Key result
Aggressive statin administration before PCI in patients with non-ST elevation ACS significantly reduced CK elevation at 3 days compared to no statin (84 vs 180 IU/l, p=0.02).
Why the study?
Does aggressive preprocedural statin administration reduce periprocedural myocardial damage in Japanese patients with non-ST elevation ACS undergoing PCI?
RCT (n=50)
Randomized
Yes
Does aggressive preprocedural statin administration reduce periprocedural myocardial damage in Japanese patients with non-ST elevation ACS undergoing PCI?
Absolute Event Rate: 84% vs 180%
p-value: p=0.02
Aggressive statin therapy prior to PCI in patients with NSTE-ACS significantly reduces periprocedural myocardial enzyme release.
Supports pre-PCI statin loading in NSTE-ACS to limit injury; extends evidence to Japanese patients.
BACKGROUND: While preprocedural statin treatment for acute coronary syndrome (ACS) is widely regarded as beneficial, there has been no prospective randomized multicenter trial of patients with non-ST elevation ACS in the Japanese population to examine the efficacy of preprocedural aggressive statin use. The aim of this study was to confirm this effect by prospective randomized multicenter design. METHODS: Fifty patients who presented with non-ST elevation ACS were enrolled, and randomly assigned to aggressive statin administration before percutaneous coronary intervention (PCI). Troponin-T (TnT), creatine phosphokinase (CK), CK-myocardial band (CK-MB), high-sense C-reactive protein (hs-CRP), and brain natriuretic peptide (BNP) were measured at baseline and/ or after procedure. RESULTS: Three days after PCI, the statin group had significantly less CK elevation compared with the nonstatin group (84+/-17 IU/l versus 180+/-68 IU/l, respectively, p = 0.02). CK-MB elevation also tended to be lower in the statin group than in the nonstatin group (3.2+/-1.9 versus. 7.0+/-3.0, respectively, p = 0.07), as was BNP level (3.2+/-1.9 versus 7.0+/-3.0 pg/ml, respectively, p = 0.07). The change of serum LDL cholesterol was significantly correlated with CK (p = 0.01) and TnT (p = 0.02) at 1 day after PCI. CONCLUSIONS: Aggressive statin usage before PCI to Japanese patients with non-ST elevation ACS appears to reduce myocardial damage after procedure. The degree of serum lipid level reduction may reflect the vulnerability of atheromatous plaques that could cause cardiac damage after PCI.
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Hara et al. (2009) conducted an RCT in Non-ST elevation acute coronary syndrome (n=50). Aggressive statin therapy vs. No statin was evaluated on Creatine phosphokinase (CK) elevation 3 days after PCI (p=0.02). Aggressive statin administration before PCI in patients with non-ST elevation ACS significantly reduced CK elevation at 3 days compared to no statin (84 vs 180 IU/l, p=0.02).
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