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PERSPECTIVE

Why do cyclo-oxygenase-2 inhibitors cause cardiovascular events?

^a Huntington Medical Research Institutes, Department of Experimental Cardiology, Pasadena, California, USA

Manuscript received October 11, 2001; accepted November 2, 2001.

^* Reprint requests and correspondence: Dr. Richard J. Bing, Huntington Medical Research Institutes, 99 North El Molino Ave., Pasadena, California 91101, USA.
cardio{at}hmri.org

This report confirms evidence that selective nonsteroidal anti-inflammatory drugs (NSAIDs), such as celecoxib, can lead to thrombotic cardiovascular events. Aspirin, a nonselective COX-1 (cyclo-oxygenase) and COX-2 inhibitor may result in gastric toxicity. For this reason, selective COX-2 inhibitors have been developed to reduce erosion of the gastric mucosa. Both selective and nonselective NSAIDs reduce prostacyclin formation in the infarcted heart; they accomplish this by tipping the balance of prostacyclin/thromboxane in favor of thromboxane, a prothrombotic eicosanoid. The relative increase in thromboxane, coupled with a diminution in prostacyclin in infarcted heart muscle, can lead to the development of thrombotic cardiovascular events. This may be prevented by the addition of a nitric oxide donor to NSAIDs.

Abbreviations and Acronyms   NSAID   COX   cyclo-oxygenase   iNOS   inducible form of nitric oxide-synthase   NO   nitric oxide   NSAID   nonsteroidal anti-inflammatory drug

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