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J Am Coll Cardiol, 2004; 43:519-525, doi:10.1016/j.jacc.2003.09.043
© 2004 by the American College of Cardiology Foundation
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Nonsteroidal Anti-Inflammatory drugs and cardiovascular risk

Patricia A. Howard, PharmD, FCCP, BCPS (AQ CV)*,* and Patrice Delafontaine, MD, FACC, FESC, FAHA, FACP{dagger}

* Department of Pharmacy Practice, University of Kansas Medical Center, Kansas City, Kansas, USA
{dagger} Division of Cardiovascular Diseases, University of Kansas Medical Center, Kansas City, Kansas, USA



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  		Figure 1 Action of nonsteroidal anti-inflammatory drugs (NSAID). Arachidonic acid, liberated from membrane phospholipids in response to multiple stimuli, is converted to prostaglandin H2 by cytosolic prostaglandin G/H synthases (cyclooxygenase [COX]-1 and -2). Prostaglandin H2 is converted by tissue-specific isomerases to multiple prostanoids. Aspirin and other nonselective nonaspirin nonsteroidal anti-inflammatory drugs (NANSAID) inhibit both COX-1 and -2, whereas coxibs selectively inhibit COX-2.

 




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