Lipoprotein-associated phospholipase A2 activity is a marker of small, dense LDL particles in human plasma

Background: Recent, clinical studies showed that lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) is a predictor for incident atherosclerotic disease. We have previously shown that among the LDL subfractions, Lp-PLA(2) activity is preferentially associated with the atherogenic small, dense (sdLDL) particles in vitro. We investigated whether Lp-PLA(2) could be a marker of sdLDL in human plasma. Methods: One hundred and seventy-six individuals participated in the study. LDL subclass analysis was performed by polyacrylamide gel electrophoresis. LpPLA(2) activity and mass were determined in total plasma and in apolipoprotein B-depleted plasma (HDL-LpPLA(2)). Non-HDL-Lp-PLA(2) activity and mass were calculated by subtracting the HDL-Lp-PLA(2) from total plasma Lp-PLA(2). Results: On the basis of the LDL subclass analysis, participants were categorized into phenotype A and non-A (total cholesterol mass of the sdLDL subfractions <= 0.155 and >0.155 mmol/L, respectively). Unlike total plasma Lp-PLA(2) mass, total plasma Lp-PLA(2) activity and non-HDL-Lp-PLA(2) activity and mass were significantly higher in persons with phenotype non-A compared with persons with phenotype A, whereas HDLLp-PLA, activity and mass were lower in persons with phenotype non-A compared with phenotype A. Total plasma activity and non-HDL-Lp-PLA(2) activity and mass, but not Lp-PLA(2) mass, were correlated with sdLDL-cholesterol mass, proportion, and mean LDL particle size. In multiple regression analysis, total plasma and non-HDL-Lp-PLA(2) activities were the second best predictors of the presence of sdLDL particles in human plasma after serum triglyceride concentrations. At serum triglyceride concentrations >1.356 mmol/L, total plasma and non-HDL-Lp-PLA(2) activity added significantly to the prediction of the presence of sdLDL in plasma. Conclusions: Lp-PLA2 activity, but not the enzyme mass, is a marker of sdLDL in human plasma. (c) 2005 American Association for Clinical Chemistry.