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Apolipoprotein E polymorphism and coronary artery disease.
Author(s) -
H J Menzel,
R.G. Kladetzky,
Gerd Assmann
Publication year - 1983
Publication title -
arteriosclerosis an official journal of the american heart association inc
Language(s) - English
Resource type - Journals
eISSN - 2330-9180
pISSN - 0276-5047
DOI - 10.1161/01.atv.3.4.310
Subject(s) - medicine , apolipoprotein b , apolipoprotein e , coronary artery disease , coronary atherosclerosis , cardiology , phenotype , lipoprotein , loss of heterozygosity , cholesterol , coronary angiography , heterozygote advantage , high density lipoprotein , artery , endocrinology , gastroenterology , allele , disease , biology , genetics , myocardial infarction , gene
Lipid status and apolipoprotein E phenotypes were tested in 1000 patients who underwent coronary angiography. The same number of factory employees was chosen as a control group. We distinguished between six different apolipoprotein E phenotypes and determined their frequencies in all groups. For the three homozygous phenotypes E3/3, E4/4, and E2/2, the percentage distribution in the group of factory employees was 62.7%, 2.3%, and 0.8%, respectively; for the three heterozygous phenotypes E4/3, E3/2, and E4/2, we determined frequencies of 20.3%, 11.0%, and 3.0%, respectively. In the group of patients with and without signs of coronary atherosclerosis, we observed almost the same frequencies except that heterozygotes (E3/2) occurred significantly more frequently in the group of coronary angiography patients unaffected by coronary sclerosis. Cholesterol and triglyceride values were significantly elevated in patients with coronary artery disease, whereas high density lipoprotein cholesterol levels were not significantly different. The data further suggest that apolipoprotein E2/2 homozygosity, despite the presence of beta-very low density lipoproteins in the plasma of these patients, cannot be considered a biochemical indicator of an increased risk of coronary atherosclerosis. On the other hand, apolipoprotein E3/2 heterozygosity may have a protective effect on the development of early atherosclerosis.

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