BACKGROUND: The aim of this study was to assess the effects of N-acetylcysteine (N-ACC) on contrast-induced nephropathy (CIN) defined by Cystatin C (Cys-C) serum levels and to evaluate the influence of Cys-C on clinical outcome in patients with ST-elevation myocardial infarction (STEMI). METHODS: In total, 251 patients with STEMI undergoing primary percutaneous coronary intervention (PCI) were randomized to either high-dose N-ACC (2 × 1200 mg/d for 48 h) with optimal hydration or placebo plus optimal hydration. Serum Cys-C was measured at baseline, immediately, 24, 48 and 72 h after PCI. CIN was defined as an increase in serum Cys-C levels of 25% or more from baseline within 72 h after PCI. Major adverse cardiac events (MACE)--defined as death, recurrent infarction and congestive heart failure--within 6 months were recorded. RESULTS: Baseline Cys-C was 1294 ± 611 and 1352 ± 811 ng/mL (p = 0.54) for the N-ACC and placebo group, respectively. There was a steady increase in Cys-C in both groups within the first 72 h after randomization. CIN occurred in 74.6 and in 70.4% of patients in the N-ACC and placebo group, respectively (p = 0.46). The magnitude of increase in the serum concentration of Cys-C was an independent predictor for MACE after 6 months of follow-up. CONCLUSIONS:High-dose N-ACC does not provide additional benefit over placebo with respect to Cys-C defined CIN in STEMI patients undergoing primary PCI. The magnitude of increase in Cys-C serum levels in the early course after STEMI is a predictor of medium-term MACE.
RCT Entities:
BACKGROUND: The aim of this study was to assess the effects of N-acetylcysteine (N-ACC) on contrast-induced nephropathy (CIN) defined by Cystatin C (Cys-C) serum levels and to evaluate the influence of Cys-C on clinical outcome in patients with ST-elevation myocardial infarction (STEMI). METHODS: In total, 251 patients with STEMI undergoing primary percutaneous coronary intervention (PCI) were randomized to either high-dose N-ACC (2 × 1200 mg/d for 48 h) with optimal hydration or placebo plus optimal hydration. Serum Cys-C was measured at baseline, immediately, 24, 48 and 72 h after PCI. CIN was defined as an increase in serum Cys-C levels of 25% or more from baseline within 72 h after PCI. Major adverse cardiac events (MACE)--defined as death, recurrent infarction and congestive heart failure--within 6 months were recorded. RESULTS: Baseline Cys-C was 1294 ± 611 and 1352 ± 811 ng/mL (p = 0.54) for the N-ACC and placebo group, respectively. There was a steady increase in Cys-C in both groups within the first 72 h after randomization. CIN occurred in 74.6 and in 70.4% of patients in the N-ACC and placebo group, respectively (p = 0.46). The magnitude of increase in the serum concentration of Cys-C was an independent predictor for MACE after 6 months of follow-up. CONCLUSIONS: High-dose N-ACC does not provide additional benefit over placebo with respect to Cys-C defined CIN in STEMI patients undergoing primary PCI. The magnitude of increase in Cys-C serum levels in the early course after STEMI is a predictor of medium-term MACE.
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