Abstract 1194: Lp-PLA2 is Weakly to Modestly Correlated with Insulin, Visceral Fat, and Lipids and Lipoproteins, but is Uncorrelated with C-Reactive Protein (hsCRP) and Blood Pressure: The HERITAGE Family Study
Introduction: Lipoprotein-associated phospholipase A2 (Lp-PLA2) has been proposed as a novel, independent risk factor for CAD, with higher values increasing risk. While limited data suggest a small, but significant relationship between Lp-PLA2 and lipids and lipoproteins, there are few data available to establish the relationship between Lp-PLA2 and other recognized risk factors for CAD.
Hypothesis: It was hypothesized that Lp-PLA2 would have significant, but low correlations with other risk factors for CAD and that these results would be independent of age, sex and race.
Methods: Subjects were 753 participants in the biracial and two generational (fathers, mothers, sons, daughters) HERITAGE Family Study. Plasma samples were drawn in a fasted state in the morning and analyzed for Lp-PLA2, hsCRP and plasma lipids and lipoprotein. Fasting insulin and glucose were assayed. An IVGTT was used to determine insulin sensitivity index (Si), disposition index (Di), and the acute insulin response to glucose (AIRglucose). Fat mass, fat-free mass and visceral fat were assessed by hydrostatic weighing and CT scan, and resting blood pressure by a Colin-STBP-780 automated blood pressure monitor. VO2max was determined twice on a cycle ergometer. Relationships were determined by using Pearson partial correlations, controlling for age, sex and race.
Results: At baseline, Lp-PLA2 was significantly related to: total cholesterol (r=0.303d), LDL-C (r=0.299d), VLDL-C (r=0.179d), HDL-C (r= -0.105b), HDL2-C (r= -0.084a), HDL3-C (r= -0.088a), Apo-B (r=0.275d), triglycerides (r=0.152d), insulin (r=0.132c), Si (r= -0.110b), visceral fat (r=0.138c), % fat (r=0.113b), fat-free mass (r=0.100b), BMI (r=0.125c), waist circumference (r=0.144c), waist/hip ratio (r=0.107b), and VO2max (r= -0.133c), but unrelated to hsCRP and blood pressure. These results were relatively consistent across age, sex and race.
Conclusions: Lp-PLA2 is weakly to modestly correlated with many of the established CAD risk factors, but uncorrelated with the others, including hsCRP. These trends appear to hold across age, sex, and race. These results suggest the independence of Lp-PLA2 as a risk factor for CAD. Note: a = p < 0.05; b = p < 0.01; c = p < 0.001; d = p < 0.0001