[Anil Tuladhar]

This is add-on to my above comments:

It has been proposed that coxibs may adversely influence the prostacyclin (antithrombotic): thromboxane (prothrombotic) ratio in the vascular wall. Coxibs may inhibit the production of prostacyclin (antithrombotic) and leave thromboxane (prothrombotic) generation unaffected (as there are no COX-2 receptors in platelets), thus promoting platelet aggregation and atherosclerosis.

Furthermore, inhibition of prostacyclin in the kidney could lead to sodium and water retention, causing hypertension. These biological actions might increase the risk of cardiovascular events, including myocardial infarction and stroke.

The mechanism postulated for naproxen’s possible cardioprotective effect is its inhibition of thromboxane with consequent platelet aggregation.

Readers may find following attached review article helpful.