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Chronic inhibition of lipoprotein-associated phospholipase A2 does not improve coronary endothelial function: A

Megha Prasad1, Ryan Lennon2, Gregory W Barsness1

  • 1Mayo Clinic, Department of Cardiovascular Diseases, Rochester, MN, United States.

International Journal of Cardiology
|January 8, 2018
PubMed

Insights

Darapladib, an inhibitor of Lipoprotein-associated phospholipase A2 (Lp-PLA2), did not improve coronary endothelial dysfunction in patients. Despite reducing Lp-PLA2 activity, the drug showed no significant effect on vascular function, suggesting Lp-PLA2 may not be a primary target in humans.

Area of Science:

  • Cardiovascular Research
  • Pharmacology
  • Biomarker Discovery

Background:

  • Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a biomarker linked to vascular inflammation and cardiovascular events.
  • Coronary endothelial dysfunction (CED) is a critical factor in cardiovascular disease progression.

Purpose of the Study:

  • To investigate the efficacy of darapladib, an Lp-PLA2 inhibitor, in improving CED.
  • To assess the impact of Lp-PLA2 inhibition on endothelial function in patients with CED.

Main Methods:

  • A double-blinded, randomized placebo-controlled trial involving 54 patients with CED.
  • Patients received either oral darapladib (160mg daily) or a placebo for 6 months.
  • Coronary angiography and endothelial function tests (vasoreactivity to acetylcholine) were performed at baseline and follow-up.

Main Results:

  • Darapladib significantly reduced Lp-PLA2 activity compared to placebo (p<0.001).
  • No significant improvement was observed in coronary artery diameter response to acetylcholine in the darapladib group versus placebo (p=0.87).
  • Coronary blood flow response to acetylcholine also showed no significant difference between groups (p=0.41).

Conclusions:

  • Inhibition of Lp-PLA2 with darapladib did not improve coronary endothelial function in patients with CED.
  • These findings suggest that endogenous Lp-PLA2 may not play a pivotal role in human coronary endothelial function.
  • Further research is needed to fully elucidate the role of Lp-PLA2 in cardiovascular pathophysiology.
Abstract

Keywords:
Endothelial functionInflammationLipoprotein-associated phospholipase A2

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