Key result
Greater coronary plaque regression after intensive statin therapy is not linked to fewer CV events.
Why the study?
The clinical implications of statin-induced coronary plaque regression for long-term clinical outcomes in ACS patients had not been established.
Does greater coronary plaque regression predict reduced cardiovascular events in ACS patients treated with intensive statin therapy?
Cohort
Does greater coronary plaque regression predict reduced cardiovascular events in ACS patients treated with intensive statin therapy?
Absolute Event Rate: 1.7% vs 3.4%
p-value: p=0.4
In ACS patients on intensive statin therapy, reverse vessel remodeling and baseline HDL-C, rather than coronary plaque regression, independently predicted future cardiovascular events.
Suggests plaque regression alone may not adequately capture statin benefit in ACS; challenges traditional surrogate.
Background: The JAPAN-ACS study demonstrated that statins significantly reduced coronary plaque volume in patients with acute coronary syndrome (ACS). The clinical implications of plaque regression for clinical outcomes in ACS patients has not been established. The Extended JAPAN-ACS study was conducted to evaluate the relationship between coronary plaque regression and long-term clinical outcome, and to explore the factors associated with cardiovascular events. Methods and Results: Patients with intravascular ultrasound (IVUS) data at both enrollment and follow-up in the JAPAN-ACS study were enrolled and observed for at least 3 years. Patients were divided into lesser and greater coronary plaque regression groups. The primary endpoint was defined as a composite of the following events: cardiovascular death, nonfatal myocardial infarction, nonfatal cerebral infarction, and unstable angina. The median value of the percent change in plaque volume, 18.0%, was used as a cutoff point. There were 4 primary events (3.4%) in the lesser regression group, and 2 events (1.7%) in the greater regression group (P=0.4). Cumulative secondary cardiovascular events did not differ between the 2 groups. Multivariate analysis identified the high-density lipoprotein cholesterol (HDL-C) at baseline and the % change of the external elastic membrane volume as independent risk factors of cardiovascular events. Conclusions: Coronary plaque regression induced by an intensive statin regimen did not predict future cardiovascular events in ACS patients. Rather, the baseline HDL-C level and reverse vessel remodeling might serve as predictors for cardiovascular events. (Circ J 2012; 76: 825-832)
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Miyauchi et al. (2012) conducted a cohort in Acute coronary syndrome (ACS). Greater coronary plaque regression (≥18.0%) vs. Lesser coronary plaque regression (<18.0%) was evaluated on Composite of cardiovascular death, nonfatal myocardial infarction, nonfatal cerebral infarction, and unstable angina (p=0.4). Greater coronary plaque regression following intensive statin therapy did not significantly reduce future cardiovascular events compared to lesser regression in ACS patients (1.7% vs 3.4%, P=0.4).
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