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Thrombus of the Ascending Aorta as a Source of Cerebral Embolism
REFERENCES
1 Martini N, Melamed MR. Multiple primary lung cancers. J Thorac Cardiovasc Surg I975; 70:606-I2 2 Mathisen DJ, Jensik RJ, Faber LP, Kittle CF. Survival following resection for second and third primary lung cancers. J Thorac Cardiovasc Surg 1984; 88:502-10 3 Ferguson MK, De Meester TR, DesLauriers J, Little AG, Piraux M, Golomb H. Diagnosis and management of synchronous lung cancers. J Thorac Cardiovasc Surg 1985; 89:378-85 4 Mountain CF. A new international staging system for lung cancer. Chest 1986; 89:225S-33S 5 Takahashi Y, Hirata Y, Saito T, Yamashina T, Arisato N, Watanabe N, et al. Enzyme immunoassay for human serum glutathione Stransferase 1r using monoclonal and polyclonal antibodies. Cancer J 1989; 2:225-29 6 Takahashi T, Ueda R, Song X, Nishida K, Shinzato M, Namikawa R, et al. Two novel cell surface antigens on small cell lung carcinoma defined by mouse monoclonal antibodies NE-25 and PE-35. Cancer Res I986; 46:4770-75 7 Souhami RL, Beverley PCL, Bobrow LG . Antigens of small-cell lung cancer. Lancet I987; 2:325-26 8 Hida T, Koike K, Sekido Y, Nishida K, Sugiura T, Ariyoshi Y, et al. Epitope analysis of cluster I and NK cell-related monoclonal antibodies. Br J Cancer I99I; 63(suppl14):24-8 9 Ueda R, Takahashi T, Watanabe H, Nishida K, Utsumi KR, Ariyoshi Y, et al. Serological and biochemical analysis of four antigens associated with small cell lung cancer. Lung Cancer I988; 4:96-8 10 Warren S, Gates 0 . Multiple primary malignant tumors: a survey of the literature and a statistical study. Am J Cancer 1932; 16:1358-414 11 Gazdar AF, Carney, ON, Guccion JG, Baylin SB. Small cell carcinoma of the lung: cellular origin and relationship to other pulmonary tumors. In: Greco FA, Oldham R, Bunn PA, eds. Small cell lung cancer. New York: Grune and Stratton, 1981; 145-75 I2 Auerbach 0, Stout AP, Hammond EC, Gar6nkel L. Changes in bronchial epithelium in relation to cigarette smoking and in relation to lung cancer. N Eng! J Med 1961; 265:253-67 13 Mclemore T, Martin R. Pulmonary carcinogenesis: aryl hydrocarbon hydroxylase. In: Livingston RB , ed. Lung cancer 1. The Hague, the Netherlands: Martinus Nijhoff Publishers, 1981; 134
T
ransesophageal echocardiography is superior to transthoracic echocardiography in detecting cardiac source of embolism such as left atrial tumors or thrombus, atrial septal defect or aneurysm with patent foramen ovale, and mitral valve prolapse in patients with cerebral ischemia or stroke.'"" Aortic disease with atherosclerotic debris was recently shown by transesophageal echocardiography to be another source of embolism. 1•7• 10 To our knowledge, this is the first report of a patient presenting with a stroke who had a thrombus in the ascending aorta detected by transesophageal echocardiography that was no longer present after treatment with heparin. CASE REPORT
A 74-year-old woman with history of treated hypertension had the sudden onset of left hemiparesis and slurred speech and was admitted to the neurology service for treatment of a stroke. She had normal blood pressure and normal results of physical examination except for the neurologic examination that showed apraxia, left hemiparesis with three of 6ve motor strength , and a left Babinski. Computed tomographic scan of the head showed right frontal and left occipital areas of hypodensity consistent with nonhemorrhagic infarction. A transthoracic echocardiogram was obtained that showed mild left ventricular hypertrophy with normal left ventricular systolic function and no cardiac sourceof emboli. Transesophageal Echocardiography
A 74-year-old woman presented with a stroke. Transesophageal echocardiography showed evidence of a thrombus attached to the wall of the ascending aorta that was not detected by the transthoracic approach. The thrombus was no longer present after treatment with heparin with no recurrent embolic event. To our knowledge, this is the first report of a thrombus attached to the ascending aorta that was no longer present after treatment with heparin, was detected by transesophageal echocardiography, and was thought to be the source of cerebral embolic event. (Chest 1993; 104:1604-0S)
Transesophageal echocardiography was performed using a 5-MHz transducer and an echograph (Sono 1000 Hewlett Packard Echograph) after sedation with midazolam. The left atrium and left atrial appendage were normal with no evidence of tumor or thrombi. The patient was in normal rhythm and there was no evidence of left atrial spontaneous contrast. Imaging of the ascending aorta showed a large and mobile mass that is triangular in shape and appeared at times to be attached at its tip to the wall of the ascending aorta about 2 em superior to the level of the aortic cusps (Fig I, left). This mass was thought to represent a thrombus or a tumor. The valves appeared normal. There was evidence of atheroma involving the ascending aorta, the descending aorta, and left coronary artery. The patient was started on a regimen of heparin drip at I,OOO Ulh and cardiothoracic surgery service was consulted. The plan was to excise that mass from the ascending aorta. Since the J?!ltient had been receiving heparin for six days, a repeated transesophageal echocardiogram was performed to confirm the presence of the mass just prior to cardiac surgery. The repeated transesophageal echocardiogram that was six days apart from the previous test showed the mass in the ascending aorta to be no longer present (Fig 1B, right). The test findings were otherwise unchanged. Since the patient had no clinical evidence of embolism and her condition had improved during the six days, it was assumed that lyses of the thrombus had occurred with heparin preventing further thrombosis. While the patient was receiving heparin she had a positive stool hemoccult test and underwent colonoscopy that showed evidence of a mass in the proximal descending colon that was hemorrhagic; a biopsy specimen showed cancer of the (.'()lon. The heparin therapy was discontinued ten days after her hospital admission, and four days later, repeated transesophageal echocardiogram showed no recurrence of thrombus in the ascending aorta; the patient underwent left hemicolectomy, and a biopsy specimen of the liver showed metastatic adenocarcinoma. The patient was referred to the oncology department.
*From the Department of Medicine, Case Western Reserve University, Cleveland. Reprint requests: Dr. Farah , 2074 Abington Road, Cleveland 44106
Transesophageal echocardiography provides high-resolution imaging of the heart and aorta because of the close
Thrombus of the Ascending Aorta as a Source of Cerebral Embolism* Michel G. Farah, M.D.; and Hani Hawawini , M.D .
1604
DISCUSSION
Thrombus of the Ascending Aorta (Farah, Hawawini)
FIGURE 1A (left). Transesophageal echocardiograrn of the ascending aorta (AO) shows a large mobile thrombus (arrow). B(right) . The thrombus is no longer present after treatment with heparin. LA= left atrium; PA = pulmonary artery. proximity of the esophagus to these structures. The advantage of transesophageal echocardiography over transthoracic echocardiography relates to imaging of posterior structures that are difficult to visualize by standard ec~ocardiography such as the posterior regions of the atria, left'atrial appendage, atrial septum, ascending aorta, descending aorta, and aortic arch. In detecting a cardiac source of embolism in patients with cerebral ischemia or stroke, transesophageal echocardiography was found to be superior to transthoracic echocardiography. •.a Cardiac source of embolism include left atrial thrombus or tumor, left atrial spontaneous contrast "smoke;' atrial septal defect, atrial septal aneurysm associated with patient foramen ovale, and mitral valve prolapse. Recent reports suggest that aortic disease with intra-aortic atherosclerotic debris can be a potential source of embolism .1·7·•• This patient, presenting with a stroke, had atheroma of the ascending and descending aorta and in addition had a large mobile mass with a small pedicle attached to the wall of the ascending aorta suggestive of a thrombus (Fig lA, left) that was detected only by transesophageal echocardiography with no abnormality to suggest a source of embolism by transthoracic echocardiography. The mass, . presumed to be a thrombus, was no longer present on a repeated study six days later (Fig IB, right) while the patient was receiving treatment with heparin. It is assumed that the thrombus lysed and the heparin prevented further thrombosis. The patient was improving neurologically with no evidence of any new embolic events to suggest breaking of the mass or thrombus. To our knowledge, this is the first report of a thrombus attached to the wall of an atheromatous ascending aorta that was no longer present after treatment with heparin, was detected only by transesophageal echocardiography, and is thought to be the source of cerebral embolism. REFERENCES
1 Pop G, Sutherland GR, Koudstaal PJ, Sit Tw, de Jong G,
2
3
4
5
6
7
8
9
10
Roelandt JRTC. Transesophageal echocardiography in the detection of intracardiac embolic sources in patients with transient ischemic attacks. Stroke 1990; 21 :560-65 Zenker G, Erbel R, Kramer G, et al. Transesophageal twodimensional echocardiography in young patients with cerebral ischemic events. Stroke 1988; 19:345-48 Castello R, Pearson AC, Labovitz AJ, Wallace P. Atrial spontaneous contrast in patients undergoing transesophageal echocardiography; prevalence and clinical implications. Am J Cardiol 1990; 65:1149-53 Pearson AC, Labovitz AJ, Tatineni S, Gomez CR. Superiority of transesophageal echocardiography in detecting cardiac source of embolism in patients with cerebral ischemia of uncertain etiology. JAm Coli Cardiol1991; 17:66-72 Pearson AC, Nagelhout D, Castello R, Gomez CR, Labovitz AJ. Atrial septal aneurysm and stroke: a transesophageal echocardiographic study. JAm Coli Cardiol1991; 18:1223-29 Black 1\V, Hopkins AP, Lee LCL, Walsh WF. Left atrial spontaneous echo contrast: a clinical and echocardiographic analysis. JAm Coil Cardiol1991; 18:398-404 Tunick PA, Kronzon I. Protruding atherosclerotic plaque in the aortic arch of patients with systemic embolization: a new finding seen by transesophageal echocardiography. Am Heart J 1990; 120:658-60 Karalis DC, Chandrasekaran K, Victor MF, Ross JJ, Mintz GS. Recognition and embolic potential of intraaortic atherosclerotic debris. JAm Coli Cardiol1991; 17:73-8 Tunick PA, Gulliford AT, Lamparello PJ, Kronzon I. Atheromatosis of the aortic arch as an occult source of multiple systemic emboli. Ann Intern Med 1991; 114:391-92 Tunick PA, Perez JL. Kronzon I. Protruding atheromas in the thoracic aorta and systemic embolization. Ann Intern Med 1991; 115:423-27 CHEST I 104 I 5 I NOVEMBER, 1993
1605
1 Martini N, Melamed MR. Multiple primary lung cancers. J Thorac Cardiovasc Surg I975; 70:606-I2 2 Mathisen DJ, Jensik RJ, Faber LP, Kittle CF. Survival following resection for second and third primary lung cancers. J Thorac Cardiovasc Surg 1984; 88:502-10 3 Ferguson MK, De Meester TR, DesLauriers J, Little AG, Piraux M, Golomb H. Diagnosis and management of synchronous lung cancers. J Thorac Cardiovasc Surg 1985; 89:378-85 4 Mountain CF. A new international staging system for lung cancer. Chest 1986; 89:225S-33S 5 Takahashi Y, Hirata Y, Saito T, Yamashina T, Arisato N, Watanabe N, et al. Enzyme immunoassay for human serum glutathione Stransferase 1r using monoclonal and polyclonal antibodies. Cancer J 1989; 2:225-29 6 Takahashi T, Ueda R, Song X, Nishida K, Shinzato M, Namikawa R, et al. Two novel cell surface antigens on small cell lung carcinoma defined by mouse monoclonal antibodies NE-25 and PE-35. Cancer Res I986; 46:4770-75 7 Souhami RL, Beverley PCL, Bobrow LG . Antigens of small-cell lung cancer. Lancet I987; 2:325-26 8 Hida T, Koike K, Sekido Y, Nishida K, Sugiura T, Ariyoshi Y, et al. Epitope analysis of cluster I and NK cell-related monoclonal antibodies. Br J Cancer I99I; 63(suppl14):24-8 9 Ueda R, Takahashi T, Watanabe H, Nishida K, Utsumi KR, Ariyoshi Y, et al. Serological and biochemical analysis of four antigens associated with small cell lung cancer. Lung Cancer I988; 4:96-8 10 Warren S, Gates 0 . Multiple primary malignant tumors: a survey of the literature and a statistical study. Am J Cancer 1932; 16:1358-414 11 Gazdar AF, Carney, ON, Guccion JG, Baylin SB. Small cell carcinoma of the lung: cellular origin and relationship to other pulmonary tumors. In: Greco FA, Oldham R, Bunn PA, eds. Small cell lung cancer. New York: Grune and Stratton, 1981; 145-75 I2 Auerbach 0, Stout AP, Hammond EC, Gar6nkel L. Changes in bronchial epithelium in relation to cigarette smoking and in relation to lung cancer. N Eng! J Med 1961; 265:253-67 13 Mclemore T, Martin R. Pulmonary carcinogenesis: aryl hydrocarbon hydroxylase. In: Livingston RB , ed. Lung cancer 1. The Hague, the Netherlands: Martinus Nijhoff Publishers, 1981; 134
T
ransesophageal echocardiography is superior to transthoracic echocardiography in detecting cardiac source of embolism such as left atrial tumors or thrombus, atrial septal defect or aneurysm with patent foramen ovale, and mitral valve prolapse in patients with cerebral ischemia or stroke.'"" Aortic disease with atherosclerotic debris was recently shown by transesophageal echocardiography to be another source of embolism. 1•7• 10 To our knowledge, this is the first report of a patient presenting with a stroke who had a thrombus in the ascending aorta detected by transesophageal echocardiography that was no longer present after treatment with heparin. CASE REPORT
A 74-year-old woman with history of treated hypertension had the sudden onset of left hemiparesis and slurred speech and was admitted to the neurology service for treatment of a stroke. She had normal blood pressure and normal results of physical examination except for the neurologic examination that showed apraxia, left hemiparesis with three of 6ve motor strength , and a left Babinski. Computed tomographic scan of the head showed right frontal and left occipital areas of hypodensity consistent with nonhemorrhagic infarction. A transthoracic echocardiogram was obtained that showed mild left ventricular hypertrophy with normal left ventricular systolic function and no cardiac sourceof emboli. Transesophageal Echocardiography
A 74-year-old woman presented with a stroke. Transesophageal echocardiography showed evidence of a thrombus attached to the wall of the ascending aorta that was not detected by the transthoracic approach. The thrombus was no longer present after treatment with heparin with no recurrent embolic event. To our knowledge, this is the first report of a thrombus attached to the ascending aorta that was no longer present after treatment with heparin, was detected by transesophageal echocardiography, and was thought to be the source of cerebral embolic event. (Chest 1993; 104:1604-0S)
Transesophageal echocardiography was performed using a 5-MHz transducer and an echograph (Sono 1000 Hewlett Packard Echograph) after sedation with midazolam. The left atrium and left atrial appendage were normal with no evidence of tumor or thrombi. The patient was in normal rhythm and there was no evidence of left atrial spontaneous contrast. Imaging of the ascending aorta showed a large and mobile mass that is triangular in shape and appeared at times to be attached at its tip to the wall of the ascending aorta about 2 em superior to the level of the aortic cusps (Fig I, left). This mass was thought to represent a thrombus or a tumor. The valves appeared normal. There was evidence of atheroma involving the ascending aorta, the descending aorta, and left coronary artery. The patient was started on a regimen of heparin drip at I,OOO Ulh and cardiothoracic surgery service was consulted. The plan was to excise that mass from the ascending aorta. Since the J?!ltient had been receiving heparin for six days, a repeated transesophageal echocardiogram was performed to confirm the presence of the mass just prior to cardiac surgery. The repeated transesophageal echocardiogram that was six days apart from the previous test showed the mass in the ascending aorta to be no longer present (Fig 1B, right). The test findings were otherwise unchanged. Since the patient had no clinical evidence of embolism and her condition had improved during the six days, it was assumed that lyses of the thrombus had occurred with heparin preventing further thrombosis. While the patient was receiving heparin she had a positive stool hemoccult test and underwent colonoscopy that showed evidence of a mass in the proximal descending colon that was hemorrhagic; a biopsy specimen showed cancer of the (.'()lon. The heparin therapy was discontinued ten days after her hospital admission, and four days later, repeated transesophageal echocardiogram showed no recurrence of thrombus in the ascending aorta; the patient underwent left hemicolectomy, and a biopsy specimen of the liver showed metastatic adenocarcinoma. The patient was referred to the oncology department.
*From the Department of Medicine, Case Western Reserve University, Cleveland. Reprint requests: Dr. Farah , 2074 Abington Road, Cleveland 44106
Transesophageal echocardiography provides high-resolution imaging of the heart and aorta because of the close
Thrombus of the Ascending Aorta as a Source of Cerebral Embolism* Michel G. Farah, M.D.; and Hani Hawawini , M.D .
1604
DISCUSSION
Thrombus of the Ascending Aorta (Farah, Hawawini)
FIGURE 1A (left). Transesophageal echocardiograrn of the ascending aorta (AO) shows a large mobile thrombus (arrow). B(right) . The thrombus is no longer present after treatment with heparin. LA= left atrium; PA = pulmonary artery. proximity of the esophagus to these structures. The advantage of transesophageal echocardiography over transthoracic echocardiography relates to imaging of posterior structures that are difficult to visualize by standard ec~ocardiography such as the posterior regions of the atria, left'atrial appendage, atrial septum, ascending aorta, descending aorta, and aortic arch. In detecting a cardiac source of embolism in patients with cerebral ischemia or stroke, transesophageal echocardiography was found to be superior to transthoracic echocardiography. •.a Cardiac source of embolism include left atrial thrombus or tumor, left atrial spontaneous contrast "smoke;' atrial septal defect, atrial septal aneurysm associated with patient foramen ovale, and mitral valve prolapse. Recent reports suggest that aortic disease with intra-aortic atherosclerotic debris can be a potential source of embolism .1·7·•• This patient, presenting with a stroke, had atheroma of the ascending and descending aorta and in addition had a large mobile mass with a small pedicle attached to the wall of the ascending aorta suggestive of a thrombus (Fig lA, left) that was detected only by transesophageal echocardiography with no abnormality to suggest a source of embolism by transthoracic echocardiography. The mass, . presumed to be a thrombus, was no longer present on a repeated study six days later (Fig IB, right) while the patient was receiving treatment with heparin. It is assumed that the thrombus lysed and the heparin prevented further thrombosis. The patient was improving neurologically with no evidence of any new embolic events to suggest breaking of the mass or thrombus. To our knowledge, this is the first report of a thrombus attached to the wall of an atheromatous ascending aorta that was no longer present after treatment with heparin, was detected only by transesophageal echocardiography, and is thought to be the source of cerebral embolism. REFERENCES
1 Pop G, Sutherland GR, Koudstaal PJ, Sit Tw, de Jong G,
2
3
4
5
6
7
8
9
10
Roelandt JRTC. Transesophageal echocardiography in the detection of intracardiac embolic sources in patients with transient ischemic attacks. Stroke 1990; 21 :560-65 Zenker G, Erbel R, Kramer G, et al. Transesophageal twodimensional echocardiography in young patients with cerebral ischemic events. Stroke 1988; 19:345-48 Castello R, Pearson AC, Labovitz AJ, Wallace P. Atrial spontaneous contrast in patients undergoing transesophageal echocardiography; prevalence and clinical implications. Am J Cardiol 1990; 65:1149-53 Pearson AC, Labovitz AJ, Tatineni S, Gomez CR. Superiority of transesophageal echocardiography in detecting cardiac source of embolism in patients with cerebral ischemia of uncertain etiology. JAm Coli Cardiol1991; 17:66-72 Pearson AC, Nagelhout D, Castello R, Gomez CR, Labovitz AJ. Atrial septal aneurysm and stroke: a transesophageal echocardiographic study. JAm Coli Cardiol1991; 18:1223-29 Black 1\V, Hopkins AP, Lee LCL, Walsh WF. Left atrial spontaneous echo contrast: a clinical and echocardiographic analysis. JAm Coil Cardiol1991; 18:398-404 Tunick PA, Kronzon I. Protruding atherosclerotic plaque in the aortic arch of patients with systemic embolization: a new finding seen by transesophageal echocardiography. Am Heart J 1990; 120:658-60 Karalis DC, Chandrasekaran K, Victor MF, Ross JJ, Mintz GS. Recognition and embolic potential of intraaortic atherosclerotic debris. JAm Coli Cardiol1991; 17:73-8 Tunick PA, Gulliford AT, Lamparello PJ, Kronzon I. Atheromatosis of the aortic arch as an occult source of multiple systemic emboli. Ann Intern Med 1991; 114:391-92 Tunick PA, Perez JL. Kronzon I. Protruding atheromas in the thoracic aorta and systemic embolization. Ann Intern Med 1991; 115:423-27 CHEST I 104 I 5 I NOVEMBER, 1993
1605