Recent studies shed light on the cardiovascular risk of NSAIDs, in particular COX-2–specific inhibitors such as rofecoxib.1 These drugs were thought to increase the risk of myocardial infarction and other thrombotic events through specific inhibition of prostacyclin, shifting prostanoid balance to favor thromboxane A2.2 Predictably, attention then turned toward traditional nonselective COX inhibitors