|Wilson Peter W F, - FRAMINGHAM HEART STUDY|
|Myers Richard H, - BOSTON UNIVERSITY|
|Larson Michael G, - FRAMINGHAM HEART STUDY|
|Ordovas Jose M, - TUFTS-HNRCA|
|Wolf Philip A, - BOSTON UNIVERSITY|
|Schaefer Ernst J, - TUFTS-HNRCA|
Submitted to: Journal of the American Medical Association
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: December 7, 1994
Publication Date: N/A
Interpretive Summary: Lipoproteins are particles that carry cholesterol and fats in the bloodstream. Apolipoprotein E is a protein component of lipo- proteins. Three different kinds of apolipoprotein E are found in the general population: Apo E-2, apoE-3 and apoE-4. We have studied the effects of these different apoE's on abnormalities of circulating blood lipid levels and risk of coronary heart disease. Our results indicate that these common genetic variants are responsible for a significant proportion of abnormal levels of lipids in the population and are important markers for coronary heart disease risk.
Technical Abstract: Objective: To describe the association between apolipoprotein E al- leles (e2, e3, and e4), dyslipidemias, and coronary heart disease (CHD). Design: Cross-sectional prevalence study. Setting and Participants: Community-based sample of men (n=1034) and women (n=916) aged 40 to 77 yrs participating in a long-term study of cardiovascular disease. Subjects underwent fasting lipid measurements, coronary risk factor determinations, and a comprehensive evaluation for the presence of current or previous CHD. Results: Compared with the e3 allele, the e4 allele was associated with elevated low-density (>4.14 mmol/L) in women, the e2 and e4 alleles were associated with moderately elevated triglyceride values (>2.82 mmol/L) in men, and the e2 allele was associated with severely elevated triglyceride values (>5.64 mmol/L) in men. The apolipoprotein E alleles were not as- sociated with hypertension, obesity, smoking, or diabetes, but the e4 allele frequency was reduced in women after age 60. The age-adjusted prevalence of CHD was associated with the e4 allele in both men (relative odds=1.53, P=0.04) and women (relative odds=1.99, P=0.05). In analyses for women and for both sexes combined, this relation persisted after adjustment by hypertension, smoking, diabetes, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol. Conclusions: Apolipoprotein E alleles are important genetic markers for dyslipidemia and CHD. The estimated CHD odds associated with the e4 allele appear to be greater than those for any genetic lipid abnormality. The association of the e4 allele with CHD remains significant in women and both sexes combined after adjustment by coronary risk factors and lipids.