Abstract 2666: Randomized Controlled Trial to Compare High-Dose N-Acetylcystein Versus Placebo to Prevent Contrast-Induced Nephropathy and Myocardial Reperfusion Injury in Patients with ST-Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention

STEMI patients undergoing PCI are at high risk for contrast-induced nephropathy (CIN) because of hemodynamic instability and lack of effective prophylaxis. High-dose N-Acetylcystein (N-ACC) reduced the incidence of CIN in patients with high contrast volumes. In addition, previous animal trials showed that the antioxidant effects of N-ACC reduce reperfusion injury. Aim of this randomized, controlled, single-blinded trial was to assess the effects of N-ACC on CIN and reperfusion injury in patients undergoing primary PCI with moderate contrast volumes. Two hundred-fifty patients undergoing primary PCI were randomized to either high-dose N-ACC (2x1200 mg/d for 48 hours) or placebo plus optimal hydratation. The two primary endpoints were: 1) occurrence of CIN defined as an increase in the serum creatinine concentration of >25% from the baseline value within 72 h; 2) Myocardial salvage measured by T2-weighted STIR-images and delayed enhancement MRI at day 2– 4 after primary PCI. Secondary endpoints were infarct size and microvascular obstruction, ST-resolution at 90 minutes and occurrence of MACE at 30 day follow-up. The median volume of an isoosmolar 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 μmol/l and 90 vs 95 ml/min, respectively. 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.). Lipid peroxidation as a marker for oxidative stress was reduced by 20% in the N-ACC group (p<0.05), whereas no change was evident in placebo. 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 PCI with moderate doses of contrast medium and optimal hydratation.