Key result
Cyclo-oxygenase inhibitors may not have a major effect on the thromboembolic complications of arterial disease.
Why the study?
Do cyclo-oxygenase inhibitors reduce thromboembolic complications in patients with arterial disease?
Do cyclo-oxygenase inhibitors reduce thromboembolic complications in patients with arterial disease?
Despite the mechanistic role of prostaglandins and thromboxanes in platelet aggregation, cyclo-oxygenase inhibitors may not have a major clinical effect on thromboembolic complications of arterial disease.
Challenges expectations for cyclo-oxygenase inhibitors in arterial thromboembolic prevention; leaves open definitive randomized trials.
Release of arachidonate from cell membrane phospholipids by activation of phospholipase A1 is a key step in the formation of prostaglandins and thromboxanes. In platelets PGH2 and TXA2 are formed from arachidonate and can cause aggregation and the release of granule contents; in vascular tissue, PGI2 is formed instead and, by increasing platelet cAMP, inhibits platelet reactions. There is considerable interest in inhibitors of the enzymes in these pathways as drugs to modify thrombus formation. Results of the clinical trials, however, indicate that drugs which inhibit cyclo-oxygenase may not have a major effect on the thromboembolic complications of arterial disease.
No takes yet. Share an insight, caveat, or question.
Mustard et al. (1980) conducted a review in Arterial disease. Cyclo-oxygenase inhibitors was evaluated on Thromboembolic complications. Cyclo-oxygenase inhibitors may not have a major effect on the thromboembolic complications of arterial disease.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: