NSAIDs and cardiovascular disease

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 rheu-matoid 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 selec-tive for COX-2, named cyclooxygenase-2 inhibitors, developed to reduce the gastro-intestinal (GI) toxicity of tNSAIDs, which is dependent, at least in part, on the inhibition of COX-1. Placebo-controlled trials have estab-lished that cyclooxygenase-2 inhibitors (rofecoxib, valdecoxib and celecoxib) con-fer 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) predomi-nates over stroke.3 The cardiovascular (CV) hazard associated with the use of cyclooxygenase-2 inhibitors led to the voluntary withdrawal from the Unite