Key result
Previous statin therapy prior to primary PCI for STEMI was associated with a significantly lower rate of MACE at 1 month compared to no previous statin therapy (4.4% vs. 13.9%, p=0.014).
Why the study?
Does previous statin therapy reduce MACE in patients with STEMI undergoing primary PCI?
Cohort (n=350)
Does previous statin therapy reduce MACE in patients with STEMI undergoing primary PCI?
Absolute Event Rate: 4.4% vs 13.9%
p-value: p=0.014
Previous statin therapy is associated with enhanced coronary flow, reduced infarct size, and improved short-term clinical outcomes in STEMI patients undergoing primary PCI.
Hypothesis-generating for pre-PCI statin benefit in STEMI; leaves open need for randomized confirmation before practice change.
Background: Statin treatment has been shown to reduce the risk of coronary artery disease and improve the outcome of patients with acute myocardial infarction. However, the effects of previous statin treatment on the clinical course of subsequent acute myocardial infarction remain unclear. This study was designed to investigate whether previous statin therapy influences the clinical outcome of patients with ST-Segment Elevation Myocardial Infarction (STEMI) treated with primary Percutaneous Coronary Intervention (PCI). Methods: We evaluated the clinical outcome of 350 patients with STEMI undergoing primary PCI, of which 91 received previous statin treatment (statin group) and 259 did not (non-statin group). Myocardial perfusion, infarct size, inflammatory responses, and Major Adverse Cardiovascular Events (MACE) were evaluated. Results: The frequency of MACE at 1 month after PCI was significantly lower in the statin group than the nonstatin group (4.4% vs. 13.9%, p=0.014). Post-PCI peak creatine kinase was significantly lower in the statin group median, (interquartile range): (1246 [504-3301] vs. 2235 [952-4083] IU/ml; p=0.002), whereas peak high-sensitivity C-reactive protein did not significantly differ between the two groups (p=0.287). The frequency of ST-segment resolution after PCI was significantly higher in the statin group (90.1% vs. 76.8%; p=0.006), as was the frequency of Thrombolysis in Myocardial Infarction grade 3 coronary flow (p=0.008). Myocardial blush grade was similar in both groups (p=0.839). Multivariate logistic regression analysis revealed previous statin treatment, hs-CRP, blood glucose, and age to be independent predictors of MACE. Conclusion: Previous statin therapy enhances coronary flow, reduces infarct size, and improves clinical outcome of STEMI patients treated with primary PCI.
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Murakawa et al. (2016) conducted a cohort in ST-Segment Elevation Myocardial Infarction (STEMI) (n=350). Previous statin treatment vs. No previous statin treatment was evaluated on Major Adverse Cardiovascular Events (MACE) at 1 month after PCI (p=0.014). Previous statin therapy prior to primary PCI for STEMI was associated with a significantly lower rate of MACE at 1 month compared to no previous statin therapy (4.4% vs. 13.9%, p=0.014).
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