The cardiovascular safety of celecoxib.
Ever since the VIoxx Gastrointestinal Outcomes Research (VIGOR) trial first suggested that rofecoxib may increase the risk of cardiovascular disease, and especially since it was withdrawn from the market based on mounting evidence of this risk, celecoxib has had to bear intense scrutiny regarding its own potential cardiovascular effects. This article reviews the current body of evidence regarding the cardiovascular effects of celecoxib, considered under two distinct, but non-mutually exclusive, headings: cardiorenal and thromboembolic. In terms of cardiorenal effects, celecoxib appears to cause a slight increase in blood pressure, and probably to the same extent as nonselective nonsteroidal anti-inflammatory drugs (NS NSAIDs) but less than rofecoxib. Limited observational data suggest that celecoxib is not associated with an increased risk of hospitalization for heart failure, but clinical studies are required. The current body of evidence regarding the thromboembolic effects of celecoxib is equivocal. If an increased risk of thromboembolic events is present at all, then it would seem to be small. This contrasts with the situation for rofecoxib, for which the evidence of an increased thromboembolic risk is much more consistent. There are emerging data that suggest that NS NSAIDs may also elevate the risk of thromboembolic events. If true, then switching patients from coxibs to NS NSAIDs for reasons of cardiovascular safety would be flawed. Certainly it would not appear at this stage that celecoxib poses any more thromboembolic risk than NS NSAIDs. A limitation of the current body of evidence regarding the cardiovascular safety of celecoxib is that most of it has only been drawn from observational studies and noncardiovascular clinical trials. A definitive answer to whether or not celecoxib increases cardiovascular risk can really only be derived from purpose-designed, adequately-powered, prospective randomized trials that include appropriate cardiovascular end points and comparators.
Liew
Danny
D
NHMRC Centre of Clinical Research Excellence in Therapeutics, Department of Medicine and Epidemiology, Monash University Central and Eastern Clinical School, Alfred Hospital, Melbourne, Victoria 3004, Australia. danny.liew@med.monash.edu.au
Krum
Henry
H