Epidemiology of Atherosclerosis

BACKGROUND:

Coronary artery disease appears to be a consequence of the interaction between an individual's genotype and exposure to environmental factors. Genetic information has the potential to contribute to the identification of families and individuals with a biological predisposition for developing coronary artery disease. Although numerous studies have suggested the possibility of a link between polymorphic genetic variation and coronary heart disease, it has not been possible to use any single genetic locus or combination of loci to establish a person's risk except for the case of familial hypercholesterolemia.

Apolipoproteins play a critical role in regulating cellular uptake of lipoproteins by specific receptors, regulating the activities of lipoprotein lipase and lecithin-cholesterol acyl transferase, and in the indirect regulation of the intracellular enzymes, acyl-cholesterol acyl transferase and HMG Co-A reductase. This study provided insight into the role of environmental and genetic effects on phenotypic variation of the individual components of the molecules of lipid metabolism as well as on the relationships between components.

Previous studies conducted under this grant include: the relationship between quantitative levels of apo A-I and coronary artery disease as defined by coronary angiography; the effects of exercise, alcohol, obesity, and pregnancy on apo A-I levels; the relationship between apo A-I and HDL levels in children and the mode of inheritance of apo A-I levels in pedigrees in the Rochester, Minnesota community; and characterization of the antigenic structure of apolipoproteins in coronary artery disease.

DESIGN NARRATIVE: