Patients with rheumatoid arthritis (RA) have an increased burden of atherosclerotic cardiovascular disease which cannot be explained by an increased prevalence of traditional cardiovascular risk factors alone. Atherosclerosis is now being viewed as an inflammatory condition and the cumulative inflammation experienced in RA may contribute to accelerated atherosclerosis. It has been hypothesised that treatment with anti-tumour necrosis factor (TNF) alpha in RA may reduce both intra-articular inflammation and the inflammation associated with atherosclerosis. Thus, TNFalpha blockade may reduce the cardiovascular morbidity and mortality associated with RA. This review examines the pathophysiological role of TNFalpha in atherosclerosis and the evidence to date that anti-TNFalpha treatment modifies this process in RA.