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      Coronary Artery Disease but Not Coronary Calcification Is Associated with Elevated Levels of Cardiolipin, Beta-2-Glycoprotein-I, and Oxidized LDL Antibodies

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          Abstract

          Background: Autoimmune factors have been shown to play a role in atherosclerosis. The aim of this study is to correlate 5 autoantibodies (anticardiolipin, anti-CL, β<sub>2</sub>-glycoprotein-I, β<sub>2</sub>GPI, phosphatidylcholine, oxidized low-density lipoprotein, oxLDL, endothelial cell) with the presence of coronary heart disease, angiographic findings, and with coronary artery calcification. Methods: The levels of the 5 autoantibodies and a control antifibroblast line of 126 coronary heart disease patients and 20 healthy controls were measured. Fifty-one patients underwent coronary angiography, and 98 patients had coronary artery calcium determination using spiral computerized tomography (dual mode). Results: Levels of 3 autoantibodies (anti-CL, β<sub>2</sub>GPI, oxLDL) were significantly elevated in coronary heart disease patients compared with controls (p < 0.001,p = 0.001, p < 0.001, respectively). Within the subgroup of patients with significant coronary artery stenosis, anti-CL antibodies were also elevated (p = 0.008). No correlation was found between anti-CL, and anti-β<sub>2</sub>GPI autoantibody levels and coronary calcium scores as measured by spiral computerized tomography. However, anti-oxLDL antibodies were raised in patients with no calcification detected by spiral computerized tomography, compared with the patients with any coronary calcification (p = 0.046). Conclusion: Anti-CL, β<sub>2</sub>GPI and oxLDL antibodies are elevated in coronary heart disease patients regardless of coronary calcification.

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          Most cited references 1

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          Enhancement of Atherosclerosis in Beta-2-Glycoprotein I-Immunized Apolipoprotein E-Deficient Mice

          We have previously shown that low density lipoprotein receptor-deficient (LDL-RD) mice immunized with β 2 -glycoprotein I (β2GPI; a target of autoimmune anticardiolipin antibodies) developed enhanced early atherosclerosis, when fed a normal chow diet. The current study was undertaken to evaluate the effect of immunization with β2GPI and the addition of a high fat diet on the progression of atherosclerosis in the apolipoprotein E (ApoE)-deficient mouse. Six-week-old female ApoE-deficient mice (n = 10) were immunized subcutaneously with either human β2GPI or with ovalbumin, both emulsified in complete Freund’s adjuvant and fed a high fat diet for 6 weeks. The β2GPI-immunized mice were found to develop accelerated atherosclerosis when compared with their ovalbumin-immunized littermates (aortic lesion area of 137,500 ± 13,801 vs. 72,444 ± 14,465 µm 2 , respectively; p = 0.0067). The β2GPI-immunized mice developed high titers of anti-β2GPI antibodies, 10 days after the procedure, which were sustained until the sacrifice. LDL extracted from both study groups displayed similar susceptibility to ex vivo oxidation. These results confirm our previous study in which we found increased atherosclerosis in β2GPI-immunized LDL-RD mice fed a chow diet. In the current study we show that the proatherogenic effect of β2GPI immunization is maintained despite high cholesterol levels and is not associated with increased susceptibility of LDL to ex vivo oxidation.
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            Author and article information

            Journal
            CRD
            Cardiology
            10.1159/issn.0008-6312
            Cardiology
            S. Karger AG
            0008-6312
            1421-9751
            2001
            May 2001
            25 May 2001
            : 95
            : 1
            : 20-24
            Affiliations
            aDepartment of Medicine ‘B’ and Center of Autoimmune Diseases, bCardiac Rehabilitation Institute, cInstitute of Lipid and Atherosclerosis Research, Sheba Medical Center, Tel-Hashomer, and Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel, and dSpecialty Laboratory, Santa Monica, Calif., USA
            Article
            47338 Cardiology 2001;95:20–24
            10.1159/000047338
            11385187
            © 2001 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: 1, Tables: 2, References: 21, Pages: 5
            Categories
            General Cardiology

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