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Mobile Ascending Aortic Atheroma Diagnosed by Transesophageal Echocardiography as Source of Peripheral Vascular Embolism
CASE REPORTS
Mobile Ascending Aortic Atheroma Diagnosed by Transesophageal Echocardiography as Source of Peripheral Vascular Embolism Leon J. Frazin, MD, and Jason W. Glowney, MD, Chicago, Illinois
Complex aortic atheromas are an important differential diagnosis to consider in evaluating sources of arterial embolization. Diagnosis of the embolic source is an essential first step, so treatment can then be initiated to prevent further reoccurrence. We report the case of a 36-year-old man, without significant medical history, who presented to the University of Illinois at Chicago with peripheral vascular embolism to the lower extremities. Computed tomography with contrast angiography and transthoracic echocardiography failed to reveal a source of the thromboembolism. A complex mobile atheroma was discovered in the ascending aorta during transesophageal echocardiography. The case presented is noteworthy when considering the following: the relative rarity of complex atheromas of the ascending aorta, the young age of the patient with no history of atherosclerotic disease, and the failure of computed tomography angiography to reveal the embolic source despite literature supporting high sensitivities for aortic plaque detection compared with transesophageal echocardiography. (J Am Soc Echocardiogr 2009;22:972.e1-972.e4.) Keywords: Aortic atheromas, TEE
Aortic atheromas (aortic atheromatous plaques) are defined by an irregular thickening of the intima of $ 2 mm with increased echogenicity seen on transesophageal echocardiography (TEE). Oftentimes these lesions will have extending mobile components that usually represent thrombi. A complex plaque is defined as a protruding atheroma $ 4 mm with or without or an attached mobile component. They are further classified as stable and unstable, with an unstable plaque being mobile, nonhomogeneous, ulcerated, or spongiform, in contrast with stable plaques, which are calcified, immobile, echo dense, homogenous, and without signs of ulceration or rupture.1 Complex atheromas are more prone to embolization than simple atheromas. The criteria that define complex atheromas (thickness $ 4 mm and/or mobile component) have been associated independently with an increased risk of arterial embolism. It is further thought that a lack of calcification poses the greatest risk of embolization compared with the other complex plaque features, with a proposed mechanism being that these atheromas are more lipid-laden and thus more prone to ulceration, thrombosis, and rupture.2 Most studies of aortic atheroma to date have taken symptomatic subjects who were referred for diagnostic evaluation. The Stroke Prevention: Assessment of Risk in a Community (SPARC) study enrolled random patients and as such was not subject to referral bias. A total of 579 patients of an average age of 66.9 years underwent evaluation with TEE. Atheroma was noted in 43.7% of enrolled subjects, with 7.6% being identified as complex ($ 4 mm or mobile).3 In regard to aortic segment location, the data showed that prevalence of both From the University of Illinois at Chicago, Chicago, Illinois (L.J.F., J.W.G.) Reprint requests: Jason W. Glowney, MD, Internal Medicine/Emergency Medicine, University of Illinois at Chicago, 808 South Wood Street, Chicago, IL 60612. (E-mail: [email protected]). 0894-7317/$36.00 Copyright 2009 by the American Society of Echocardiography. doi:10.1016/j.echo.2009.03.006
972.e1
simple and complex atheroma increased from the ascending aorta distally. Only 1 patient (0.2%) in the SPARC study had a lesion defined as a complex ascending aortic artheroma.4 The prevalence of aortic atheromatous disease increases with age and is usually indicative of generalized atherosclerosis. The average age of subjects with lesions $ 4 mm on TEE is 70 years. Other risk factors for its development are hyperlipidemia, hypertension, smoking, left ventricular hypertrophy, Caucasian race, and an inflammatory state.4
CASE STUDY A 36-year-old man presented to the medicine clinic with symptoms of acute onset of bilateral limb pain and purple discoloration of the left foot that occurred 2 weeks previously. He stated that the discoloration improved to redness shortly thereafter, but he continued to have severe pain with the left lower extremity being worse than the right. He reported that with walking his pain increased to intolerable levels after less than 1 block. The patient denied any medical history, had a 25 pack-year history of tobacco, and reported nonsteroidal antiinflammatory drug as the only medications he took. On examination, the patient had nonpalpable pulses of bilateral dorsalis pedis and posterior tibial arteries and a nonpalpable popliteal pulse on the left. Doppler examination revealed biphasic signals of the right posterior tibial and dorsalis pedis arteries, but monophasic signals of both on the left side. With symptoms suggestive of subacute claudication, the patient was admitted to the vascular surgery service. A contrast-enhanced computed tomography angiography of the chest, abdomen, pelvis, and lower extremities was performed. The results revealed occlusions of both the left common femoral and right popliteal arteries with a normal thoracic aorta. Given the clinical history, physical examination findings, and computed tomography results, the vascular surgery service thought this
Frazin and J. W. Glowney 972.e2
Journal of the American Society of Echocardiography Volume 22 Number 8
Figure 1 TEE image of long-axis view of the ascending aorta showing a complex mobile atheroma (arrow). LV, Left ventricle; LA, left atrium; Ao, aorta.
Figure 2 TEE 3-dimensional image of a complex atheroma of the ascending aorta (arrow). View obtained looking superior from the aortic valve. simvastatin maintained. He continues to do well without further arterial embolism and is awaiting right popliteal bypass surgery.
patient’s presentation was likely secondary to embolic events, and anticoagulation with heparin was administered. Workup included a negative venous duplex ultrasound of the lower extremities, a negative hypercoagulable workup (antithrombin III, factor V Leiden mutation, protein c/s, prothrombin mutation, and anti-cardiolipin antibody), and no evidence of atrial fibrillation. Lipid profile showed low-density lipoprotein of 111 mg/dL, high-density lipoprotein of 44 mg/dL, and triglycerides of 133 mg/dL. The cardiology service was consulted to assist in the patient’s care, and a transthoracic echocardiogram was performed to further evaluate for embolic causes. The transthoracic echocardiogram study was technically limited, had a nondiagnostic saline contrast study, but was otherwise normal and unremarkable for an embolic source. At this point cardiology suggested proceeding to transesophageal echocardiography as the next step in the patient’s embolic workup. A transesophageal echocardiogram revealed normal systolic function, normal valves, normal chamber sizes and wall thickness, and no evidence of clot in the atrium or appendage. On the ascending aorta long-axis view, a large protruding, mobile, noncalcified, nonulcerated atheroma was observed that measured 15 10 mm involving the ascending aorta on the inner curvature 3.5 cm superior to the aortic valve (Figure 1, Video 1). Saline contrast study did not reveal evidence of a patent foramen ovale. Three-dimensional images were rendered to further assess the atheroma and better revealed a highly mobile complex atheroma (Figure 2, Video 2). Given the findings on transesophageal echocardiogram, the patient was maintained on anticoagulation and 2 weeks later underwent excision of his ascending aortic wall atheroma with Dacron patch aortoplasty as a definitive treatment to avoid the risk of further arterial embolization. Pathology evaluation of surgical specimens revealed a 0.4 0.4 0.4-cm aortic wall lesion consistent with atheromatous changes and an attached thrombus. The patient had an uneventful postoperative course and 3 weeks later underwent thromboendarterectomy of the left profunda, superficial, and common femoral arteries with patch. Pathology would yield a specimen consistent with a chronic thrombus. The patient went on to have normal dipyridamole stress test and carotid duplex study results. As primary prevention for the patient’s newly diagnosed peripheral vascular disease, 81 mg of aspirin was begun by the vascular surgery service with adjusted-dose Coumadin and
DISCUSSION We defined our patient’s aortic lesion as a complex unstable atheroma based on a size $ 4 mm, a lack of calcification, and having a mobile component. Having a large mobile atheroma, as described on TEE and verified via surgical pathology specimen, increased his likelihood of arterial embolism. Evidence for this increased risk comes from a study by Di Tullio et al,5 who calculated an increased adjusted odds ratio of 4.3 for stroke in patients with large aortic arch atheromas ($ 4 mm) in comparison with those without atheromas. When the large atheroma group (68 patients) was further delineated, they found 10 patients with complex mobile aortic arch atheromas. Their data would underline the highly embolic nature of complex mobile aortic arch atheromas when they calculated an adjusted odds ratio of 21.3 in this select group for ischemic stroke. The age of this patient (36 years) would be considered young for complex aortic lesions, because atheromatous changes increase with advancing age and the average age of individuals with complex aortic plaques by size criteria ($ 4 mm) is 70 years old.4 The only identifiable risk factors from his history were his 25 pack-year history of smoking and Caucasian race. His lipid profile was normal, he had no history of hypertension, he had a negative hypercoagulable workup, and he appeared to have only a solitary ascending aortic lesion, because he had no evidence of other atheromatous disease of the aorta or carotids. In 1997, Laperche et al6 presented 23 cases from more than 27,000 TEE examinations performed in medical centers throughout France of mobile thrombi of the aortic arch in which an arterial embolic event led to the TEE evaluation. The mean age of 45 years found in this group was younger than the average age of 70 years cited by Kronzon and Tunick4 in patients with complex aortic plaques. The mobile masses observed in these studies were proven to be thrombi by way of surgical retrieval or autopsy in 78% of the cases (18/23 patients), and it was stated that the rest were suggestive for thrombus on TEE imaging. The authors would go on to conclude that these cases of mobile thrombi superimposed on atheromatous plaques likely represented a subset of aortic atherosclerosis with
972.e3 Frazin and J. W. Glowney
Journal of the American Society of Echocardiography August 2009
Figure 3 Coronal cut of computed tomography angiography scan with view of ascending aorta with no atheroma noted. AA, Ascending aorta; LVOT, left ventricular outflow tract; LV, left ventricle.
a high embolic potential and a tendency to occur in a younger patient population.6 The aforementioned patient in our presentation parallels the cases presented by Laperche et al, given his younger age, with a mobile thrombus superimposed on an aortic plaque confirmed by pathology, an otherwise intact aorta on TEE (no other aortic debris), and an embolic event as the initial presentation. In contrast, our case study does differ from these 23 patients in that all of their aortic lesions were distal to the innominate artery takeoff on TEE, whereas the mobile atheroma we present was proximal to the innominate artery in the ascending aorta. The images obtained on TEE are noteworthy because complex atheromas are rare in the ascending aorta, with data from the SPARC study finding only 1 case in 297 subjects with plaques (0.2%).3 This is further corroborated by research by Tunick et al4 who found only 10 cases of complex ascending aortic atheroma of 1111 patients (1%) studied with severe thoracic aortic plaques ($ 4 mm). Computed tomography is a modality frequently used to assess the aorta and its branches. Sensitivities compared with TEE have ranged from 87% to 95% in detecting protruding aortic plaques, making it an appealing choice given that it can be rapidly obtained and may better visualize the ascending aorta that is obscured by the bronchial air column during TEE.1 Drawbacks of the technique are the exposure to intravenous contrast, radiation, and reported decreased sensitivity in detecting noncalcified plaques.1 This decreased sensitivity to noncalcified plaques may have been to blame for the failure to detect the complex unstable atheroma in our case study (Figures 3 and 4). TEE remains the imaging modality of choice in detecting and evaluating aortic atheromas. The resolution of images produced is higher when compared with transthoracic echocardiography and thus makes plaque characterizations more accurate (thickness, ulceration, calcification, and mobile components). When compared with magnetic resonance and computed tomography, TEE is better able to assess embolic potential by determining plaque mobility, is not limited
Figure 4 Sagittal cut of computed tomography angiography scan with view of ascending aorta with no atheroma noted. AA, Ascending aorta; LVOT, left ventricular outflow tract. by lack of plaque calcification, and can be performed at bedside if needed. With cases of atheroma that have a mobile thrombus component, treatment with adjusted-dose warfarin (goal international normalized ratio 2.0-3.0) is generally recommended. Evidence supporting this recommendation comes from the Stroke Prevention in Atrial Fibrillation III trials, which showed a relative risk increase of approximately 4.0 in patients with complex aortic plaque treated with combination low-dose warfarin (international normalized ratio 1.2-1.5) and aspirin (325 mg) versus adjusted-dose warfarin.7 The use of surgical endarterectomy in the treatment of complex atheromas remains less well defined. Laperche et al6 reported that of the 15 patients with arterial embolic events and mobile, pedunculated aortic arch thrombi not undergoing surgical endarterectomy, 27% had recurrence of thromboembolism despite anticoagulation with heparin versus no recurrence in those that proceeded directly to surgery. This contrasts with data collected by Stern et al,8 who studied the merits of prophylactic intraoperative endarterectomy in patients with protruding aortic atheromas undergoing heart surgery. The data would show the incidence of intraoperative stroke was approximately 3 times higher in patients undergoing prophylactic aortic arch endarterectomy when compared with patients with aortic arch atheromas not undergoing endarterectomy during their scheduled cardiac surgery.
CONCLUSIONS The treatment strategy for patients with aortic atheromas is still not well defined because there have not been any randomized clinical
Journal of the American Society of Echocardiography Volume 22 Number 8
trails to evaluate to date.1 Treatment modalities that have been used include anticoagulation therapy, platelet inhibition, surgery, and statins.
REFERENCES 1. Thenappan T, Ali Raza J, Movahed A. Aortic atheromas: current concepts and controversies - a review of the literature. Echocardiography 2008;25: 198-207. 2. Cohen A, Amarenco P. Atherosclerosis of the thoracic aorta: from risk stratification to treatment. Am J Cardiol 2002;90:1333-5. 3. Meissner I, Khandheria BK, Sheps SG, Schwartz GL, Wiebers DO, Whisnant JP, et al. Atherosclerosis of the aorta: risk factor, risk marker, or innocent bystander? A prospective population-based transesophageal echocardiography study. J Am Coll Cardiol 2004;44:1018-24.
Frazin and J. W. Glowney 972.e4
4. Kronzon I, Tunick PA. Aortic atherosclerotic disease and stroke. Circulation 2006;114:63-75. 5. Di Tullio MR, Sacco RL, Savoia MT, Sciacca RR, Homma S. Aortic atheroma morphology and the risk of ischemic stroke in a multiethnic population. Am Heart J 2000;139(2 Pt 1):329-36. 6. Laperche T, Laurian C, Roudaut R, Steg PG. Mobile thromboses of the aortic arch without aortic debris. A transesophageal echocardiographic finding associated with unexplained arterial embolism. The Filiale Echocardiographie de la Socie´te´ Franc¸aise de Cardiologie. Circulation 1997;96:288-94. 7. Transesophageal echocardiographic correlates of thromboembolism in high-risk patients with nonvalvular atrial fibrillation. The Stroke Prevention in Atrial Fibrillation Investigators Committee on Echocardiography. Ann Intern Med 1998;128:639-47. 8. Stern A, Tunick PA, Culliford AT, Lachmann J, Baumann FG, Kanchuger MS, et al. Protruding aortic arch atheromas: risk of stroke during heart surgery with and without aortic arch endarterectomy. Am Heart J 1999;138(4 Pt 1):746-52.
Mobile Ascending Aortic Atheroma Diagnosed by Transesophageal Echocardiography as Source of Peripheral Vascular Embolism Leon J. Frazin, MD, and Jason W. Glowney, MD, Chicago, Illinois
Complex aortic atheromas are an important differential diagnosis to consider in evaluating sources of arterial embolization. Diagnosis of the embolic source is an essential first step, so treatment can then be initiated to prevent further reoccurrence. We report the case of a 36-year-old man, without significant medical history, who presented to the University of Illinois at Chicago with peripheral vascular embolism to the lower extremities. Computed tomography with contrast angiography and transthoracic echocardiography failed to reveal a source of the thromboembolism. A complex mobile atheroma was discovered in the ascending aorta during transesophageal echocardiography. The case presented is noteworthy when considering the following: the relative rarity of complex atheromas of the ascending aorta, the young age of the patient with no history of atherosclerotic disease, and the failure of computed tomography angiography to reveal the embolic source despite literature supporting high sensitivities for aortic plaque detection compared with transesophageal echocardiography. (J Am Soc Echocardiogr 2009;22:972.e1-972.e4.) Keywords: Aortic atheromas, TEE
Aortic atheromas (aortic atheromatous plaques) are defined by an irregular thickening of the intima of $ 2 mm with increased echogenicity seen on transesophageal echocardiography (TEE). Oftentimes these lesions will have extending mobile components that usually represent thrombi. A complex plaque is defined as a protruding atheroma $ 4 mm with or without or an attached mobile component. They are further classified as stable and unstable, with an unstable plaque being mobile, nonhomogeneous, ulcerated, or spongiform, in contrast with stable plaques, which are calcified, immobile, echo dense, homogenous, and without signs of ulceration or rupture.1 Complex atheromas are more prone to embolization than simple atheromas. The criteria that define complex atheromas (thickness $ 4 mm and/or mobile component) have been associated independently with an increased risk of arterial embolism. It is further thought that a lack of calcification poses the greatest risk of embolization compared with the other complex plaque features, with a proposed mechanism being that these atheromas are more lipid-laden and thus more prone to ulceration, thrombosis, and rupture.2 Most studies of aortic atheroma to date have taken symptomatic subjects who were referred for diagnostic evaluation. The Stroke Prevention: Assessment of Risk in a Community (SPARC) study enrolled random patients and as such was not subject to referral bias. A total of 579 patients of an average age of 66.9 years underwent evaluation with TEE. Atheroma was noted in 43.7% of enrolled subjects, with 7.6% being identified as complex ($ 4 mm or mobile).3 In regard to aortic segment location, the data showed that prevalence of both From the University of Illinois at Chicago, Chicago, Illinois (L.J.F., J.W.G.) Reprint requests: Jason W. Glowney, MD, Internal Medicine/Emergency Medicine, University of Illinois at Chicago, 808 South Wood Street, Chicago, IL 60612. (E-mail: [email protected]). 0894-7317/$36.00 Copyright 2009 by the American Society of Echocardiography. doi:10.1016/j.echo.2009.03.006
972.e1
simple and complex atheroma increased from the ascending aorta distally. Only 1 patient (0.2%) in the SPARC study had a lesion defined as a complex ascending aortic artheroma.4 The prevalence of aortic atheromatous disease increases with age and is usually indicative of generalized atherosclerosis. The average age of subjects with lesions $ 4 mm on TEE is 70 years. Other risk factors for its development are hyperlipidemia, hypertension, smoking, left ventricular hypertrophy, Caucasian race, and an inflammatory state.4
CASE STUDY A 36-year-old man presented to the medicine clinic with symptoms of acute onset of bilateral limb pain and purple discoloration of the left foot that occurred 2 weeks previously. He stated that the discoloration improved to redness shortly thereafter, but he continued to have severe pain with the left lower extremity being worse than the right. He reported that with walking his pain increased to intolerable levels after less than 1 block. The patient denied any medical history, had a 25 pack-year history of tobacco, and reported nonsteroidal antiinflammatory drug as the only medications he took. On examination, the patient had nonpalpable pulses of bilateral dorsalis pedis and posterior tibial arteries and a nonpalpable popliteal pulse on the left. Doppler examination revealed biphasic signals of the right posterior tibial and dorsalis pedis arteries, but monophasic signals of both on the left side. With symptoms suggestive of subacute claudication, the patient was admitted to the vascular surgery service. A contrast-enhanced computed tomography angiography of the chest, abdomen, pelvis, and lower extremities was performed. The results revealed occlusions of both the left common femoral and right popliteal arteries with a normal thoracic aorta. Given the clinical history, physical examination findings, and computed tomography results, the vascular surgery service thought this
Frazin and J. W. Glowney 972.e2
Journal of the American Society of Echocardiography Volume 22 Number 8
Figure 1 TEE image of long-axis view of the ascending aorta showing a complex mobile atheroma (arrow). LV, Left ventricle; LA, left atrium; Ao, aorta.
Figure 2 TEE 3-dimensional image of a complex atheroma of the ascending aorta (arrow). View obtained looking superior from the aortic valve. simvastatin maintained. He continues to do well without further arterial embolism and is awaiting right popliteal bypass surgery.
patient’s presentation was likely secondary to embolic events, and anticoagulation with heparin was administered. Workup included a negative venous duplex ultrasound of the lower extremities, a negative hypercoagulable workup (antithrombin III, factor V Leiden mutation, protein c/s, prothrombin mutation, and anti-cardiolipin antibody), and no evidence of atrial fibrillation. Lipid profile showed low-density lipoprotein of 111 mg/dL, high-density lipoprotein of 44 mg/dL, and triglycerides of 133 mg/dL. The cardiology service was consulted to assist in the patient’s care, and a transthoracic echocardiogram was performed to further evaluate for embolic causes. The transthoracic echocardiogram study was technically limited, had a nondiagnostic saline contrast study, but was otherwise normal and unremarkable for an embolic source. At this point cardiology suggested proceeding to transesophageal echocardiography as the next step in the patient’s embolic workup. A transesophageal echocardiogram revealed normal systolic function, normal valves, normal chamber sizes and wall thickness, and no evidence of clot in the atrium or appendage. On the ascending aorta long-axis view, a large protruding, mobile, noncalcified, nonulcerated atheroma was observed that measured 15 10 mm involving the ascending aorta on the inner curvature 3.5 cm superior to the aortic valve (Figure 1, Video 1). Saline contrast study did not reveal evidence of a patent foramen ovale. Three-dimensional images were rendered to further assess the atheroma and better revealed a highly mobile complex atheroma (Figure 2, Video 2). Given the findings on transesophageal echocardiogram, the patient was maintained on anticoagulation and 2 weeks later underwent excision of his ascending aortic wall atheroma with Dacron patch aortoplasty as a definitive treatment to avoid the risk of further arterial embolization. Pathology evaluation of surgical specimens revealed a 0.4 0.4 0.4-cm aortic wall lesion consistent with atheromatous changes and an attached thrombus. The patient had an uneventful postoperative course and 3 weeks later underwent thromboendarterectomy of the left profunda, superficial, and common femoral arteries with patch. Pathology would yield a specimen consistent with a chronic thrombus. The patient went on to have normal dipyridamole stress test and carotid duplex study results. As primary prevention for the patient’s newly diagnosed peripheral vascular disease, 81 mg of aspirin was begun by the vascular surgery service with adjusted-dose Coumadin and
DISCUSSION We defined our patient’s aortic lesion as a complex unstable atheroma based on a size $ 4 mm, a lack of calcification, and having a mobile component. Having a large mobile atheroma, as described on TEE and verified via surgical pathology specimen, increased his likelihood of arterial embolism. Evidence for this increased risk comes from a study by Di Tullio et al,5 who calculated an increased adjusted odds ratio of 4.3 for stroke in patients with large aortic arch atheromas ($ 4 mm) in comparison with those without atheromas. When the large atheroma group (68 patients) was further delineated, they found 10 patients with complex mobile aortic arch atheromas. Their data would underline the highly embolic nature of complex mobile aortic arch atheromas when they calculated an adjusted odds ratio of 21.3 in this select group for ischemic stroke. The age of this patient (36 years) would be considered young for complex aortic lesions, because atheromatous changes increase with advancing age and the average age of individuals with complex aortic plaques by size criteria ($ 4 mm) is 70 years old.4 The only identifiable risk factors from his history were his 25 pack-year history of smoking and Caucasian race. His lipid profile was normal, he had no history of hypertension, he had a negative hypercoagulable workup, and he appeared to have only a solitary ascending aortic lesion, because he had no evidence of other atheromatous disease of the aorta or carotids. In 1997, Laperche et al6 presented 23 cases from more than 27,000 TEE examinations performed in medical centers throughout France of mobile thrombi of the aortic arch in which an arterial embolic event led to the TEE evaluation. The mean age of 45 years found in this group was younger than the average age of 70 years cited by Kronzon and Tunick4 in patients with complex aortic plaques. The mobile masses observed in these studies were proven to be thrombi by way of surgical retrieval or autopsy in 78% of the cases (18/23 patients), and it was stated that the rest were suggestive for thrombus on TEE imaging. The authors would go on to conclude that these cases of mobile thrombi superimposed on atheromatous plaques likely represented a subset of aortic atherosclerosis with
972.e3 Frazin and J. W. Glowney
Journal of the American Society of Echocardiography August 2009
Figure 3 Coronal cut of computed tomography angiography scan with view of ascending aorta with no atheroma noted. AA, Ascending aorta; LVOT, left ventricular outflow tract; LV, left ventricle.
a high embolic potential and a tendency to occur in a younger patient population.6 The aforementioned patient in our presentation parallels the cases presented by Laperche et al, given his younger age, with a mobile thrombus superimposed on an aortic plaque confirmed by pathology, an otherwise intact aorta on TEE (no other aortic debris), and an embolic event as the initial presentation. In contrast, our case study does differ from these 23 patients in that all of their aortic lesions were distal to the innominate artery takeoff on TEE, whereas the mobile atheroma we present was proximal to the innominate artery in the ascending aorta. The images obtained on TEE are noteworthy because complex atheromas are rare in the ascending aorta, with data from the SPARC study finding only 1 case in 297 subjects with plaques (0.2%).3 This is further corroborated by research by Tunick et al4 who found only 10 cases of complex ascending aortic atheroma of 1111 patients (1%) studied with severe thoracic aortic plaques ($ 4 mm). Computed tomography is a modality frequently used to assess the aorta and its branches. Sensitivities compared with TEE have ranged from 87% to 95% in detecting protruding aortic plaques, making it an appealing choice given that it can be rapidly obtained and may better visualize the ascending aorta that is obscured by the bronchial air column during TEE.1 Drawbacks of the technique are the exposure to intravenous contrast, radiation, and reported decreased sensitivity in detecting noncalcified plaques.1 This decreased sensitivity to noncalcified plaques may have been to blame for the failure to detect the complex unstable atheroma in our case study (Figures 3 and 4). TEE remains the imaging modality of choice in detecting and evaluating aortic atheromas. The resolution of images produced is higher when compared with transthoracic echocardiography and thus makes plaque characterizations more accurate (thickness, ulceration, calcification, and mobile components). When compared with magnetic resonance and computed tomography, TEE is better able to assess embolic potential by determining plaque mobility, is not limited
Figure 4 Sagittal cut of computed tomography angiography scan with view of ascending aorta with no atheroma noted. AA, Ascending aorta; LVOT, left ventricular outflow tract. by lack of plaque calcification, and can be performed at bedside if needed. With cases of atheroma that have a mobile thrombus component, treatment with adjusted-dose warfarin (goal international normalized ratio 2.0-3.0) is generally recommended. Evidence supporting this recommendation comes from the Stroke Prevention in Atrial Fibrillation III trials, which showed a relative risk increase of approximately 4.0 in patients with complex aortic plaque treated with combination low-dose warfarin (international normalized ratio 1.2-1.5) and aspirin (325 mg) versus adjusted-dose warfarin.7 The use of surgical endarterectomy in the treatment of complex atheromas remains less well defined. Laperche et al6 reported that of the 15 patients with arterial embolic events and mobile, pedunculated aortic arch thrombi not undergoing surgical endarterectomy, 27% had recurrence of thromboembolism despite anticoagulation with heparin versus no recurrence in those that proceeded directly to surgery. This contrasts with data collected by Stern et al,8 who studied the merits of prophylactic intraoperative endarterectomy in patients with protruding aortic atheromas undergoing heart surgery. The data would show the incidence of intraoperative stroke was approximately 3 times higher in patients undergoing prophylactic aortic arch endarterectomy when compared with patients with aortic arch atheromas not undergoing endarterectomy during their scheduled cardiac surgery.
CONCLUSIONS The treatment strategy for patients with aortic atheromas is still not well defined because there have not been any randomized clinical
Journal of the American Society of Echocardiography Volume 22 Number 8
trails to evaluate to date.1 Treatment modalities that have been used include anticoagulation therapy, platelet inhibition, surgery, and statins.
REFERENCES 1. Thenappan T, Ali Raza J, Movahed A. Aortic atheromas: current concepts and controversies - a review of the literature. Echocardiography 2008;25: 198-207. 2. Cohen A, Amarenco P. Atherosclerosis of the thoracic aorta: from risk stratification to treatment. Am J Cardiol 2002;90:1333-5. 3. Meissner I, Khandheria BK, Sheps SG, Schwartz GL, Wiebers DO, Whisnant JP, et al. Atherosclerosis of the aorta: risk factor, risk marker, or innocent bystander? A prospective population-based transesophageal echocardiography study. J Am Coll Cardiol 2004;44:1018-24.
Frazin and J. W. Glowney 972.e4
4. Kronzon I, Tunick PA. Aortic atherosclerotic disease and stroke. Circulation 2006;114:63-75. 5. Di Tullio MR, Sacco RL, Savoia MT, Sciacca RR, Homma S. Aortic atheroma morphology and the risk of ischemic stroke in a multiethnic population. Am Heart J 2000;139(2 Pt 1):329-36. 6. Laperche T, Laurian C, Roudaut R, Steg PG. Mobile thromboses of the aortic arch without aortic debris. A transesophageal echocardiographic finding associated with unexplained arterial embolism. The Filiale Echocardiographie de la Socie´te´ Franc¸aise de Cardiologie. Circulation 1997;96:288-94. 7. Transesophageal echocardiographic correlates of thromboembolism in high-risk patients with nonvalvular atrial fibrillation. The Stroke Prevention in Atrial Fibrillation Investigators Committee on Echocardiography. Ann Intern Med 1998;128:639-47. 8. Stern A, Tunick PA, Culliford AT, Lachmann J, Baumann FG, Kanchuger MS, et al. Protruding aortic arch atheromas: risk of stroke during heart surgery with and without aortic arch endarterectomy. Am Heart J 1999;138(4 Pt 1):746-52.