It is well known that rheumatoid arthritis (RA) causes significant morbidity as a result of synovial inflammation, joint destruction, and associated disability. In addition to these articular manifestations of RA, there is growing recognition of an excess mortality, which is due to increased atherosclerosis.

Approximately 50% of atherosclerotic coronary artery disease in the community occurs in the absence of traditional risk factors, such as smoking, hypertension, diabetes mellitus, and hypercholesterolemia. Recently, inflammation has emerged as an important pathogenic mechanism of atherosclerosis. Inflammation has a role in both the initiation and the progression of atherosclerosis. C-reactive protein (CRP) is a sensitive marker for underlying systemic inflammation. Prospective studies indicate that baseline levels of CRP are associated with increased risk of myocardial infarction and stroke among apparently healthy individuals. Furthermore, the value of high-sensitivity testing for CRP appears to be additive to that of total and HDL- cholesterol for cardiovascular risk prediction.

RA is a typical chronic inflammatory disease and CRP well reflects on the disease activity of RA. Several studies have reported increased cardiovascular disease and mortality among patients with RA. As a potential underlying mechanism for this observation, the inflammation of RA may play an important role. Studies have shown evidences that patients with RA have accelerated atherosclerosis, which is associated with the inflammation of RA. In this article, we reviewed the relationship between RA and accelerated atherosclerosis.

Keywords: Rheumatoid arthritis, Atherosclerosis, Inflammation