LIPOPROTEIN(A) IS INCREASED IN TRIGLYCERIDE-RICH LIPOPROTEINS IN MEN WITH CORONARY HEART-DISEASE, BUT DOES NOT CHANGE ACUTELY FOLLOWING ORAL FAT INGESTION

Association of apo(a)/Lp(a) with triglyceride-rich lipoproteins (TGR-L ps) is determined by different factors that are poorly understood. Som e previous studies suggested that apo(a) in TGR-Lps may affect the ath erogenicity of the TGR particles. To study whether there are any pecul iarities in postprandial (pp) Lp(a) metabolism, we have determined apo (a) phenotypes and Lp(a) concentrations in 46 subjects with coronary h eart disease (CHD) and in six normolipidemic individuals at different lime points (4, 6 and 8 h) following an oral fat tolerance test. While mean triglyceride concentration reached its maximum 6 h after a stand ardized fat meal, no change in total cholesterol and in mean Lp(a) pla sma concentration was detected at any time point after the fat load. I n 6 normolipidemic probands and in 8 patients with CHD, who were match ed for apo(a) phenotype, lipoprotein levels, age and body weight, we f ollowed the distribution of apo(a) in plasma density gradient fraction s in the fasting and pp state. In the CHD patients a significant large r percentage of apo(a) reactivity was detected in TGR-Lps in the pre- as well as in the postprandial state, compared to control subjects. Th e fat intake did not induce a significant change of apo(a) reactivity in the TGR-Lp fractions in both groups. The apo(a) isoform-size and th e Lp(a) plasma concentration in the fasting state had no influence on the individual variation of the Lp(a) concentration in pp TGR-Lp fract ions. Our results provide evidence that TGR-Lp fractions of CHD patien ts are enriched in apo(a) reactivity compared to healthy controls, but do not support the hypothesis that Lp(a) acts atherogenically through a pp increase of its plasma concentration.