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The problem of the atherothrombotic potential of nonsteroidal anti-inflammatory drugs.

Bolten WW

Klaus Miehlke-Klinik Wiesbaden, Germany.

Inflammatory vascular processes have a modulating influence on the pathogenesis of atherosclerosis. Through their enzymatic inhibition of systemic inflammation, e.g. in the context of antirheumatic therapy, traditional nonsteroidal nonselective anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2 (COX-2) selective inhibitors have differing effects on the inhibition of prostacyclin (PGI2) and thromboxane (TXA2) synthesis in the vessel wall and in platelets. The resulting loss of homeostasis may, in addition to other factors, increase the atherogenic cardiovascular (CV) risk for treated patients. In clinical studies, myocardial infarction (MI) or cerebrovascular accident occurred more frequently during treatment with rofecoxib, celecoxib, valdecoxib, naproxen and acetylsalicylic acid compared with placebo or comparator substances with an anti-inflammatory action. Lumiracoxib, naproxen and ibuprofen did not show any differences in the incidence of CV side effects in a large outcomes study. For other NSAIDs and selective COX- 2 inhibitors there are no conclusive published data available with regard to the assessment of CV risk. At present, an increased atherogenic potential has to be assumed for all NSAIDs and selective COX-2 inhibitors. Until adequate results are available, treatment recommendations must take into account a potential atherothrombotic risk in any NSAID or selective COX-2 inhibitor therapy.

Published 8 June 2005 in Ann Rheum Dis.
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