Cyclooxygenase inhibition and thrombogenicity

Cyclooxygenase (COX)-1 and COX-2 catalyze the formation of prothrombotic and antithrombotic eicosanoids, respectively. Aspirin, conventional nonsteroidal anti-inflammatory drugs (NSAIDs), and COX-2–specific inhibitors exhibit different patterns of inhibition of COX-1–mediated thromboxane biosynthesis and COX-2–mediated prostacyclin biosynthesis. The relationship between the pharmacologic inhibition of these vasoactive eicosanoids and the thromboprophylaxis or thrombogenicity exhibited by different therapeutic agents is currently unclear. Future studies are needed to assess the antithrombotic properties of commonly used NSAIDs, the hypothetical thrombogenicity of COX-2–specific inhibitors in high-risk patients, the need for concomitant aspirin with selective versus nonselective COX inhibitors, and the antiplatelet and gastric toxicity of the aspirin/COX-2–specific inhibitor combination in comparison with the aspirin/conventional NSAID combination.