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Aortic Thromboembolism Successfully Treated with Anticoagulation and Antiplatelet Therapy
CLINICAL COMMUNICATION TO THE EDITOR
Aortic Thromboembolism Successfully Treated with Anticoagulation and Antiplatelet Therapy To the Editor: We report a case of an aortic thromboembolism that had a positive outcome after prompt treatment with anticoagulation and antiplatelet therapy.
CASE REPORT A 52-year-old male smoker with a history of hypertension and hypercholesterolemia presented to the Emergency Department for right arm numbness and weakness followed by discoloration of the fingers on his left hand. His blood pressure was 130/70 mm Hg in the right arm and his heart rate was 80 beats per minute and regular. The physical examination revealed an absent left brachial and radial pulse with intact right arm pulses and ischemic changes on his left hand. There were no carotid bruits and no cardiac murmurs. The electrocardiogram showed normal sinus rhythm with early repolarization. The head computed tomography scan showed a wedge-shaped hypodensity in the left posteroparietal area. The transthoracic echocardiogram showed no evidence for a cardiac source of thromboembolism. In light of acute cerebrovascular attack and ischemic left arm, a transesophageal echocardiogram (TEE) was ordered to look for an occult cardiac source of emboli and aortic pathology. The TEE showed a calcified ulcerated atheroma in the distal aortic arch, with a large (15 mm ⫻ 10 mm) slightly mobile thrombus and an adjacent small (4 mm ⫻ 4 mm) immobile thrombus (Figure 1). Based on the TEE results, we concluded that this 52-year-old man had emboli to the left carotid and left subclavian arteries from aortic arch thrombi. The patient was started on heparin infusion and was bridged to warfarin with an international normalized ratio goal of 2-3. He also received
Funding: None. Conflict of Interest: Both authors declare no conflicts of interest. Authorship: Both authors had access to the material published and a role in writing the article. Requests for reprints should be addressed to Rejmon Dedaj, MD, Department of Medicine, Berkshire Medical Center, 725 North Street, Pittsfield MA 01021. E-mail address: [email protected]
0002-9343/$ -see front matter © 2009 Elsevier Inc. All rights reserved.
Figure 1 Transesophageal echocardiogram at the time of presentation to the emergency room.
clopidogrel and lipid-lowering agent therapy and was discharged after 5 days of hospitalization. A repeat TEE 3 months after discharge showed complete resolution of the thrombi (Figure 2). He is currently doing well on warfarin and clopidogrel, with normal pulses in his left arm and no neurologic deficits.
DISCUSSION Aortic atherosclerotic plaques are an important source of systemic emboli.1 Two clinical syndromes result from the embolic phenomena, atheroemboli and, more commonly, thromboemboli.2 Thromboembolism may occur when an
Figure 2 Follow-up transesophageal echocardiogram at 3 months after discharge.
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The American Journal of Medicine, Vol 122, No 12, December 2009
aortic atherosclerotic plaque ruptures, leading to acute thrombus formation. The thromboemboli tend to be single and lodge in medium or large arteries, resulting most often in stroke, transient ischemic attack, or limb ischemia. TEE is an excellent technique for detecting complex plaques of the aortic arch, and its frequent use has led to the increased recognition of aortic atheromas.3 Mobile elements on these plaques have been shown to represent thrombus4 and are frequently associated with embolic events. The severity of aortic atherosclerosis graded by TEE correlates with the risk for future embolism, especially if mobile lesions or superimposed thrombi are present.5,6 The optimal medical treatment for patients with aortic thromboembolism is yet to be determined. Full-dose anticoagulation with warfarin may be efficacious in preventing stroke in these patients.7 Large complex plaques (those with ulcerations or mobile components) confer an increased risk of recurrent cerebrovascular attacks.8 Based on the TEE findings, our patient had a high risk of recurrent cardiovascular events and was started on dual anticoagulation and antiplatelet therapy. Surgery is rarely used to remove the aortic thrombi because of the high perioperative mortality and morbidity. Rejmon Dedaj, MD Department of Internal Medicine Berkshire Medical Center/University of Massachusetts Pittsfield
William Levy, MD Echocardiography, Department of Cardiology Berkshire Health Systems Pittsfield, Mass
doi:10.1016/j.amjmed.2009.06.015
References 1. Tunick PA, Kronzon I. Atheromas of the thoracic aorta: clinical and therapeutic update. J Am Coll Cardiol. 2000;35:545. 2. Tunick PA, Lackner H, Katz ES, et al. Multiple emboli from a large aortic arch thrombus in a patient with thrombotic diathesis. Am Heart J. 1992;124:239-241. 3. Thenappan T, Ali Raza J, Movahed A. Aortic atheromas: current concepts and controversies—a review of the literature. Echocardiography. 2008;25:198-207. 4. Vaduganathan P, Ewton A, Nagueh SF, et al. Pathologic correlates of aortic plaques, thrombi and mobile “aortic debris” imaged in vivo with transesophageal echocardiography. J Am Coll Cardiol. 1997;30:357. 5. Sheikhzadeh A, Ehlermann P. Atheromatous disease of the thoracic aorta and systemic embolism. Clinical picture and therapeutic challenge. Z Kardiol. 2004;93:10-17. 6. Casella G, Greco C, Perugini E, et al. Atheromatosis of the thoracic aorta and risk of stroke. G Ital Cardiol (Rome). 2006;7:309-316. 7. Dressler FA, Craig WR, Castello R, Labovitz AJ. Mobile aortic atheroma and systemic emboli: efficacy of anticoagulation and influence of plaque morphology on recurrent stroke. J Am Coll Cardiol. 1998;31:134-138. 8. Di Tullio MR, Russo C, Jin Z, et al. Patent Foramen Ovale in Cryptogenic Stroke Study Investigators. Aortic arch plaques and risk of recurrent stroke and death. Circulation. 2009;119:2376-2382.
Aortic Thromboembolism Successfully Treated with Anticoagulation and Antiplatelet Therapy To the Editor: We report a case of an aortic thromboembolism that had a positive outcome after prompt treatment with anticoagulation and antiplatelet therapy.
CASE REPORT A 52-year-old male smoker with a history of hypertension and hypercholesterolemia presented to the Emergency Department for right arm numbness and weakness followed by discoloration of the fingers on his left hand. His blood pressure was 130/70 mm Hg in the right arm and his heart rate was 80 beats per minute and regular. The physical examination revealed an absent left brachial and radial pulse with intact right arm pulses and ischemic changes on his left hand. There were no carotid bruits and no cardiac murmurs. The electrocardiogram showed normal sinus rhythm with early repolarization. The head computed tomography scan showed a wedge-shaped hypodensity in the left posteroparietal area. The transthoracic echocardiogram showed no evidence for a cardiac source of thromboembolism. In light of acute cerebrovascular attack and ischemic left arm, a transesophageal echocardiogram (TEE) was ordered to look for an occult cardiac source of emboli and aortic pathology. The TEE showed a calcified ulcerated atheroma in the distal aortic arch, with a large (15 mm ⫻ 10 mm) slightly mobile thrombus and an adjacent small (4 mm ⫻ 4 mm) immobile thrombus (Figure 1). Based on the TEE results, we concluded that this 52-year-old man had emboli to the left carotid and left subclavian arteries from aortic arch thrombi. The patient was started on heparin infusion and was bridged to warfarin with an international normalized ratio goal of 2-3. He also received
Funding: None. Conflict of Interest: Both authors declare no conflicts of interest. Authorship: Both authors had access to the material published and a role in writing the article. Requests for reprints should be addressed to Rejmon Dedaj, MD, Department of Medicine, Berkshire Medical Center, 725 North Street, Pittsfield MA 01021. E-mail address: [email protected]
0002-9343/$ -see front matter © 2009 Elsevier Inc. All rights reserved.
Figure 1 Transesophageal echocardiogram at the time of presentation to the emergency room.
clopidogrel and lipid-lowering agent therapy and was discharged after 5 days of hospitalization. A repeat TEE 3 months after discharge showed complete resolution of the thrombi (Figure 2). He is currently doing well on warfarin and clopidogrel, with normal pulses in his left arm and no neurologic deficits.
DISCUSSION Aortic atherosclerotic plaques are an important source of systemic emboli.1 Two clinical syndromes result from the embolic phenomena, atheroemboli and, more commonly, thromboemboli.2 Thromboembolism may occur when an
Figure 2 Follow-up transesophageal echocardiogram at 3 months after discharge.
e4
The American Journal of Medicine, Vol 122, No 12, December 2009
aortic atherosclerotic plaque ruptures, leading to acute thrombus formation. The thromboemboli tend to be single and lodge in medium or large arteries, resulting most often in stroke, transient ischemic attack, or limb ischemia. TEE is an excellent technique for detecting complex plaques of the aortic arch, and its frequent use has led to the increased recognition of aortic atheromas.3 Mobile elements on these plaques have been shown to represent thrombus4 and are frequently associated with embolic events. The severity of aortic atherosclerosis graded by TEE correlates with the risk for future embolism, especially if mobile lesions or superimposed thrombi are present.5,6 The optimal medical treatment for patients with aortic thromboembolism is yet to be determined. Full-dose anticoagulation with warfarin may be efficacious in preventing stroke in these patients.7 Large complex plaques (those with ulcerations or mobile components) confer an increased risk of recurrent cerebrovascular attacks.8 Based on the TEE findings, our patient had a high risk of recurrent cardiovascular events and was started on dual anticoagulation and antiplatelet therapy. Surgery is rarely used to remove the aortic thrombi because of the high perioperative mortality and morbidity. Rejmon Dedaj, MD Department of Internal Medicine Berkshire Medical Center/University of Massachusetts Pittsfield
William Levy, MD Echocardiography, Department of Cardiology Berkshire Health Systems Pittsfield, Mass
doi:10.1016/j.amjmed.2009.06.015
References 1. Tunick PA, Kronzon I. Atheromas of the thoracic aorta: clinical and therapeutic update. J Am Coll Cardiol. 2000;35:545. 2. Tunick PA, Lackner H, Katz ES, et al. Multiple emboli from a large aortic arch thrombus in a patient with thrombotic diathesis. Am Heart J. 1992;124:239-241. 3. Thenappan T, Ali Raza J, Movahed A. Aortic atheromas: current concepts and controversies—a review of the literature. Echocardiography. 2008;25:198-207. 4. Vaduganathan P, Ewton A, Nagueh SF, et al. Pathologic correlates of aortic plaques, thrombi and mobile “aortic debris” imaged in vivo with transesophageal echocardiography. J Am Coll Cardiol. 1997;30:357. 5. Sheikhzadeh A, Ehlermann P. Atheromatous disease of the thoracic aorta and systemic embolism. Clinical picture and therapeutic challenge. Z Kardiol. 2004;93:10-17. 6. Casella G, Greco C, Perugini E, et al. Atheromatosis of the thoracic aorta and risk of stroke. G Ital Cardiol (Rome). 2006;7:309-316. 7. Dressler FA, Craig WR, Castello R, Labovitz AJ. Mobile aortic atheroma and systemic emboli: efficacy of anticoagulation and influence of plaque morphology on recurrent stroke. J Am Coll Cardiol. 1998;31:134-138. 8. Di Tullio MR, Russo C, Jin Z, et al. Patent Foramen Ovale in Cryptogenic Stroke Study Investigators. Aortic arch plaques and risk of recurrent stroke and death. Circulation. 2009;119:2376-2382.