Relationship between Plasma Lipoprotein-Associated Phospholipase A2 Concentrations and Apolipoprotein in Stable Coronary Artery Disease Patients.
Background: Increasing evidence states that the plasma lipoprotein-associated phospholipase A2 (Lp-PLA2) levels and apolipoprotein particles are regarded as the risk maker for cardiovascular heart disease. Nevertheless, the issue about whether Lp-PLA2 is associated with apolipoprotein particles in individuals who have been diagnosed as stable coronary artery disease (CAD) remains largely unexplored.
Methods: All 569 participants engaged in this research, who never took lipid-lowering drugs, had been divided into groups by the coronary angiography (CAG), namely, stable CAD: n = 291; non-CAD: n = 278. The results concerning Lp-PLA2 levels were calculated by Elisa Kit, while apolipoprotein particles were measured by the department of laboratory.
Results: The plasma concentration of Lp-PLA2 was remarkably higher in stable CAD group than the non-CAD group (136.0 ± 60.5 ng/mL vs. 113.2 ± 65.6 ng/mL, P < 0.001). Pearson correlation analyses explained the plasma Lp-PLA2 concentration was correlated with apoB (r = 0.390, P < 0.001) and apoB/apoA1 (r = 0.450, P < 0.001), not associated with apoA1 (r = -0.099, P = 0.101). Conversely, the association remains unobserved among non-CAD patients except apoA1. Moreover, multiple linear regression revealed the relations between Lp-PLA2 concentrations and apoB (β = 0.390, P < 0.001), as well as apoB/apoA1 (β = 0.450, P < 0.001), but not apoA1 (β = -0.099, P = 0.121). After adjustment for several risk factors regarding CAD, like hypertension, gender, smoking, age, and diabetes mellitus, there had still been positive associations between the Lp-PLA2 concentration and apoB (β = 0.364, P < 0.001), as well as apoB/apoA1 (β = 0.390, P < 0.001).
Conclusions: The plasma levels of Lp-PLA2 provide positively a key link with apoB, apoB/apoA-1 among stable CAD, denoting the communication between Lp-PLA2 and apolipoprotein particles in the state of CAD.