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      Ultrasound and Arterial Wall Disease

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          Abstract

          Rapid progress in non-invasive ultrasound techniques has resulted in a wide variety of clinical applications for the assessment of cerebrovascular diseases. Recent highlights in ultrasound research include the evaluation of vascular ageing as a degenerative process, the demonstration of plaque development, motion and vulnerability in atherosclerosis and multi-dimensional as well as innovative imaging techniques (e.g., compound imaging) to depict early and small vascular lesions. In addition, echo-contrast agents have been used to compensate for difficulties in visualising late, severe or subtotal obstructive plaques, but failed to be really superior to conventional techniques as evidenced in a prospective, multi-centre trial (Contrast Enhanced Duplex sonography versus Arteriography Studies – CEDAS). With increasing sophistication of ultrasound methodology, it becomes essential to establish standards for data acquisition and interpretation: three consensus meetings have provided detailed recommendations on quantification of carotid atherosclerosis, characterisation of carotid artery plaques and detection of microembolism by transcranial Doppler as a potential indicator of stroke risk.

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          Most cited references19

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          Risk of stroke in the distribution of an asymptomatic carotid artery

          (1995)
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            Critical carotid stenoses: morphologic and chemical similarity between symptomatic and asymptomatic plaques.

            To identify microanatomic and chemical features that may mark the transition from asymptomatic to symptomatic atherosclerotic carotid lesions, we evaluated 62 carotid artery bifurcation plaques including 45 high-grade stenoses removed at endarterectomy and 17 nonstenotic plaques recovered at autopsy. Morphologic features were evaluated on multiple-interval histologic sections and were graded for the presence of hemorrhage, ulceration, thrombosis, lumen surface irregularity, and calcification. Plaque hemorrhage, recent and remote, was found in most of the specimens, and did not discriminate between symptomatic and asymptomatic stenotic plaques. High-grade carotid stenotic plaques were associated with a significantly higher incidence of ulceration (53%), thrombosis (49%), and lumen irregularity (78%) when compared to nonstenotic asymptomatic plaques (6%, 0%, and 17%, respectively; p less than 0.01). Although these features were more prominent in lesions that produced symptoms, they were present in 80% of the stenotic bifurcations, and did not distinguish between symptomatic and asymptomatic endarterectomy plaques. No significant differences were found between symptomatic and asymptomatic high-grade lesions with respect to collagen, DNA, total cholesterol, fibrinogen, lipase, elastase, or collagenase content. We conclude that intraplaque hemorrhage is commonly seen in carotid plaques even without severe stenosis, and it does not appear to be a dominant determinant of symptoms. Ulceration and surface thrombi that may lead to cerebral embolization are prominent features in markedly stenotic plaques even when symptoms are absent. The disruptive processes that underlie plaque instability appear to be closely associated with plaque size and stenosis rather than plaque composition.
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              Paradoxic decreases in atherosclerotic plaque mass in insulin-treated diabetic patients.

              This study assessed the impact of diabetes mellitus on atherosclerotic lesion formation. Seventy insulin-treated diabetics, 150 non-insulin-treated diabetics, and 607 nondiabetics with chronic anginal syndromes and de novo native coronary stenoses were studied using (1) angiography, and (2) intravascular ultrasound (reference and lesion arterial, lumen, and plaque areas; area stenosis [reference-lesion/reference lumen area]; remodeling index [reference-lesion lumen area/lesion-reference plaque area]; and slope of the regression line relating lumen area to plaque burden [plaque/arterial area]). Despite being diabetic for longer and having similar lumen compromise, insulin-treated patients had (1) less reference plaque (8.3 +/- 3.4 vs 10.5 +/- 4.5 mm2, p = 0.0015), (2) less stenosis plaque (13.0 +/- 4.9 vs 16.9 mm2, p or = 1 year had (paradoxically) less reference segment and stenosis plaque accumulation. Possible explanations include impaired adaptive remodeling and/or arterial (and plaque) shrinkage.
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                Author and article information

                Journal
                CED
                Cerebrovasc Dis
                10.1159/issn.1015-9770
                Cerebrovascular Diseases
                S. Karger AG
                978-3-8055-7680-2
                978-3-318-01047-3
                1015-9770
                1421-9786
                2004
                December 2003
                29 December 2003
                : 17
                : Suppl 1
                : 19-33
                Affiliations
                Department of Neurology, University of Heidelberg, Universitätsklinikum Mannheim, Mannheim, Germany
                Article
                74792 Cerebrovasc Dis 2004;17(suppl 1):19–33
                10.1159/000074792
                14694277
                1ce6438a-edde-4af4-a670-626efe2c2ac4
                © 2004 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.

                History
                Page count
                Figures: 5, References: 133, Pages: 15
                Categories
                New Frontiers in the Diagnosis of Ischemic Stroke

                Geriatric medicine,Neurology,Cardiovascular Medicine,Neurosciences,Clinical Psychology & Psychiatry,Public health
                Ultrasound,Carotid artery,Atherogenesis,Contrast-enhanced ultrasound,Vascular ageing,Plaque development and atherosclerosis,Intima-media thickness

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