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      Aortic Sinotubular Atherosclerotic Debris Associated with Cerebral Embolic Events Can Be Identifiedby Transthoracic Echocardiography

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          Abstract

          Objective: To evaluate the association between the presence of aortic sinotubular debris (STAD) identified by transthoracic echocardiography (TTE) and embolic strokes. Background: The presence of atherosclerotic debris in the ascending aorta or aortic arch detected by transesophageal echocardiography or epiaortic echocardiography has been well established to be correlated with embolic stroke or other thromboembolic events. No data are available on the role of TTE in describing aortic pathology in thromboembolic events. Methods: We identified 60 transthoracic echocardiographic studies from 11,275 studies, in which STAD was diagnosed. The charts of these patients (group 1; mean age 67 ± 10 years) were reviewed and compared with those of 57 patients (group 2) without STAD, matched for age, gender and risk factors for advanced atherosclerosis. The results of brain imaging procedures, carotid duplex and coronary angiography were also reviewed. Results: Ischemic stroke was found in 15 of group 1 (25%) and 4 patients of group 2 (7%, odds ratio = 4.4; 95% confidence interval, 1.3–19.4, p = 0.008). The average thickness of STAD was 0.7 ± 0.2 cm in stroke patients and 0.6 ± 0.2 cm in patients without stroke (p = n.s.). STAD was associated with ≤40% carotid artery stenosis. Conclusion: STAD detected by TTE is strongly associated with embolic strokes. Our findings expand the role of TTE in the evaluation of patients with embolic strokes.

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          Most cited references 3

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          Atherosclerotic disease of the aortic arch and the risk of ischemic stroke.

          Atherosclerotic disease of the aortic arch has been suspected to be a potential source of cerebral emboli. We conducted a study to quantify the risk of ischemic stroke associated with atherosclerotic disease of the aortic arch. Using transesophageal echocardiography, we performed a prospective case-control study of the frequency and thickness of atherosclerotic plaques in the ascending aorta and proximal arch in 250 consecutive patients admitted to the hospital with ischemic stroke and 250 consecutive controls, all over the age of 60 years. Atherosclerotic plaques > or = mm in thickness were found in 14.4 percent of the patients but in only 2 percent of the controls. After adjustment for atherosclerotic risk factors, the odds ratio for ischemic stroke among patients with such plaques was 9.1 (95 percent confidence interval, 3.3 to 25.2; P or = 4 mm in thickness, as compared with 8.1 percent of the 172 patients who had infarcts whose possible or likely causes were known (odds ratio, 4.7; 95 percent confidence interval, 2.2 to 10.1; P or = 4 mm in the aortic arch were not associated with the presence of atrial fibrillation or stenosis of the extracranial internal carotid artery. In contrast, plaques that were 1 to 3.9 mm thick were frequently associated with carotid stenosis of > or = 70 percent. These results indicate a strong, independent association between atherosclerotic disease of the aortic arch and the risk of ischemic stroke. The association was particularly strong with thick plaques. Atherosclerotic disease of the aortic arch should be regarded as a risk factor for ischemic stroke and as a possible source of cerebral emboli.
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            Atherosclerotic disease of the aortic arch as a risk factor for recurrent ischemic stroke. The French Study of Aortic Plaques in Stroke Group.

            Atherosclerotic disease of the aortic arch is found in 60 percent of patients 60 years of age or older who have had brain infarction. The aim of this study was to determine whether atherosclerotic plaques in the aortic arch are a risk factor for recurrent brain infarction and for vascular events in general (i.e., brain infarction, myocardial infarction, peripheral embolism, and death from vascular causes). For a period of two to four years, we followed a cohort of 331 patients 60 years of age or older who were consecutively admitted to the hospital with brain infarction (a total of 788 person-years of follow up). All patients underwent transesophageal echocardiography to determine whether atherosclerotic plaques were present in the aortic arch proximal to the ostium of the left subclavian artery. The patients were divided into three groups according to the thickness of the wall of the aortic arch ( or = 4 mm). The incidence of recurrent brain infarction was 11.9 per 100 person-years in patients with an aortic-wall thickness of > or = 4 mm, as compared with 3.5 per 100 person-years in patients with a wall thickness of 1 to 3.9 mm and 2.8 per 100 person-years in patients with a wall thickness of or = 4 mm thick (including the thickness of the aortic wall) were found to be independent predictors of recurrent brain infarction (relative risk, 3.8; 95 percent confidence interval, 1.8 to 7.8; P = 0.0012) and of all vascular events (relative risk, 3.5; 95 percent confidence interval, 2.1 to 5.9; P or = 4 mm thick in the aortic arch are significant predictors of recurrent brain infarction and other vascular events.
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              Intraoperative Transesophageal Echocardiography and Epiaortic Ultrasound for Assessment of Atherosclerosis of the Thoracic Aorta11This study was supported in part by a Minority Scientist Development Award from the American Heart Association, Dallas, Texas, to Dr. Dávila-Román.

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                Author and article information

                Journal
                CRD
                Cardiology
                10.1159/issn.0008-6312
                Cardiology
                S. Karger AG
                0008-6312
                1421-9751
                1998
                March 1999
                22 March 1999
                : 90
                : 4
                : 253-257
                Affiliations
                Division of Cardiology, Department of Internal Medicine, University of Texas-Houston Medical School, and Hermann Hospital, Houston, Tex., USA
                Article
                6854 Cardiology 1998;90:253–257
                10.1159/000006854
                10085485
                © 1998 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 3, Tables: 2, References: 18, Pages: 5
                Categories
                General Cardiology

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