Current use of cyclooxygenase-2 inhibitors was associated with an increase in 30-day mortality after ischemic stroke in a population-based cohort study published Nov. 5 in Neurology.
Since the association between COX-2 inhibitors and ischemic stroke mortality was associated only with current use and not former use, the researchers, led by Dr. Morten Schmidt of Aarhus (Denmark) University Hospital, believe that alternative treatment options – such as nonselective NSAIDs, which did not have an impact on overall mortality after ischemic stroke – may be more suitable for treating potential ischemic stroke patients, such as those with atrial fibrillation and a high CHA2DS2-VASc score.
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Records of over 100,000 patients hospitalized for a first-time stroke were examined to determine if COX-2 inhibitors influenced 30-day mortality rates.
If the association is truly causal, it constitutes a strong argument for increasing the efforts to ensure that patients with a high predicted risk of arterial thromboembolism are not prescribed COX-2 inhibitors when alternative treatment options are available,” Dr. Schmidt and his associates wrote.
In order to determine whether COX-2 inhibitors influenced 30-day mortality at the time of hospitalization for stroke, the researchers examined records of 100,243 people hospitalized for a first-time stroke in Denmark during 2004-2012 and deaths within 1 month after the stroke (Neurology 2014 Nov. 5 [doi:10.1212/WNL.0000000000001024]).
The hazard ratio for ischemic stroke was 1.19 (95% confidence interval, 1.02-1.38) for current users of COX-2 inhibitors, while current users of nonselective NSAIDs had an HR of 1.00 (95% CI, 0.87-1.15), compared with nonusers.
The COX-2 inhibitors in the study included diclofenac, etodolac, nabumeton, and meloxicam, as well as coxibs including celecoxib and rofecoxib. The nonselective NSAIDs in the study were ibuprofen, naproxen, ketoprofen, dexibuprofen, piroxicam, tolfenamic acid, and indomethacin.
Though the researchers acknowledged more studies are needed to truly examine the effects of COX-2 inhibitors on stroke mortality, they hypothesized that the increased mortality rate may be caused by COX-2 inhibition interfering with the pathophysiologic response to a stroke, or unwanted effects from the thromboembolic properties of COX-2 inhibitors.
“Our study adds to the increasing body of evidence concerning the vascular risk and prognostic impact associated with use of COX-2 inhibitors,” Dr. Schmidt and his associates wrote.
The study was funded by several Danish research foundations and the Program for Clinical Research Infrastructure, which was established by the Lundbeck Foundation and the Novo Nordisk Foundation. The authors reported no relevant disclosures.