Selective cyclooxygenase-2 (COX-2) inhibitors and potential risk of cardiovascular events.
Selective cyclooxygenase-2 (COX-2) inhibitors were developed as a response to the gastrointestinal toxicity of conventional nonsteroidal anti-inflammatory agents (NSAIDs). However, COX-2 inhibitors decrease vascular prostacyclin (PGI(2)) production and may disrupt the homeostatic mechanisms that limit the effects of platelet activation. Basic and clinical data raise concerns about a potential prothrombotic effect of this class of drugs. The widespread popularity of these agents mandates their prospective evaluation in patients with cardiovascular diseases or who are at risk for cardiovascular events.
Mukherjee
Debabrata
D
Division of Cardiology, University Hospital, University of Michigan Health System, B1-F245, 1500 East Medical Center Drive, Ann Arbor, MI 48103-0022, USA. dmukherj@umich.edu
D000818:Animals; D000068579:Celecoxib; D002986:Clinical Trials as Topic; D051546:Cyclooxygenase 2; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors / Q000009:adverse effects* / Q000494:pharmacology; D011464:Epoprostenol / Q000378:metabolism; D006801:Humans; D007527:Isoenzymes / Q000037:antagonists & inhibitors*; D007783:Lactones / Q000009:adverse effects / Q000494:pharmacology; D008565:Membrane Proteins; D015539:Platelet Activation / Q000187:drug effects; D011451:Prostaglandin-Endoperoxide Synthases; D011720:Pyrazoles; D013449:Sulfonamides / Q000009:adverse effects / Q000494:pharmacology; D013450:Sulfones; D013927:Thrombosis / Q000209:etiology*
D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors; D007527:Isoenzymes; D007783:Lactones; D008565:Membrane Proteins; D011720:Pyrazoles; D013449:Sulfonamides; D013450:Sulfones; C116926:rofecoxib; D011464:Epoprostenol; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases; D000068579:Celecoxib