Dew, many moons ago I promised you a reference to the effects of Cox-2 inhibitors on the heart; a recent news report of a statement by the FDA's David Graham reminded me of that promise:
"I'm attracted to the Cox-2 hypothesis," Graham said, referring to suggestions that the heart problems cover the class of drugs called Cox-2 inhibitors, which includes the three under review."
The reference is from the Journal of the American College of Cardiology, vol 39, #3, 2002, from the paper: "Why do Cyclo-Oxygenase-2 Inhibitors Cause Cardiovascular Events?" by Richard J Bing and Magdelana Lomnicka.
The summary:
"This report confirms evidence that selective nonsteriodal 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 cardivasuclar events. This may be prevented by the addition of a nitric oxide donor to NSAIDs"
Sorry I don't have the report in an online version.
