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Updated: Aug 15, 2026

High-Density Lipoprotein-Specific Phospholipid Efflux Assay
Published on: September 30, 2025
Lipoprotein-associated phospholipase A2 is an independent marker for coronary endothelial dysfunction in humans
Eric H Yang1, Joseph P McConnell, Ryan J Lennon
1Division of Cardiovascular Diseases, Mayo College of Medicine, Rochester, MN 55905, USA.
Insights
Lipoprotein-associated phospholipase A2 (Lp-PLA2) is linked to coronary endothelial dysfunction. Higher Lp-PLA2 levels predict endothelial dysfunction in humans, indicating its role in cardiovascular health.
Area of Science:
- Cardiovascular Research
- Biomarkers
- Endothelial Function
Background:
- Coronary endothelial dysfunction is a key factor in cardiovascular disease.
- Identifying reliable predictors of endothelial dysfunction is crucial for risk stratification.
Purpose of the Study:
- To investigate the association between lipoprotein-associated phospholipase A2 (Lp-PLA2) and coronary endothelial dysfunction.
- To determine if Lp-PLA2 predicts endothelial dysfunction in humans.
Main Methods:
- 172 patients without significant coronary artery disease were assessed for endothelial function.
- Endothelial function was evaluated using coronary blood flow and diameter changes in response to acetylcholine.
- Plasma Lp-PLA2 concentrations were measured and analyzed across tertiles.
Main Results:
- Patients in higher Lp-PLA2 tertiles showed reduced coronary blood flow and increased vasoconstriction.
- Significantly higher serum Lp-PLA2 concentrations were found in patients with coronary endothelial dysfunction.
- The odds ratio for endothelial dysfunction was 3.3 in the highest Lp-PLA2 tertile.
Conclusions:
- Lipoprotein-associated phospholipase A2 (Lp-PLA2) is independently associated with coronary artery endothelial dysfunction.
- Lp-PLA2 serves as a strong predictor of endothelial dysfunction in the human population.
Objective:
The purpose of the current study was to determine whether lipoprotein-associated phospholipase A2 (Lp-PLA2) is associated with coronary endothelial dysfunction and is a predictor of endothelial dysfunction in humans.
Methods And Results:
Patients (172) with no significant coronary artery disease (<30% stenosis) undergoing assessment of coronary endothelial function were studied. Endothelial function was assessed by the change in coronary blood flow and coronary artery diameter in response to intracoronary acetylcholine. Plasma concentrations of Lp-PLA2 were measured, and patients were divided into tertiles. Patients in tertiles 2 and 3 had a significantly lower change in coronary blood flow (63.8+/-73.2 and 32.0+/-71.7 versus 78.4+/-73.2%; P<0.001) and greater epicardial coronary artery vasoconstriction (-14.1+/-14.7 and -23.3+/-25.1 versus -9.5+/-15.2% mean diameter change; P<0.001) in response to acetylcholine. Patients with coronary endothelial dysfunction had significantly higher serum concentrations of Lp-PLA2 than those with normal endothelial function (246.2+/-71.6 versus 209+/-56.7 ng/mL; P=0.001). The odds ratio for coronary endothelial dysfunction in patients with Lp-PLA2 in the highest tertile was 3.3 (95% CI, 1.6 to 6.6).
Conclusions:
Lp-PLA2 is independently associated with coronary artery endothelial dysfunction and is a strong predictor of endothelial dysfunction in humans.
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