Key result
COX-2 selective NSAIDs currently lack conclusive evidence of causing ischemic vascular events, and their renal and hypertensive effects appear similar to conventional NSAIDs.
Why the study?
Do COX-2 selective NSAIDs increase the risk of adverse cardiovascular events compared to conventional NSAIDs?
Do COX-2 selective NSAIDs increase the risk of adverse cardiovascular events compared to conventional NSAIDs?
At the time of publication, there was no conclusive evidence that COX-2 selective NSAIDs cause ischemic vascular events, though aspirin remains necessary for patients with cardiovascular risk.
Evidence inconclusive on CV risk of COX-2 NSAIDs; leaves open need for dedicated RCTs in high-risk patients.
The newly developed nonsteroidal antiinflammatory drugs (NSAIDs) that selectively inhibit cyclooxygenase-2 (COX-2), are effective against pain and inflammation and appear to have less gastrointestinal toxicity than conventional NSAIDs. Their COX-2 selectivity, however, has raised concerns regarding their cardiovascular safety, since they do not inhibit COX-1, the isoform of the enzyme that is active in thrombosis and vasoconstriction. At this point there is no conclusive evidence that COX-2 inhibitors cause ischemic vascular events, because retrospective post hoc analyses conflict one another, and no specific randomized trials have yet been done. Renal effects, edema and hypertension appear to be similar between conventional NSAIDs and COX-2-selective inhibitors. Aspirin is still required for patients with cardiovascular risk who are prescribed a COX-2-selective inhibitor.
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Robert E. Fowles (2003) conducted a review in Cardiovascular safety of COX-2 inhibitors. COX-2 selective NSAIDs vs. Conventional NSAIDs was evaluated on Ischemic vascular events. COX-2 selective NSAIDs currently lack conclusive evidence of causing ischemic vascular events, and their renal and hypertensive effects appear similar to conventional NSAIDs.
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