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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:1776.)
© 2005 American Heart Association, Inc.

Brief Reviews

Atherosclerosis in Patients With Autoimmune Disorders

Johan Frostegård

From the Department of Medicine, Karolinska University Hospital, Huddinge, Center for Infectious Medicine and Unit of Rheumatology, Stockholm, Sweden.

Correspondence to Johan Frostegård, MD, PhD, Department of Medicine, Karolinska University Hospital, Huddinge, Center for Infectious Medicine and Rheumatology Unit, 141 86 Stockholm, Sweden. E-mail johan.frostegard{at}medhs.ki.se

Series Editor: Göran K. Hansson
Immunity and Atherosclerosis
ATVB In Focus

Previous Brief Review in this Series:

•Nilsson J, Hansson GK, Shah PK. Immunomodulation of atherosclerosis: implications for vaccine development. 2005;25:18–28.

Recent findings indicate that presence of activated immune competent cells and inflammation are typical of atherosclerosis, the main cause of cardiovascular disease (CVD). The risk of CVD is very high in a prototypic autoimmune disease, systemic lupus erythematosus (SLE), and is also raised in other autoimmune diseases such as rheumatoid arthritis. Autoimmunity-related CVD and atherosclerosis are important clinical problems. They may also shed light on interactions between immune reactions and atherosclerosis development and manifestations, not least in women, who have a much higher risk of autoimmune disease than men. In general, a combination of traditional and nontraditional risk factors, including dyslipidemia (and to a varying degree, hypertension, diabetes, and smoking), inflammation, antiphospholipid antibodies (aPLs), and lipid oxidation, contribute to CVD in autoimmune diseases. Premature atherosclerosis is likely to be a major underlying mechanism, although distinctive features, if any, of autoimmunity-related atherosclerosis compared with "normal" atherosclerosis are not clear. One interesting possibility is that factors such as inflammation, neoepitopes on endothelial cells, or aPLs make atherosclerotic lesions in autoimmune disease more prone to rupture than in "normal" atherosclerosis. Some cases of autoimmunity-related CVD may be more related to thrombosis than atherosclerosis. Whether premature atherosclerosis is a general feature of autoimmune diseases such as SLE or only affects a subgroup of patients whereas others do not have an increased risk remains to be demonstrated. Treatment of patients with autoimmune disease should also include CVD aspects and be focused on traditional risk factors as well as on disease-related factors. Hopefully novel therapeutic principles will be developed that target the causes of the inflammation present in atherosclerotic lesions.

The risk of cardiovascular disease is very high in systemic lupus erythematosus and is also raised in other autoimmune diseases like rheumatoid arthritis. This may shed light on the role of immune reactions in atherothrombosis. Traditional risk factors and also non-traditional like inflammation, antiphospholipid antibodies and lipid oxidation are implicated.

Key Words: antibodies • atherosclerosis • autoimmunity • inflammation

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