Syntheses of published interventional and observational studies conclude that both selective and nonselective COX-2 inhibitors increase the risk of acute myocardial infarction (AMI), and this risk varies across individual NSAIDs.4–7 Cardiovascular toxicity associated with selective COX-2 and some traditional NSAIDs is mediated through a common mechanism involving the inhibition of COX-2-dependent prostacyclin. Here, PTGS2 is linked to acute myocardial infarction.