Abstract 5766: Reduction of Oxidized Stress by High-Dose N-Acetylcysteine versus Placebo in Patients With ST-Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention

Abstract

Background STEMI patients undergoing primary PCI develop oxidative stress which might have an impact on reperfusion injury. High-dose N-Acetylcysteine (N-ACC) might prevent oxidative stress with subsequent reduction of reperfusion injury and also the incidence of contrast-induced nephropathy (CIN). Aim of this randomized, controlled, single-blind trial was to assess the effects of N-ACC on oxidative stress, reperfusion injury and CIN in patients undergoing primary PCI. Methods Two hundred-fifty patients undergoing primary PCI were randomized to either N-ACC (2×1200 mg/d for 48 hours) or placebo plus optimal hydration. The two primary endpoints were: occurrence of CIN defined as an increase in the serum creatinine concentration of >25% from the baseline value within 72 h; Myocardial salvage measured by T2-weighted STIR-images and delayed enhancement MRI at day 2–4 after primary PCI. Secondary endpoints were oxidative stress, infarct size, microvascular obstruction, ST-resolution at 90 minutes and occurrence of MACE at 30 day follow-up. Results The median volume of contrast agent during PCI was 190 ml (IQR 130, 250 ml) in the N-ACC and 180 (IQR 143; 228 ml) in the placebo group (p= n.s.). Baseline creatinine and creatinine clearance were 88 vs 86 μ mol/l and 90 vs 95 ml/min, respectively. Oxidized low-density lipoprotein and advance oxidative protein products as marker for oxidative stress were reduced by 20% in the N-ACC group (p<0.05), whereas no change was evident in placebo. The primary endpoint CIN occurred in 14% in the N-ACC group and in 18% in the placebo group (p=n.s.). The primary endpoint reperfusion injury measured by myocardial salvage was also not different between both treatment groups (25.4%; IQR 14.1; 38.1 versus 22.5%; IQR 16.8; 36.5; p=n.s.). In addition, no differences in infarct size and microvascular obstruction as well as in ST-segment resolution were observed. The MACE rate after N-ACC was similar to placebo (19.4% versus 19.4%, p=n.s.). Conclusion High-dose N-ACC reduces oxidative stress. However, it does not provide an additional clinical benefit to placebo with respect to CIN and prevention of myocardial reperfusion injury in patients undergoing primary PCI with moderate doses of contrast medium and optimal hydration.