FEATURED EDITORIAL
NSAIDs and cardiovascular disease
Department of Medicine and Center of Excellence on Aging, "G d’Annunzio" University, and CeSI, Italy
Correspondence to:
Dr P Patrignani, Department of Medicine and Center of Excellence on Aging, "G d’Annunzio" University, Via dei Vestini, 31, 66013 Chieti, Italy; ppatrignani@unich.it
| The first 150 words of the full text of this article appear below. |
Non-steroidal anti-inflammatory drugs (NSAIDs) are a chemically heterogeneous group of agents to treat symptoms of acute pain and chronic inflammatory and degenerative joint diseases, such as rheumatoid arthritis (RA) and osteoarthritis (OA).1 They act mostly through the inhibition of cyclooxygenase-2 (COX-2)-dependent prostanoids. They comprise traditional (t) NSAIDs and NSAIDs selective for COX-2, named cyclooxygenase-2 inhibitors, developed to reduce the gastrointestinal (GI) toxicity of tNSAIDs, which is dependent, at least in part, on the inhibition of COX-1.
Placebo-controlled trials have established that cyclooxygenase-2 inhibitors (rofecoxib, valdecoxib and celecoxib) confer a small but absolute increase in the incidence of thrombotic vascular events.2 An overview of data derived from trials with cyclooxygenase-2 inhibitors suggests that myocardial infarction (MI) predominates over stroke.3 The cardiovascular (CV) hazard associated with the use of cyclooxygenase-2 inhibitors led to the voluntary withdrawal from the United States (US) and European Union (EU) markets of rofecoxib and valdecoxib, in 2004
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