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BMJ 2006;332:895-898 (15 April), doi:10.1136/bmj.332.7546.895
Harald E Vonkeman, rheumatologist1, Jacobus R B J Brouwers, professor of pharmacotherapeutics2, Mart A F J van de Laar, professor of rheumatology1
1 Department of Rheumatology and Clinical Immunology, Medisch Spectrum Twente Hospital and University of Twente, Enschede, Netherlands, 2 Groningen University Institute for Drug Exploration and Groningen Research Institute of Pharmacy, Department of Social Pharmacy, Pharmacoepidemiology and Pharmacotherapy, Groningen, Netherlands
Correspondence to: H E Vonkeman H.Vonkeman@ziekenhuis-mst.nl
| The first 150 words of the full text of this article appear below. |
Concern is growing about an increased risk of thrombotic events (including myocardial infarction and stroke) during the use of non-steroidal anti-inflammatory drugs (NSAIDs), in particular the so called selective cyclo-oxygenase-2 (COX 2) inhibitors. Although clinical trials give conflicting results with respect to the incidence of vascular events, increasing evidence shows that a class effect might exist for selective COX 2 inhibitors. Even before the massive introduction of selective COX 2 inhibitors, observational studies showed that the use of NSAIDs causes congestive heart failure in elderly patients.1 2 Conversely, the discontinuation of NSAIDs has also been associated with increased risk of myocardial infarction, especially in the first several weeks after stopping chronic NSAID treatment.3
Many different mechanisms could explain the different effects of classic NSAIDs and selective COX 2 inhibitors in relation to thrombotic vascular events. In this review we link biochemical facts concerning NSAIDs and COX inhibitors with data from clinical
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