, Volume 21, Issue 2, pp 77-79
Date: 03 Apr 2007

Cerebrovascular Events After Discontinuation of Rofecoxib Treatment

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The pain-relieving nonsteroidal antiinflammatory drugs (NSAIDs) exhibit different degrees of selectivity for the isoforms COX-1 and COX-2 which differ substantially in their localization and function. While COX-1 plays an important role in the cytoprotection of the gastric mucosa, in platelet activation, and in other homeostatic processes, COX-2 is thought to largely account for prostaglandin formation at the site of tissue injury [1]. With the objective of treating pain and inflammation without affecting gastric mucosa, COX-2 selective NSAIDs (“Coxibs”) were developed and introduced on the market. The finding of an excess of thrombotic cardiovascular events, primarily of myocardial infarction, in the VIGOR trial [2] raised concern about the cardiovascular safety of rofecoxib, and also of COX-2 inhibitors in general. The relative risk (RR) of myocardial infarction was 5.00 (95% confidence interval (CI) 1.68–20.13) for patients treated with rofecoxib as compared with naproxen [3]. The p ...