Early statin treatment prior to primary PCI for acute myocardial infarction: REPERATOR, a randomized placebo‐controlled pilot trial

S Post, MC Post, BJ van den Branden… - Catheterization and …, 2012 - Wiley Online Library
S Post, MC Post, BJ van den Branden, FD Eefting, MJ Goumans, PR Stella, HW van Es…
Catheterization and Cardiovascular Interventions, 2012Wiley Online Library
Objective: The aim of this pilot study was to determine whether early atorvastatin treatment
will reduce left ventricle (LV) remodeling, infarct size, and improve microvascular perfusion.
Background: In animal studies, early statin therapy reduces reperfusion injury after a
percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI). Methods:
Forty‐two consecutive patients (82% male, mean age 61.2±9.8) who underwent a primary
PCI for a first ST‐elevated AMI were randomized for pretreatment with atorvastatin 80 mg (n …
Abstract
Objective: The aim of this pilot study was to determine whether early atorvastatin treatment will reduce left ventricle (LV) remodeling, infarct size, and improve microvascular perfusion. Background: In animal studies, early statin therapy reduces reperfusion injury after a percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI). Methods: Forty‐two consecutive patients (82% male, mean age 61.2 ± 9.8) who underwent a primary PCI for a first ST‐elevated AMI were randomized for pretreatment with atorvastatin 80 mg (n = 20) or placebo (n = 22) and continued with the same dosage daily for 1 week. All patients received atorvastatin 80 mg once daily 7 days after primary PCI. The LV function and infarct size were measured by magnetic resonance imaging within 1 day, at 1 week, and 3 months follow up. The primary endpoint was the end‐systolic volume index (ESVI) at 3 months. Secondary endpoints were global LV function measurements, myocardial infarct size, biochemical cardiac markers, TIMI flow, and ST‐T elevation resolution. Results: ESVI 3 months after AMI was 25.1 mL/m2 in the atorvastatin arm and 25.0 mL/m2 in the placebo arm (P = 0.74). The differences in change from baseline to 3 months follow up in global LV function and myocardial infarct size did not differ between both treatment arms. Furthermore, biochemical markers, TIMI flow, and ST‐T elevation resolution did not differ between atorvastatin and placebo arm. Conclusions: In this pilot study, pretreatment with atorvastatin in an acute myocardial infarction does not result in an improved cardiac function, microvascular perfusion, or decreased myocardial infarct size. © 2012 Wiley Periodicals Inc.
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