GENETIC-POLYMORPHISM OF APOLIPOPROTEIN-B, APOLIPOPROTEIN-E, AND LIPOPROTEIN-LIPASE, AND SERUM-LIPOPROTEIN LEVELS IN SURVIVORS OF MYOCARDIAL-INFARCTION

We assayed three DNA polymorphisms (XbaI, MspI, and EcoRI) of the apol ipoprotein (apo) B gene, the Hind polymorphism of the lipoprotein lipa se (LPL) gene, and the common phenotypes of apo E in 77 survivors of m yocardial infarction (64 men and 13 women) and 96 healthy control subj ects (61 men and 35 women). There was no association between the frequ encies of specific apo B genotypes or apo E phenotypes and the history of myocardial infarction (MI), although an association between the ap o B XbaI polymorphism and serum LDL protein concentration was found in MI survivors. Homozygosity for the LPL H+ allele (HindIII site presen t) was associated with reduced LPL activity in postheparin plasma and elevation of serum triglyceride concentration among the control subjec ts; this polymorphism was not, however, associated with the history of MI. Both male and female patients had higher VLDL and LDL mass concen trations than controls. Total HDL, HDL2 cholesterol, and phospholipid concentrations as well as apo A-I levels were lower and apo B levels h igher in patients than in controls. Serum Lp(a) concentrations or post heparin plasma LPL activities among controls and patients were not sig nificantly different. Our data illustrate the complex relation between lipoproteins, lipases, and coronary heart disease (CHD) and demonstra te that allelic variation of apo B and LPL may influence lipoprotein m etabolism without necessarily affecting the risk of myocardial infarct ion.