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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 . . . [Full text of this article]