In recent years, the scientific community has gained significant insight into the complex interaction between inflammation and
the cardiovascular system in patients with rheumatoid arthritis (RA), which leads to increased cardiovascular (CV) morbidity and mortality
in these patients. Our common understanding of this association is that persistent inflammation contributes to the development of
premature atherosclerosis. Consequently, the question arises whether control of inflammation with antirheumatic treatment will be able to
improve CV outcome. While there are a lot of data that demonstrate improvement of numerous CV surrogate markers in patients treated
with virtually all antirheumatic drug classes, there is much less information about the possible translation of these beneficial effects into
improved CV outcome. In summary, the published evidence suggests that tumor necrosis factor (TNF) alpha inhibitors may improve CV
outcome. The same is true for methotrexate (MTX). However, it is not clear whether MTX works via suppression of inflammation or
through drug specific mechanisms. For other traditional disease-modifying antirheumatic drugs and biologic therapies, there are no convincing
data for improved CV outcome. Only a few drugs (glucocorticoids and NSAIDs) have been associated with increased CV risk.
Treating RA aggressively, as recommended by current guidelines, is likely to have a beneficial effect on CV outcomes.