Rosuvastatin versus atorvastatin to prevent contrast induced nephropathy in patients undergoing primary percutaneous

Ahmet Kaya1, Mustafa Kurt, Ibrahim Halil Tanboğa

  • 1Dept. of Cardiology, Ordu University Medical School, Ordu, Turkey. drkayaahmet69@gmail.com

Acta Cardiologica
|November 29, 2013
PubMed

Insights

Atorvastatin and rosuvastatin showed similar effectiveness in preventing contrast-induced nephropathy (CIN) in ST-segment elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (p-PCI). The amount of contrast agent was the main predictor of CIN.

Area of Science:

  • Cardiology
  • Nephrology
  • Pharmacology

Background:

  • Contrast-induced nephropathy (CIN) is a significant complication following percutaneous coronary intervention (PCI).
  • Statins are frequently used peri-procedurally to mitigate CIN risk.
  • Atorvastatin and rosuvastatin are commonly prescribed statins with differing pharmacokinetic profiles.

Purpose of the Study:

  • To compare the incidence of CIN between high-dose atorvastatin and rosuvastatin in ST-segment elevation myocardial infarction (STEMI) patients undergoing primary PCI.
  • To identify predictors of CIN in this patient population.

Main Methods:

  • A randomized controlled trial involving 192 STEMI patients undergoing primary PCI.
  • Patients received either atorvastatin 80 mg or rosuvastatin 40 mg prior to the procedure.
  • Renal function was assessed at baseline and 48 hours post-procedure.

Main Results:

  • The overall incidence of CIN was 8.9%.
  • No statistically significant difference in CIN incidence or renal dysfunction markers was observed between the atorvastatin and rosuvastatin groups.
  • The volume of contrast agent administered was the sole independent predictor of CIN (OR 1.08, 95% CI 1.03-1.13, P<0.001).

Conclusions:

  • High-dose atorvastatin and rosuvastatin demonstrate comparable efficacy in preventing CIN in STEMI patients undergoing primary PCI.
  • Contrast volume is a critical factor influencing CIN development, independent of statin choice.
Abstract

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