POSTPRANDIAL PLASMA-LIPOPROTEIN CHANGES IN RELATION TO APOLIPOPROTEIN-E PHENOTYPES AND LOW-DENSITY-LIPOPROTEIN SIZE IN MEN WITH AND WITHOUTCORONARY-ARTERY DISEASE

Postprandial lipoprotein metabolism may play a role in the etiology of premature coronary artery disease (CAD). To determine whether apolipo protein E (apo E) polymorphism and the size of low density lipoprotein (LDL) influence postprandial lipemia we studied 39 healthy men and 35 men with CAD. Venous blood samples were obtained before an oral fat l oad and 3, 5 and 7 h thereafter. Total cholesterol and high density li poprotein (HDL) cholesterol concentrations did not change in either gr oup during the fat load, but triglycerides increased more markedly in CAD patients compared with controls independently of apo E phenotypes. There was a positive correlation between the size of LDL and the conc entration of HDL cholesterol (r = 0.541, P < 0.001); conversely, an in verse correlation was observed between LDL size and the level of fasti ng triglycerides (r = -0.582; P < 0.001). The patients with CAD had si gnificantly smaller LDL particles (25.89 +/- 0.56 nm) than in controls (26.21 +/- 0.63 nm) (P < 0.05). The increase in triglyceride levels d uring the fat load was highest in CAD patients with a small size of LD L particles (<25.5 nm) and lowest in controls with large LDL (>25.5 nm ). Our results suggest that the magnitude of the triglyceride response is a better indicator of CAD risk than the fasting triglyceride conce ntration. The best model in our logistic regression analysis selected as significant risk factors the change of triglyceride concentration f rom the baseline at 5 h after a fat meal and HDL cholesterol. This mod el classified 83% of the subjects correctly.