[Lornoxicam for prevention of myocardial injury during acute ST-elevation myocardial infarction].

10% of patients with acute ST-elevation myocardial infarction (STEMI) treated with reperfusion therapy fail to develop an enzyme rise, but do exhibit transient ECG changes, which are consistent with an aborted myocardial infarction. Following reperfusion by primary PCI in STEMI, oxidative stress and an inflammatory response are induced immediately. Inflammation is a critical component of STEMI. Both COX isoforms are involved in reperfusion and ischemic myocardial injury. To evaluate the effectiveness of lornoxicam - nonselective NSAID, in decrease of myocardial injury during acute ST-elevation myocardial infarction. We analyzed 22 patients with STEMI, 14 of them received 16 mg and 8 mg lornoxicam after 20 min and 8 hours, respectively, after arrival to hospital. 12 f them received alteplase, 10 patients with cardiac pain up to 24 hours from the beginning, did not receive reperfusion therapy. All patients received anticoagulants, antiplatlet therapy, -blockers. The primary end point was all-cause mortality by the day 30 and hospitalization due to congestive heart failure by the 1st year. There was no difference in mortality and heart failure by the 30 day and 1st year respectively, between the patients with STEMI treated with lornoxicam or placebo. Randomized controlled trials are needed to explore potential cardioprotective effects of lornoxicam in patients with acute STEMI.