Contrast-induced nephropathy (CIN) impairs clinical outcome in patients undergoing angiographic procedures. The aim of this study was to investigate whether short-term high-dose atorvastatin load decreases the incidence of CIN after percutaneous coronary intervention (PCI). Statin-naive patients with acute coronary syndrome undergoing PCI (n = 241) randomly received atorvastatin (80 mg 12 hours before intervention with another 40-mg preprocedure dose, n = 120) or placebo (n = 121). All patients had long-term atorvastatin treatment thereafter (40 mg/day). Primary end point was incidence of CIN defined as postintervention increase in serum creatinine >= 0.5 mg/dl or >25% from baseline. Five percent of patients in the atorvastalin arm developed CIN versus 13.2% of those in the placebo arm (p = 0.046). In the atorvastatin group, postprocedure serum creatinine was significantly lower (1.06 +/- 0.35 vs 1.12 +/- 0.27 mg/dl in placebo, p = 0.01), creatinine clearance was decreased (80.1 +/- 32.2 vs 72.0 +/- 26.6 ml/min, p = 0.034), and C-reactive protein peak levels after intervention were decreased (8.4 +/- 10.5 vs 13.1 +/- 20.8 mg/l, p = 0.01). Multivariable analysis showed that atorvastatin pretreatment was independently associated with a decreased risk of CIN (odds ratios 0.34, 95% confidence interval 0.12 to 0.97, p = 0.043). Prevention of CIN with atorvastatin was paralleled by a shorter hospital stay (p = 0.007). In conclusion, short-term pretreatment with high-dose atorvastatin load prevents CIN and shortens hospital stay in patients with acute coronary syndrome undergoing PCI; anti-inflammatory effects may be involved in this renal protection. These results lend further support to early use of high-dose statins as adjuvant pharmacologic therapy before percutaneous coronary revascularization. (C) 2011 Elsevier Inc. All rights reserved. (Am J Cardiol 2011;108:1-7)

Short-Term, High-Dose Atorvastatin Pretreatment to Prevent Contrast-Induced Nephropathy in Patients With Acute Coronary Syndromes Undergoing Percutaneous Coronary Intervention (from the ARMYDA-CIN [Atorvastatin for Reduction of MYocardial Damage during Angioplasty Contrast-Induced Nephropathy] Trial

Patti G;
2011

Abstract

Contrast-induced nephropathy (CIN) impairs clinical outcome in patients undergoing angiographic procedures. The aim of this study was to investigate whether short-term high-dose atorvastatin load decreases the incidence of CIN after percutaneous coronary intervention (PCI). Statin-naive patients with acute coronary syndrome undergoing PCI (n = 241) randomly received atorvastatin (80 mg 12 hours before intervention with another 40-mg preprocedure dose, n = 120) or placebo (n = 121). All patients had long-term atorvastatin treatment thereafter (40 mg/day). Primary end point was incidence of CIN defined as postintervention increase in serum creatinine >= 0.5 mg/dl or >25% from baseline. Five percent of patients in the atorvastalin arm developed CIN versus 13.2% of those in the placebo arm (p = 0.046). In the atorvastatin group, postprocedure serum creatinine was significantly lower (1.06 +/- 0.35 vs 1.12 +/- 0.27 mg/dl in placebo, p = 0.01), creatinine clearance was decreased (80.1 +/- 32.2 vs 72.0 +/- 26.6 ml/min, p = 0.034), and C-reactive protein peak levels after intervention were decreased (8.4 +/- 10.5 vs 13.1 +/- 20.8 mg/l, p = 0.01). Multivariable analysis showed that atorvastatin pretreatment was independently associated with a decreased risk of CIN (odds ratios 0.34, 95% confidence interval 0.12 to 0.97, p = 0.043). Prevention of CIN with atorvastatin was paralleled by a shorter hospital stay (p = 0.007). In conclusion, short-term pretreatment with high-dose atorvastatin load prevents CIN and shortens hospital stay in patients with acute coronary syndrome undergoing PCI; anti-inflammatory effects may be involved in this renal protection. These results lend further support to early use of high-dose statins as adjuvant pharmacologic therapy before percutaneous coronary revascularization. (C) 2011 Elsevier Inc. All rights reserved. (Am J Cardiol 2011;108:1-7)
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11697/127513
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