Article

[Influence of Intensive Hypolipidemic Therapy on Blood Concentration of Lipoprotein-Associated Phospholipase A2 in Patients With Ischemic Heart Disease.]

Institute of Clinical Cardiology of Russian Cardiology Scientific and Production Center, ul. Tretiya Cherepkovskaya 15a, 121552 Moscow, Russia.
Kardiologiia (Impact Factor: 0.12). 09/2013; 53(9):4-11.
Source: PubMed

ABSTRACT

Aim:
To assess the impact of combined treatment with simvastatin and ezetimibe or treatment with simvastatin only on lipoprotein-associated phospholipase A2 in patients with ischemic heart disease.

Methods:
One hundred patients with angiographically documented coronary atherosclerosis took part in the investigation. Lp-PLA2 mass and cholesterol fractions were determined at baseline and after 6 months of treatment. Lp-PLA2 mass was determined by enzyme immunoassay method, using two highly specific monoclonal antibodies.

Results:
Combined treatment with ezetimibe and simvastatin led to significantly greater declines in Lp-PLA2 and cholesterol fractions compared with treatment only with simvastatin: Lp-PLA2 decreased by 46 vs 38%, total cholesterol by 35 vs 28%, LDL cholesterol by 50 vs 40%, respectively (p<0.05). Combination therapy with ezetimibe and simvastatin 20 and 40mg/day proved to be as effective as monotherapy with simvastatin 80 mg/day on the effect on Lp-PLA2 mass and cholesterol fractions (p<0.05). Lp-PLA2 correlated positively with total cholesterol (r=0.28) and LDL-C (r=0.33).

Conclusions:
Combined treatment led to greater reduction of total cholesterol and LDL-C, as well as significantly reduced level of Lp-PLA2 mass. The latter can be considered as target for suppression of inflammation and achievement of stabilization of atherosclerotic plaque.

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    ABSTRACT: Both increased lipoprotein-associated phospholipase A2 (Lp-PLA2) concentrations and atherogenic lipoprotein subfractions have been shown to reflect unfavourable cardiovascular risk. However, the correlation between Lp-PLA2 and lipoprotein subfractions in patients with coronary artery disease (CAD) has not been assessed yet. A total of 324 consecutive subjects who were not treated with lipid-lowering drugs were enrolled (angiographically proven CAD: n=253; non-CAD: n=71). Plasma Lp-PLA2 concentrations were measured using ELISA. The low-density lipoprotein (LDL) and high-density lipoprotein (HDL) subfractions were determined by Lipoprint System. Plasma Lp-PLA2 concentrations were higher in patients with CAD compared with those without CAD (153.61±78.73 vs. 131.41±65.49ng/ml, p=0.028). The univariable correlation analysis revealed that Lp-PLA2 concentrations were positively correlated with the cholesterol concentrations of each LDL subfractions and the intermediate as well as small HDL subfractions, while negatively linked with the LDL particle size and large HDL-cholesterol (HDL-C) concentrations in CAD group. However, no similar results were observed in the non-CAD group. Furthermore, multivariable regression analysis was performed in patients with CAD and showed that plasma Lp-PLA2 concentrations were independently correlated with the cholesterol concentrations of each LDL subfractions [large LDL-cholesterol (LDL-C): β=0.263, p<0.001; intermediate LDL-C: β=0.327, p<0.001; small LDL-C: β=0.135, p=0.033] and small HDL-C (β=0.133, p=0.034). Lp-PLA2 concentrations were positively associated with all LDL subfractions and small HDL subfraction, suggesting an interaction between Lp-PLA2 and lipoprotein subfraction phenotypes in the status of CAD. Copyright © 2015. Published by Elsevier B.V.
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