulant) were normal. Two-dimensional echocardiography, performed on the second hospital day, showed normal cardiac contractility and no evidence of valvular disease or of thrombus in the cardiac cavities. Spiral CT of the aorta was performed on the third hospital day using a CT Twin Flash system (Elscint, Haifa, Israel) with collimation of 2 × 5 mm and a pitch of 1.5 (effective slice thickness: 5.5 mm). Enhanced images (150 ml of 25% iodinated contrast material at 4 ml/s) showed a large filling defect in the ascending aorta extending towards the aortic arch (Fig. 1a). Unenhanced CT images detected subtle irregularity of the left posterior wall of the ascending aorta with a calcified component indicative of atherosclerotic plaque (Fig. 1b). Transoesophageal echocardiography (TOE) and digital subtraction aortography (DSA) confirmed a pedunculated and highly mobile endoluminal aortic mass arising from the posterior wall of the ascending aorta (Fig. 1c). DSA was performed by pulmonary artery Author for correspondence and guarantor of study: Dr S. D. Qanadli, Service de Radiologie, Hoˆpital Ambroise Pare´, 9 avenue Charles de Gaulle, 92104 Boulogne Cedex, France.
DISCUSSION
Thrombus of the non-aneurysmal aorta is a known entity, previously reported to be a source of emboli producing arterial vascular occlusion of peripheral vessels, mesenteric, splenic or renal arteries [1,3,5–10,13–16]. Most of the reported aortic thrombi were located in the aortic arch [6–9], the descending thoracic aorta [10,13] and more frequently in the abdominal aorta from the tenth thoracic vertebra to the aortic bifurcation [1,3]. The ascending aorta is an uncommon location for IT.
76
CLINICAL RADIOLOGY
(a)
(b)
(c)
(d)
Fig. 1 – (a) Enhanced spiral computed tomography (CT) of the chest (axial image) shows well defined low-density area into the aortic arch indicative of intraluminal thrombus (arrow). (b) Axial CT without contrast media at the carina level revealing a calcified atherosclerotic plaque of the ascending aorta. (c) Transoesophageal echocardiography (short-axis view) at the level of the ascending aorta. Mobile pedunculated echoes (arrow) protruding into the aortic lumen. (d) Enhanced spiral CT 3 weeks after heparin therapy at the level of (a). No thrombus is seen.
Baumgartner and Leupi [16] described, in 1993, a mass in the ascending aorta in 41-year-old man with repeated distal embolisms. Histological examination after surgery revealed that the mass was a thrombus adjacent to atherosclerotic plaque. Farah and Hawawini [14] reported, in a 74-year-old woman with stroke, a thrombus attached to the wall of the ascending aorta diagnosed by TOE. We did not find any report in the literature of IT of the ascending thoracic aorta diagnosed by spiral CT. Extensive atherosclerosis, heparin-induced thromboembolism, hypercoagulability state and post-operative status are the major suggested pathogenic factors of intraluminal aortic thrombus [1,11]. Unlike most published reports, our patients had not received heparin previously and imaging techniques had not documented extensive atherosclerosis or other aortic disease. In the first case, a focal calcified plaque was observed in the left posterior wall of the ascending aorta, which is an uncommon location for atherosclerotic plaques. Tobler et al. [17] studied the distribution of atherosclerotic plaques in the
ascending aorta and found a prevalence of 4% in this location. Furthermore, one patient had no cardiovascular risk factors and the other had only smoking. Contrast enhanced spiral CT demonstrated the intraluminal thrombus in the ascending aorta in both cases, whereas TOE was only helpful in the first case. It has been suggested that management of aortic thrombus in the descending thoracic and abdominal aorta requires invasive aortic procedures to prevent serious and even fatal complications [1]. The surgical approach is more aggressive in the ascending aorta than in other aortic segments [4,16], so heparin was used to treat our patients and there was no recurrent embolization. According to a previous report of IT of the ascending aorta or the aortic arch [8–10,14], thrombus can be successfully treated by anticoagulation alone. However, surgery should be considered if disappearance of IT is not observed or there is recurrent embolism. In conclusion, intraluminal thrombus may be located in the ascending aorta, even without extensive atherosclerotic plaques
77
CASE REPORTS
REFERENCES
(a)
(b) Fig. 2 – (a) Enhanced spiral CT scan shows intraluminal filling defect of the ascending aorta (arrow). Note the absence of atherosclerotic changes of the aorta. (b) Digital subtraction aortography (right anterior oblique view), performed by pulmonary artery approach, discloses an uncommon thrombus of the ascending aorta (arrow).
or aneurysmal changes. Patients presenting with systemic embolism without identified source should undergo spiral CT scan to evaluate the entire aorta.
1 Williams GM, Harrington D, Burdick J et al. Mural thrombus of the aorta. An important, frequently neglected cause of large peripheral emboli. Ann Surg 1981;194:737–744. 2 Feng WC, Singh AK, Bert AA et al. Perioperative paraplegia and multiorgan failure from heparin-induced thrombocytopenia. Ann Thorac Surg 1993;55:1555–1557. 3 Lozano P, Al Mousa E, Wei CF et al. Intra-aortic thrombus producing embolic arterial vascular disease. Circulation 1996;93:1471. 4 Sadony V, Walz M, Lohr E et al. Unusual cause of recurrent arterial embolism: floating thrombus in the aortic arch surgically removed under hypothermic cardiocirculatory arrest. Eur J Cardiothorac Surg 1988;2:469–471. 5 Tunick PA, Perez JL, Kronzon I. Protruding atheromas in the thoracic aorta and systemic embolization. Ann Intern Med 1991;115:423– 427. 6 Mochizuki S, Takayama S, Nishiyama T et al. Two cases of protruding atherosclerotic plaques with mobile projections in the aortic arch. Intern Med 1993;32:777–780. 7 Mitusch R, Stierle U, Tepe C et al. Systemic embolism in aortic arch atheromatosis. Eur Heart J 1994;15:1373–1380. 8 Laperche T, Laurian C, Roudant R et al. Mobile thromboses of the aortic arch without aortic debris. A transesophgeal echocardiography finding associated with unexplained arterial embolism. The Filiale Echocardiographie de la Societe Francaise de Cardiologie. Circulation 1997;96:288–294. 9 Shindo S, Iyori K, Ishimoto T et al. Localised thrombus in the distal aortic arch: its aetiology analysed by three-dimensional mould model of the thoracic aorta. Int Angiol 1997;16:171–175. 10 Bansal RC, Pauls GL, Shankel SW. Blue digit syndrome: transesophageal echocardiographic identification of thoracic aortic plaque-related thrombi and successful outcome with warfarin. J Am Soc Echocardiogr 1993;6:319–323. 11 Lindsey SM, Maddison FE, Towne JB. Heparin-induced thromboembolism: angiographic features. Radiology 1979;131:771–774. 12 Karalis DG, Quinn V, Victor MF et al. Risk of catheter-related emboli in patients with atherosclerotic debris in the thoracic aorta. Am Heart J 1996;131:1149–1155. 13 Karalis DG, Chandrasekaran K, Victor MF et al. Recognition and embolic potential of intraaortic atherosclerotic debris. J Am Coll Cardiol 1991;17:73–78. 14 Farah MG, Hawawini H. Thrombus of the ascending aorta as source of cerebral embolism. Chest 1993;104:1604–1605. 15 Belkin RN, Chaudhry S, Chung J et al. Detection of ascending aorta thrombi with transesophageal echocardiography in patients with systemic embolization. Am Heart J 1995;130:1294–1295. 16 Baumgartner J, Leupi F. Thrombosis of the ascending aorta – a rare cause for recurrent arterial embolism. Helv Chir Acta 1993;60:163– 166. 17 Tobler HG, Edwards JE. Frequency and location of atherosclerotic plaques in the ascending aorta. J Thorac Cardiovasc Surg 1988;96: 304–306.
CASE REPORTS
REFERENCES 1 Resnick D, Niwayama G. Enostosis, hyperostosis and periostitis. In: Resnick D, Niwayama G, eds. Diagnosis of Bone and Joint Disorders. Philadelphia, USA: W.B. Saunders Company, 1988:4097– 4115. 2 Greenfield GB. Cardinal roentgen features. In: Greenfield GB, ed. Radiology of Bone Diseases. Philadelphia, USA: J.B. Lippincott Company, 1990:405–578.
3 Wilner D. Periosteal and proliferative disorders. In: Wilner D, ed. Radiology of Bone Tumours and Allied Disorders. Philadelphia, USA: W.B. Saunders Company, 1982:1792–1842. 4 Dickinson CJ. The aetiology of clubbing and hypertrophic osteoarthropathy. Eur J Clin Invest 1993;23:330–338. 5 Martinez-Lavin J. Pathogenesis of hypertrophic osteoarhropathy. Clin Exp Rheumatol 1992;10:49–50. 6 Pineda C. Diagnostic imaging in hypertrophic osteoarthropathy. Clin Exp Rheumatol 1992; 10:27–33.
Intraluminal Thrombus of the Ascending Aorta with Systemic Embolism Detected by Spiral CT S. D . QAN ADL I, A . S. RANGHE ARD, P. L ACOMBE Department of Radiology, University Rene´ Descartes-Paris V, Ambroise Pare´ Hospital, Boulogne, France
Aortic thrombus without aneurysm as a source of systemic embolism is a rare entity that is little documented. It is usually described in the abdominal aorta [1–3] or in the aortic arch [4– 9]. Intraluminal thrombus (IT) in the aorta is mostly attributed to atherosclerosis [1,5–7,10] or to previous heparin therapy [2,11]. We report two unusual cases of IT of the ascending aorta diagnosed by spiral computed tomography (CT) and managed by anticoagulation therapy.
approach in order to avoid potential thrombus mobilization, and because of the reported high risk of catheter-related emboli in similar conditions [12]. The mass showed the typical features of thrombus, both on CT and on ultrasound examination. In addition, CT showed a limited left renal infarction. The patient was treated with intravenous heparin IV for one week (1000 IU/h) followed by warfarin therapy. The clinical course was favourable with complete disappearance of the thrombus 3 weeks later (Fig. 1d). There has been no recurrence of thromboembolism during 15 months follow-up.
CASE REPORTS
Case 2
Case 1
A 50-year-old woman was admitted with acute ischaemia of the left leg. She had no history of ischaemic heart disease, hypertension, vasculopathy, thromboembolic disease or malignancy. She had not received heparin previously. Smoking was her only cardiovascular risk factor. Angiography showed emboli in the left tibio-fibular trunk and in the right fibular artery without severe atherosclerosis. The patient received intravenous heparin. Spiral CT of the aorta performed on the third day showed an intraluminal filling defect in the ascending aorta (Fig. 2a). No severe atherosclerosis or evidence of intimal dissection was detected. TOE, performed 3 h previously, was normal. CT findings were confirmed by DSA of the thoracic aorta (Fig. 2b) following contrast injection into the pulmonary artery. Continuing heparin therapy resulted in resolution of the thrombus, and spiral CT performed 1 week later did not reveal any filling defect. At the time of discharge the patient was asymptomatic with no recurrence of thromboembolism on 6 months follow-up.
A 62-year-old woman was admitted to the hospital for acute ischaemia of the left hand evolving over 24 h. Six weeks previously she experienced subacute ischaemia of the right leg which spontaneously resolved. Doppler ultrasound of the left arm demonstrated an occlusion of the left brachial artery at its medial third, treated by embolectomy using a Fogarty catheter. The patient had no cardiovascular risk factors. She was normotensive and the heart was in normal sinus rhythm. Electrocardiogram, chest radiography and laboratory tests including coagulation (fibrinogen, prothrombin time, platelet count, bleeding time, dimer test, protein C, protein S, antithrombin III), and immunological studies (antinuclear and anticardiolipin antibodies, lupus anticoagulant) were normal. Two-dimensional echocardiography, performed on the second hospital day, showed normal cardiac contractility and no evidence of valvular disease or of thrombus in the cardiac cavities. Spiral CT of the aorta was performed on the third hospital day using a CT Twin Flash system (Elscint, Haifa, Israel) with collimation of 2 × 5 mm and a pitch of 1.5 (effective slice thickness: 5.5 mm). Enhanced images (150 ml of 25% iodinated contrast material at 4 ml/s) showed a large filling defect in the ascending aorta extending towards the aortic arch (Fig. 1a). Unenhanced CT images detected subtle irregularity of the left posterior wall of the ascending aorta with a calcified component indicative of atherosclerotic plaque (Fig. 1b). Transoesophageal echocardiography (TOE) and digital subtraction aortography (DSA) confirmed a pedunculated and highly mobile endoluminal aortic mass arising from the posterior wall of the ascending aorta (Fig. 1c). DSA was performed by pulmonary artery Author for correspondence and guarantor of study: Dr S. D. Qanadli, Service de Radiologie, Hoˆpital Ambroise Pare´, 9 avenue Charles de Gaulle, 92104 Boulogne Cedex, France.
DISCUSSION
Thrombus of the non-aneurysmal aorta is a known entity, previously reported to be a source of emboli producing arterial vascular occlusion of peripheral vessels, mesenteric, splenic or renal arteries [1,3,5–10,13–16]. Most of the reported aortic thrombi were located in the aortic arch [6–9], the descending thoracic aorta [10,13] and more frequently in the abdominal aorta from the tenth thoracic vertebra to the aortic bifurcation [1,3]. The ascending aorta is an uncommon location for IT.
76
CLINICAL RADIOLOGY
(a)
(b)
(c)
(d)
Fig. 1 – (a) Enhanced spiral computed tomography (CT) of the chest (axial image) shows well defined low-density area into the aortic arch indicative of intraluminal thrombus (arrow). (b) Axial CT without contrast media at the carina level revealing a calcified atherosclerotic plaque of the ascending aorta. (c) Transoesophageal echocardiography (short-axis view) at the level of the ascending aorta. Mobile pedunculated echoes (arrow) protruding into the aortic lumen. (d) Enhanced spiral CT 3 weeks after heparin therapy at the level of (a). No thrombus is seen.
Baumgartner and Leupi [16] described, in 1993, a mass in the ascending aorta in 41-year-old man with repeated distal embolisms. Histological examination after surgery revealed that the mass was a thrombus adjacent to atherosclerotic plaque. Farah and Hawawini [14] reported, in a 74-year-old woman with stroke, a thrombus attached to the wall of the ascending aorta diagnosed by TOE. We did not find any report in the literature of IT of the ascending thoracic aorta diagnosed by spiral CT. Extensive atherosclerosis, heparin-induced thromboembolism, hypercoagulability state and post-operative status are the major suggested pathogenic factors of intraluminal aortic thrombus [1,11]. Unlike most published reports, our patients had not received heparin previously and imaging techniques had not documented extensive atherosclerosis or other aortic disease. In the first case, a focal calcified plaque was observed in the left posterior wall of the ascending aorta, which is an uncommon location for atherosclerotic plaques. Tobler et al. [17] studied the distribution of atherosclerotic plaques in the
ascending aorta and found a prevalence of 4% in this location. Furthermore, one patient had no cardiovascular risk factors and the other had only smoking. Contrast enhanced spiral CT demonstrated the intraluminal thrombus in the ascending aorta in both cases, whereas TOE was only helpful in the first case. It has been suggested that management of aortic thrombus in the descending thoracic and abdominal aorta requires invasive aortic procedures to prevent serious and even fatal complications [1]. The surgical approach is more aggressive in the ascending aorta than in other aortic segments [4,16], so heparin was used to treat our patients and there was no recurrent embolization. According to a previous report of IT of the ascending aorta or the aortic arch [8–10,14], thrombus can be successfully treated by anticoagulation alone. However, surgery should be considered if disappearance of IT is not observed or there is recurrent embolism. In conclusion, intraluminal thrombus may be located in the ascending aorta, even without extensive atherosclerotic plaques
77
CASE REPORTS
REFERENCES
(a)
(b) Fig. 2 – (a) Enhanced spiral CT scan shows intraluminal filling defect of the ascending aorta (arrow). Note the absence of atherosclerotic changes of the aorta. (b) Digital subtraction aortography (right anterior oblique view), performed by pulmonary artery approach, discloses an uncommon thrombus of the ascending aorta (arrow).
or aneurysmal changes. Patients presenting with systemic embolism without identified source should undergo spiral CT scan to evaluate the entire aorta.
1 Williams GM, Harrington D, Burdick J et al. Mural thrombus of the aorta. An important, frequently neglected cause of large peripheral emboli. Ann Surg 1981;194:737–744. 2 Feng WC, Singh AK, Bert AA et al. Perioperative paraplegia and multiorgan failure from heparin-induced thrombocytopenia. Ann Thorac Surg 1993;55:1555–1557. 3 Lozano P, Al Mousa E, Wei CF et al. Intra-aortic thrombus producing embolic arterial vascular disease. Circulation 1996;93:1471. 4 Sadony V, Walz M, Lohr E et al. Unusual cause of recurrent arterial embolism: floating thrombus in the aortic arch surgically removed under hypothermic cardiocirculatory arrest. Eur J Cardiothorac Surg 1988;2:469–471. 5 Tunick PA, Perez JL, Kronzon I. Protruding atheromas in the thoracic aorta and systemic embolization. Ann Intern Med 1991;115:423– 427. 6 Mochizuki S, Takayama S, Nishiyama T et al. Two cases of protruding atherosclerotic plaques with mobile projections in the aortic arch. Intern Med 1993;32:777–780. 7 Mitusch R, Stierle U, Tepe C et al. Systemic embolism in aortic arch atheromatosis. Eur Heart J 1994;15:1373–1380. 8 Laperche T, Laurian C, Roudant R et al. Mobile thromboses of the aortic arch without aortic debris. A transesophgeal echocardiography finding associated with unexplained arterial embolism. The Filiale Echocardiographie de la Societe Francaise de Cardiologie. Circulation 1997;96:288–294. 9 Shindo S, Iyori K, Ishimoto T et al. Localised thrombus in the distal aortic arch: its aetiology analysed by three-dimensional mould model of the thoracic aorta. Int Angiol 1997;16:171–175. 10 Bansal RC, Pauls GL, Shankel SW. Blue digit syndrome: transesophageal echocardiographic identification of thoracic aortic plaque-related thrombi and successful outcome with warfarin. J Am Soc Echocardiogr 1993;6:319–323. 11 Lindsey SM, Maddison FE, Towne JB. Heparin-induced thromboembolism: angiographic features. Radiology 1979;131:771–774. 12 Karalis DG, Quinn V, Victor MF et al. Risk of catheter-related emboli in patients with atherosclerotic debris in the thoracic aorta. Am Heart J 1996;131:1149–1155. 13 Karalis DG, Chandrasekaran K, Victor MF et al. Recognition and embolic potential of intraaortic atherosclerotic debris. J Am Coll Cardiol 1991;17:73–78. 14 Farah MG, Hawawini H. Thrombus of the ascending aorta as source of cerebral embolism. Chest 1993;104:1604–1605. 15 Belkin RN, Chaudhry S, Chung J et al. Detection of ascending aorta thrombi with transesophageal echocardiography in patients with systemic embolization. Am Heart J 1995;130:1294–1295. 16 Baumgartner J, Leupi F. Thrombosis of the ascending aorta – a rare cause for recurrent arterial embolism. Helv Chir Acta 1993;60:163– 166. 17 Tobler HG, Edwards JE. Frequency and location of atherosclerotic plaques in the ascending aorta. J Thorac Cardiovasc Surg 1988;96: 304–306.