COX-2 Inhibitors and Cardiovascular Risk

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Science  15 Jun 2012:
Vol. 336, Issue 6087, pp. 1386-1387
DOI: 10.1126/science.1224398

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Nonsteroidal anti-inflammatory drugs (NSAIDs) are used by millions of people worldwide to reduce pain and inflammation. They exert their pharmacologic effect by inhibiting the cyclooxygenase-1 (COX-1) and COX-2 enzymes, thereby blocking conversion of arachidonic acid to prostaglandin E2 (PGE2) and PGI2 (prostacyclin), which mediate pain (see the figure). However, because COX enzymes exist throughout the body, NSAIDs have many physiological effects, including complications, such as development of gastric ulcers and gastrointestinal bleeding. In 2004, the blockbuster drug rofecoxib (sold commercially as Vioxx) was withdrawn from the U.S. market when a study linked a selective COX-2 inhibitor with a higher rate of heart attack and stroke. However, studies on COX inhibitors have shown varying risk profiles, fueling a debate about their association with cardiovascular risk. A recent study by Yu et al. (1) now provides a biochemical explanation for the increased cardiovascular risk associated with COX-2 inhibitors, closing this part of the long-standing discussion.