Relationship between plasma phospholipase A2 concentrations and lipoprotein subfractions in patients with stable coronary artery disease

Rui-Xia Xu, Yan Zhang, Xiao-Lin Li, Sha Li, Yuan-Lin Guo, Qian Dong, Geng Liu, Jian-Jun Li
Clinica Chimica Acta; International Journal of Clinical Chemistry 2015 June 15, 446: 195-200

BACKGROUND: 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.

METHODS: 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.

RESULTS: Plasma Lp-PLA2 concentrations were higher in patients with CAD compared with those without CAD (153.61 ± 78.73 vs. 131.41 ± 65.49 ng/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).

CONCLUSION: 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.

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