Lipoprotein-associated phospholipase A2 levels, endothelial dysfunction and arterial stiffness in patients with stable coronary artery disease

Abstract

Background Lipoprotein-associated Phospholipase A2 (Lp-PLA2), can exert proinflammatory as well as proatherogenic properties on the vascular wall. The current study sought to evaluate the influence of high Lp-PLA2 levels on indices of arterial wall properties in patients with stable coronary artery disease (CAD). Methods Three hundred seventy-four consecutive patients with stable CAD (mean age 61 ± 11 years, 89% males) were enrolled in this single-center cross-sectional study. Flow-mediated dilation (FMD) was used to assess endothelial function and augmentation index (AIx) of the central aortic pressure was used to assess reflected waves. ELISA was used to determine Lp-PLA2 serum levels. Results After dividing the participants in 3 equal groups based on the tertiles of circulating Lp-PLA2 values, no significant differences were demonstrated between those in the 3rd tertile with Lp-PLA2 values > 138 μg/L, in the 2nd tertile with Lp-PLA2 values between 101 and 138 μg/L and in the 1st tertile (Lp-PLA2 values < 101 μg/L) regarding age, male gender, smoking habits, family history of CAD or history of a previous myocardial infarction, diabetes mellitus, arterial hypertension, hyperlipidemia, duration of CAD and treatment with relevant medication. Importantly, subjects with Lp-PLA2 values in the highest tertile, had significantly reduced FMD values compared to the middle and lower tertile (4.43 ± 2.37% vs. 4.61 ± 1.97% vs. 5.20 ± 2.52% respectively, P = 0.03). Patients in the highest tertile of Lp-PLA2 values had significantly higher AIx values (24.65 ± 8.69% vs. 23.33 ± 9.65%, P = 0.03), in comparison to the lowest tertile, with Lp-PLA2 values < 101 μg/L. A linear regression analysis showed that Lp-PLA2 values > 138 μg/L negatively correlated to FMD [b = − 0.45 (95% CI: − 0.79 – -0.11), P = 0.01] and AIx values [b = 1.81 (95% CI: 0.57–3.05), P < 0.001] independently of cofounders like gender, age, diabetes mellitus, arterial hypertension, dyslipidemia, smoking habits, family history of CAD, history of previous myocardial infarction, serum glucose, circulating lipid levels, duration of CAD, antihypertensive medication, antidiabetic drugs, statin therapy and treatment with β-blockers. Conclusions Elevated Lp-PLA2 levels relate to endothelial dysfunction and arterial stiffness in patients with stable CAD independently from classical risk factors for CAD, statin use, antihypertensive treatment, and duration of the disease.

Ameliorating impact of coenzyme Q10 on the profile of adipokines, cardiomyopathy, and hematological markers correlated with the glucotoxicity sequelae in diabetic rats

“…Circulating LPPLA2 is considered an indicator of inflammation and is associated with vascular dysfunction [ 126 ]. Among patients with stable CAD, a high level of LPPLA2 is associated with endothelial dysfunction and arterial stiffness as an independent risk factor [ 127 ]. In the CoQ10 treated group, the level of LPPLA2 in serum was significantly lower than in the diabetic group using the Rat LPPLA2 ELISA kit.…”

Cardiometabolic biomarker patterns associated with cardiac MRI defined fibrosis and microvascular dysfunction in patients with heart failure with preserved ejection fraction

“…PLA acetylhydrolase-7 is a member of the lipase family and is responsible for deactivating PLA, an important proinflammatory signaling molecule ( 31 ). Studies investigating the association between plasma levels of PLA acetylhydrolases and cardiovascular disease have found that higher levels of PLA acetylhydrolase-7 lead to an increased risk of cardiovascular disease ( 32 ).…”

Lipid-Derived Biomarkers as Therapeutic Targets for Chronic Coronary Syndrome and Ischemic Stroke: An Updated Narrative Review

“…In plasma, LP-PLA2 circulates mainly bound to LDL and is less associated with HDL, which are the other two essential biomarkers for monitoring cardiac and cerebrovascular disorders. Moreover, the dynamics of LP-PLA2 between LDL and HDL have clinical significance, with variations in these two fractions observed in patients with hyperlipidemia and coronary artery diseases [51]. As LP-PLA2 bound to HDL has antiatherogenic properties, while LDL-bound-LP-PLA2 has the opposite effect, the LP-PLA2 molecule has increasingly relevant roles from both pathophysiological and therapeutical points of view.…”