Abstract
Over recent years it has become clear that patients with inflammatory rheumatic diseases are at increased risk of developing atherosclerosis. The exact causes for this are probably related in part to a general adverse effect of inflammation on atherogenesis, and in part to immune mechanisms specific to individual rheumatic diseases. This review discusses proposed mechanisms of accelerated atherosclerosis, including abnormal lipid and lipoprotein profiles, oxidative stress, enhanced apoptosis, thrombophilia, immune complexes, and increased mononuclear cell infiltration of atherosclerotic lesions, and local generation of cytokines.