Effect of N-acetylcystein in Myocardial Infarction

Acute Myocardial Infarction

We designed this study to evaluate the effect of N-acetylcystein on biomarkers of platelet activation , cardiac necrosis and coronary reperfusion in patients undergoing percutaneous coronary intervention.

Percutaneous coronary intervention(PCI) is one of the standard therapies for acute coronary syndrome. Despite major advances in PCI procedure, impaired myocardial perfusion frequently occurred after primary PCI and resulted in a larger infarct size and increased morbidity and mortality.Reperfusion injury process can be resulted in additional death of cardiomyocytes and it is suggested that oxidative stress is a contributing factor to induce reperfusion injury.During PCI,trauma occurs to the arterial endothelium, causes the activation and aggregation of platelets. It is estimated that approximately 25% of patients undergoing PCI have significant postprocedural creatinine kinase (CK)/creatinine kinase myocardial band (CK-MB) elevations and approximately 50% of patients have significant post-procedural troponin elevations. The most common complication of PCI is a cell damage to cardiomyocyte that can be diagnosed by postprocedure elevation of cardiac markers. N-acetylcystein have several positive effect on platelet and vascular function and infarct size. This study is a randomized clinical trial (RCT) evaluating the effect of N-acetylcystein on biomarkers of platelet activation and coronary reperfusion in patients undergoing percutaneous coronary intervention. Double blind randomized clinical trial on 100 patients in 2 groups (intervention & control) is conducted. Patients with confirmed ST-elevation myocardial infarction included in this study. Patients were excluded if they had: emergency for cardiac bypass; cardiogenic shock and rescue percutaneous coronary intervention. Patients in Intervention group were administered 100 mg/kg Iv bolus N-acetylcystein and then 480mg intracoronary and 10mg/kg/h over 12 hours after percutaneous coronary intervention and patients in control group received standard regimens. Primary outcome was platelet activation biomarkers assessment before and 24 hours after percutaneous coronary intervention and secondary outcome was effect of N-acetylcystein on CK-MB and high sensitive Troponin T, 6 and 12 hours after percutaneous coronary intervention.Patients were assessed for coronary blood flow after percutaneous coronary intervention with the use of TIMI flow and myocardial blush grade. Major adverse cardiac events (MACE) will be evaluated as a secondary endpoint after 30 days.

Iran