We assayed three DNA polymorphisms (XbaI, MspI, and EcoRI) of the apolipoprotein (apo) B gene, the Hind polymorphism of the lipoprotein lipase (LPL) gene, and the common phenotypes of apo E in 77 survivors of myocardial infarction (64 men and 13 women) and 96 healthy control subjects (61 men and 35 women). There was no association between the frequencies of specific apo B genotypes or apo E phenotypes and the history of myocardial infarction (MI), although an association between the apo B XbaI polymorphism and serum LDL protein concentration was found in MI survivors. Homozygosity for the LPL H+ allele (HindIII site present) was associated with reduced LPL activity in postheparin plasma and elevation of serum triglyceride concentration among the control subjects; this polymorphism was not, however, associated with the history of MI. Both male and female patients had higher VLDL and LDL mass concentrations than controls. Total HDL, HDL2 cholesterol, and phospholipid concentrations as well as apo A-I levels were lower and apo B levels higher in patients than in controls. Serum Lp(a) concentrations or postheparin plasma LPL activities among controls and patients were not significantly different. Our data illustrate the complex relation between lipoproteins, lipases, and coronary heart disease (CHD) and demonstrate that allelic variation of apo B and LPL may influence lipoprotein metabolism without necessarily affecting the risk of myocardial infarction.