Inflammatory rheumatic disorders and atherosclerosis

Atherosclerosis has emerged as the leading cause of long term morbidity and mortality in inflammatory rheumatic disorders like rheumatoid arthritis and systemic lupus erythematosus. In addition to traditional risk factors such as smoking, hypertension, diabetes mellitus and dyslipidemia, non-traditional risk factors like anti-oxidized LDL antibodies, interleukin 6 and anticardiolipin antibodies may play a key role in causing accelerated atherosclerosis, which is common in these disorders. It has been shown in animal models that both humoral and cellular immune mechanisms are involved in producing atherosclerosis. Endothelial cell injury, believed to be the triggering factor in atheroma formation, can be produced by several of the inflammatory mediators whose levels are characteristically elevated in rheumatic disorders. Using measurement of carotid intima media thickness as a tool, clinical evidence of premature and accelerated atherosclerosis has been found in both rheumatoid arthritis and lupus. Similar findings have been reported in the antiphopholipid antibody syndrome and certain vasculitides.Patients with rheumatoid arthritis have a 3.6-fold higher risk of developing coronary artery disease as compared to controls and this risk may be as high as 50-fold in systemic lupus erythematosus (SLE). Control of modifiable traditional risk factors like hypertension is crucial to lowering this risk. It has also been suggested that adequate control of the inflammatory process which is a part of the underlying disease, may also reduce the incidence of coronary artery disease.