Rheumatoid arthritis (RA) is associated with excess morbidity and mortality from myocardial
infarction and allied disorders. A large body of evidence supports the involvement of
common proinflammatory cytokines in the development and progression of both RA and
atherosclerosis. The destructive proinflammatory cascade and effector mechanisms
implicated in RA resemble the chronic inflammatory processes that drive the development of
atherosclerosis in general. Proinflammatory cytokines such as interleukin (IL)-1, IL-6, and …