Percutaneous coronary intervention has been known to cause myocardial damage as a result of microvascular dysfunction due to microembolization and microinfarction. Previous studies have shown that glucose-insulin-potassium(GIK)infusion decreases mortality in patients with acute myocardial infarction. Therefore, in this study, we aimed to investigate the effect of GIK infusion on myocardial damage due to percutaneous coronary revascularization. A total of 52 consecutive no ndiabetic patients diagnosed with non-ST-elevation acute coronary syndrome and designated for elective percutaneous coronary intervention were randomized in a double-blind fashion into GIK and normal saline groups. GIK infusion(30%dextrose, 300 U insulin, and 60 mEq potassium chloride)at a dose of 1.5 ml/kg/hour wa s initiated 24 hours before the intervention and continuing during and until 1 hour after the intervention. Troponin I levels were recorded in venous blood samples before and 12 and 24 hours after the intervention. The increase in troponin I was significantly lower at 12 and 24 hours in the GIK group compared with thos e of the saline controls(p=0.022 and p=0.005, respectively). GIK infusion initia ted 24 hours before coronary stenting for non-ST-elevation acute coronary synd rome resulted in less myocardial damage as determined by postprocedure troponin I levels. Percutaneous coronary intervention has been to to cause myocardial damage as a result of micro -mbolization and microinfarction. Previous studies have shown that glucose-insulin-potassium (GIK) infusion decreases mortality in patients with acute myocardial infarction. Therefore, in this study , we aimed to investigate the effect of GIK infusion on myocardial damage due to percutaneous coronary revascularization. A total of 52 consecutive no ndiabetic patients diagnosed with non-ST-elevation acute coronary syndrome and designated for elective percutaneous coronary intervention were randomized in a double- blind fashion into GIK and normal saline groups. GIK infusion (30% dextrose, 300 U insulin, and 60 mEq potassium chloride) at a dose of 1.5 ml / kg / hour wa s initiated 24 hours before the intervention and continuing during and until 1 hour after the intervention. Troponin I levels were recorded in venous blood samples before and 12 and 24 hours after the inter The increase in troponin I was significantly lower at 12 and 24 hours in the GIK group compared with thos e of the saline controls (p = 0.022 and p = 0.005, respectively). GIK infusion initia ted 24 hours before coronary stenting for non -ST-elevation acute coronary synd rome resulted in less myocardial damage as determined by postprocedure troponin I levels.