doi: 10.1161/CIRCULATIONAHA.104.507996
(Circulation. 2005;112:3337-3347.)
© 2005 American Heart Association, Inc.
Contemporary Reviews in Cardiovascular Medicine |
Accelerated Atherosclerosis in Autoimmune Rheumatic Diseases
From the Department of Medicine B and Center for Autoimmune Diseases, Sheba Medical Center Tel-Hashomer, Sackler Faculty of Medicine, Tel-Aviv University, Israel (Y. Shoenfeld, Y. Sherer); the Center for Study of Rheumatic Diseases, Department of Clinical and Experimental Medicine, University of Perugia, Perugia, Italy (R.G.); the Division of Rheumatology, Department of Clinical and Experimental Medicine, University of Padova, Italy (A.D.); the Department of Cell Chemistry, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan (E.M.); the Department of Medicine, Division of Rheumatology, University of Florence, Firenze, Italy (M.M.C.); the Dipartimento di Clinica Medica, Nefrologia e Scienze della Prevenzione, Università degli Studi di Parma, Parma, Italy (N.R.); the Clinical Research Unit, Hospital de Especialidades, Centro Medico La Raza, and Universidad Nacional Autónoma de México, Mexico City, Mexico (L.J.J.); the Autoimmune Rheumatic Diseases Unit, Department of Medicine, Soroka Medical Center and Ben-Gurion University, Beer-Sheva, Israel (M.A.-S.); and the Department of Internal Medicine, University of Milan, Allergy and Clinical Immunology Unit, IRCCS Istituto Auxologico Italiano, Milano, Italy (P.L.M.).
Correspondence to Yehuda Shoenfeld, MD, FRCP (Hon.), Head, Department of Medicine B and Center for Autoimmune Diseases, Sheba Medical Center, 52621 Tel-Hashomer, Israel. E-mail shoenfel@post.tau.ac.il
Received October 16, 2004; revision received June 4, 2005; accepted June 7, 2005.
Key Words: atherosclerosis • cardiovascular diseases • myocardial infarction • vasculature
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
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Introduction |
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Atherosclerosis is a multifactorial process that commences in childhood but manifests clinically later in life. Atherosclerosis is increasingly considered an immune system–mediated process of the vascular system. The presence of macrophages and activated lymphocytes within atherosclerotic plaques supports the concept of atherosclerosis as an immune system–mediated inflammatory disorder.1,2 Inflammation can aggravate atherosclerosis via different mechanisms secondary to autoimmunity, infectious diseases, and other proatherogenic changes that occur during the inflammatory state.
Autoimmune rheumatic diseases (AIRDs) are associated with higher rates of cardiovascular morbidity and mortality, primarily secondary to accelerated atherosclerosis. This phenomenon can be attributed to traditional risk factors for atherosclerosis and use of specific drugs, such as corticosteroids, but also might be the result of other autoimmune and inflammatory mechanisms that are aggravated in AIRDs. Several AIRDs exhibit increased overt cardiovascular disease (CVD) prevalence as well as findings of advanced subclinical atherosclerosis, which may precede the appearance of a clinical disease and thus be a target of early identification and preventive therapy.
Cells of the immune system can be found within atherosclerotic plaques, which suggests that they have a role in the atherogenic process. Their migration and activation within the plaques can be secondary to various stimuli, including infectious agents.3 These cells probably aggravate atherosclerosis, because CD4+ and CD8+ T-cell depletion reduced fatty streak formation in C57BL/6 mice. In addition, after crossing of apolipoprotein E (ApoE)-knockout mice with immunodeficient scid/scid mice, the offspring had a 73% reduction in aortic fatty streak lesions compared with the immunocompetent apoE mice. Moreover, when
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