AMI was defined as the presence of acute myocardial injury detected by abnormal levels of cardiac biomarkers and angiographically proven atherothrombotic coronary artery disease (CAD). Cardiology specialists collected the patients’ medication lists and medical histories, such as the presence of hypertension, diabetes mellitus, and dyslipidemia. All laboratory variables were measured upon admission, except for lipid profiles, which were obtained after at least 9 h of fasting within 24 h of hospitalization. The baseline left ventricular ejection fraction (LVEF) was determined by two-dimensional echocardiography performed before or immediately after PCI. Coronary blood flow before and after PCI was classified by the thrombolysis in myocardial infarction (TIMI) score, and coronary lesion complexity was based on the American College of Cardiology (ACC)/American Heart Association (AHA) definitions. Patients who underwent PCI received 300 mg of aspirin and 600 mg of clopidogrel, 60 mg of prasugrel, or 180 mg of ticagrelor as a loading dose before PCI. Doses of 50 to 70 U/kg of unfractionated heparin were used before or during PCI to maintain an activated clotting time of 250 to 300 s. After PCI, 100 to 300 mg of aspirin and 75 mg of clopidogrel, 5 to 10 mg of prasugrel, or 45 to 90 mg of ticagrelor were prescribed daily. All patients had coronary lesions with at least 50% stenosis by quantitative coronary analysis. The study endpoint was vascular events associated with plaque instability, which consisted of recurrent AMI, stent thrombosis, and ischemic cerebral infarction. Recurrent MI was defined as the development of recurrent angina symptoms with new 12-lead electrocardiographic changes or increased cardiac-specific biomarkers.
Free full text: Click here
