Lipoprotein-associated phospholipase A2 in coronary heart disease: Review and meta-analysis

Dongze Li1, Lizhi Zhao2, Jing Yu3

  • 1Department of Emergency Medicine, West China Hospital, Sichuan University, Chengdu, China.

Insights

Higher lipoprotein-associated phospholipase A2 (Lp-PLA2) levels are linked to increased cardiovascular events in coronary heart disease (CHD) patients. This association is particularly noted in stable CHD patients not on Lp-PLA2 inhibiting therapies.

Area of Science:

  • Cardiovascular Medicine
  • Biomarkers
  • Clinical Research

Background:

  • The prognostic significance of lipoprotein-associated phospholipase A2 (Lp-PLA2) in coronary heart disease (CHD) requires further clarification.
  • Existing research presents conflicting associations between Lp-PLA2 levels and adverse outcomes in CHD patients.

Purpose of the Study:

  • To conduct a meta-analysis investigating the association between Lp-PLA2 activity or mass and the prognosis of CHD.
  • To clarify the risk associations between Lp-PLA2 and adverse outcomes in patients with established coronary heart disease.

Main Methods:

  • A systematic literature search of PubMed and Embase was performed for prospective studies published before June 2016.
  • Multivariate-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for adverse outcomes related to Lp-PLA2 were extracted and pooled using random-effect modeling.

Main Results:

  • Fifteen studies comprising 30,857 participants were included in the meta-analysis.
  • Elevated Lp-PLA2 activity or mass was not significantly associated with increased long-term all-cause mortality.
  • Higher Lp-PLA2 activity or mass showed an independent association with an increased risk of long-term cardiovascular events (pooled HRs 1.55 and 1.62).

Conclusions:

  • Increased Lp-PLA2 activity or mass is independently associated with cardiovascular events in patients with CHD.
  • The predictive value of Lp-PLA2 for cardiovascular events is most evident in stable CHD patients not undergoing Lp-PLA2 inhibiting therapies.
Abstract

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