Key result
Extended-release niacin decreased Lp-PLA2 by 8.9%, but elevated Lp-PLA2 was not independently associated with cardiovascular events after multivariable adjustment.
Why the study?
To assess the effect of extended-release niacin on Lp-PLA2 activity and clinical outcomes in patients with established cardiovascular disease and low baseline HDL-C.
Does extended-release niacin reduce the composite of CV death, MI, stroke, hospitalization for unstable angina, and symptom-driven revascularization in statin-treated patients with established CV disease and low HDL-C?
RCT (n=3,196)
randomized
Does extended-release niacin reduce the composite of CV death, MI, stroke, hospitalization for unstable angina, and symptom-driven revascularization in statin-treated patients with established CV disease and low HDL-C?
In statin-treated patients with established CV disease, extended-release niacin reduces Lp-PLA2 levels, but Lp-PLA2 does not independently predict cardiovascular risk beyond traditional risk factors.
Background: Lipoprotein-associated phospholipase A 2 (LpPLA 2 ) is an inflammatory marker that has been associated with the presence of vulnerable plaque and increased risk of cardiovascular (CV) events. Objective: To assess the effect of extended-release niacin (ERN) on Lp-PLA 2 activity and clinical outcomes. Methods: We performed a post hoc analysis in 3196 AIM-HIGH patients with established CV disease and low baseline levels of high-density lipoprotein cholesterol (HDL-C) who were randomized to ERN versus placebo on a background of simvastatin therapy (with or without ezetimibe) to assess the association between baseline Lp-PLA 2 activity and the rate of the composite primary end point (CV death, myocardial infarction, stroke, hospitalization for unstable angina, and symptom-driven revascularization). Results: Participants randomized to ERN, but not those randomized to placebo, experienced a significant 8.9% decrease in LpPLA 2 . In univariate analysis, the highest quartile of LpPLA 2 activity (>208 nmol/min/mL, Q4) was associated with higher event rates compared to the lower quartiles in the placebo group (log rank P = .032), but not in the ERN treated participants (log rank P = .718). However, in multivariate analysis, adjusting for sex, diabetes, baseline LDL-C, HDL-C, and triglycerides, there was no significant difference in outcomes between the highest Lp-PLA2 activity quartile versus the lower quartiles in both the placebo and the ERN groups. Conclusion: Among participants with stable CV disease on optimal medical therapy, elevated Lp-PLA 2 was associated with higher CV events; however, addition of ERN mitigates this effect. This association in the placebo group was attenuated after multivariable adjustment, which suggests that Lp-PLA 2 does not improve risk assessment beyond traditional risk factors.
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Lyubarova et al. (2019) conducted an RCT in Established cardiovascular disease and low HDL-C (n=3,196). Extended-release niacin vs. Placebo was evaluated on Composite of CV death, myocardial infarction, stroke, hospitalization for unstable angina, and symptom-driven revascularization. Extended-release niacin decreased Lp-PLA2 by 8.9%, but elevated Lp-PLA2 was not independently associated with cardiovascular events after multivariable adjustment.
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