Relation of apolipoprotein E phenotype to myocardial infarction and mortality from coronary artery disease

June E. Eichner, Lewis H. Kuller, Trevor J. Orchard, Gregory A. Grandits, Lisa M. McCallum, Robert E. Ferrell, James D. Neaton

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238 Scopus citations


The apolipoprotein E polymorphism is a genetic determinant of low-density lipoprotein (LDL) cholesterol. Its status as a risk factor for coronary artery disease (CAD), either through a causal relation with LDL cholesterol level or independently, is less clearly established. Data from the Multiple Risk Factor Intervention Trial were used to examine the influence of apolipoprotein E phenotype on risk of coronary events. Of the 12,866 randomized participants, 619 were studied in a nested case-control design. CAD deaths (93) and nonfatal myocardial infarctions (113) were matched to 412 controls. The allele frequencies of apolipoprotein E in the white subset (ε{lunate}2 = 0.06, ε{lunate}3 = 0.79, and ε{lunate}4 = 0.15) were very similar to other nonselected white American populations, and the relation of apolipoprotein E on total and LDL cholesterol was generally similar to that seen in other studies, with the ε{lunate}2 allele being associated with lower and the ε{lunate}4 allele with higher total and LDL cholesterol. Allele frequencies were not the same for patients and control subjects. The presence of ε{lunate}4 was associated with an increased risk of CAD that was most evident for fatal cases. There was no relation between changes in LDL cholesterol over time during the trial and apolipoprotein E phenotypes.

Original languageEnglish (US)
Pages (from-to)160-165
Number of pages6
JournalThe American Journal of Cardiology
Issue number2
StatePublished - Jan 15 1993

Bibliographical note

Funding Information:
From the Graduate School of Public Health (Departments of Epidemiology and Human Genetics), University of Pittsburgh, Pittsburgh, Pennsylvania, and Division of Biostatistics, School of Public Health, University of Minnesota, Minneapolis, Minnesota. This study was supported in part by Grant HL 41785 from the National Institutes of Health, Bethesda, Maryland. Manuscript received November 6, 1991; revised manuscript received and accepted August 14, 1992.


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