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Should acetaminophen be added to the list of anti-inflammatory agents that are associated with cardiovascular events?

See related article, pp 1008–1014 

Ever since the use of rofecoxib turned our attention toward the potential for adverse cardiovascular events associated with the use of nonsteroidal anti-inflammatory drugs (NSAIDs), other NSAIDs and other anti-inflammatory agents have been scrutinized. More recently, attention has been turned toward acetaminophen. In 2006, Chan et al1 reported (from the Nurses Health Study) the association of acetaminophen with adverse cardiovascular events and found that although the use of NSAIDs or acetaminophen at high frequency or dose was associated with increased risk, moderate use did not confer a substantial risk. Chan et al1 also observed that cardiovascular event risk was greater in women than in men and in smokers compared with nonsmokers. Small studies also suggested small increases in blood pressure of a few mm Hg in acetaminophen users that at a population level could be important.2 The mechanism(s) for the increased cardiovascular risk has been linked to selective inhibition of cyclooxygenase, officially known as prostaglandin-endoperoxide synthase of which cyclooxygenase-2 is a subfamily. It was initially thought that acetaminophen had no effect on cyclooxygenase, but recent evidence suggests it may, particularly in higher doses. Although the exact mechanism(s) by which cyclooxygenase is inhibited in various circumstances is still subject to debate, it has been postulated that >2 cyclooxygenase variants exist.3 Cyclooxygenase-2 inhibitors have been found to increase the risk of atherothrombosis even with short-term use.4 A 2006 analysis of 138 randomized trials and almost 150 000 participants showed that selective cyclooxygenase-2 inhibitors are associated with a moderately increased risk of vascular events, mainly from a 2× …