Tumour necrosis factor alpha (TNF a) has emerged as one of the key cytokines in the fields of infection and inflammation, and has been linked with disease activity and joint damage in rheumatoid arthritis. Acute myocardial infarction remains the leading cause of death in rheumatoid arthritis, and there is now a large body of evidence placing TNF a and other inflammatory cytokines at the centre of the development of atherosclerotic plaques and their subsequent rupture, which is in keeping with the observation of accelerated atherosclerosis in rheumatoid arthritis patients. TNF a might also have a role to play in the increased incidence of congestive cardiac failure seen in rheumatoid arthritis. Although anti-TNF a therapies were originally developed with a view to controlling joint disease in rheumatoid arthritis, evidence is emerging of a positive benefit in reducing heart disease as well. A range of mechanisms has been suggested by which anti-TNF a treatment might achieve a reduction in incidence of myocardial infarction and cardiac failure, some of which will have implications for the treatment of cardiovascular disease in general.
