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 tumor necrosis factor-⍺ produced within locally affected joints in RA may promote both traditional (e.g., dyslipidemia, insulin resistance) and nontraditional (e.g., oxidative stress) systemic cardiovascular risk factors. Expression of proinflammatory cytokines and inflammatory mediators influences all stages of atherosclerosis development, from early atheroma formation to thrombus development responsible for events such as myocardial infarction. Appreciation of the inflammatory process shared by RA and atherosclerosis should heighten the recognition of this morbid association and lead to better recognition and management of cardiovascular risk in patients with rheumatologic diseases.