title: Relationship of the apolipoprotein E polymorphism with carotid artery atherosclerosis.
abstract: From the cohort taking part in the Atherosclerosis Risk in Communities (ARIC) study, a multicenter investigation of atherosclerosis and its sequelae in women and men ages 45-64 years, a sample of 145 subjects with significant carotid artery atherosclerosis but without clinically recognized coronary heart disease was identified along with 224 group-matched control subjects. The aim of this paper is to measure the association of the apolipoprotein (apo) E polymorphism with the prevalence of significant carotid artery atherosclerotic disease (CAAD) after considering the contribution of established risk factor variables. The first model used a stepwise selection procedure to define a group of significant physical and lifestyle characteristics and a group of significant plasma lipid, lipoprotein, and apolipoprotein variables that were predictive of CAAD status in this sample. Those variables selected included age (years), body mass index (BMI; kg/m2), consumption of cigarettes (CigYears; number of cigarettes/d x the number of smoking years), hypertension status, high-density lipoprotein (HDL)-cholesterol (mg/dl), total cholesterol (mg/dl), and Lp[a] (micrograms/ml). The second model was built by forcing into the equation an a priori set of demographic, anthropometric, and lipoprotein variables, which were age, BMI, CigYears, hypertensive status, LDL-cholesterol, and HDL-cholesterol. In both models, the apo E genotype epsilon 2/3 was related to CAAD status. For both models, the estimated odds ratio of being a CAAD case associated with the apo E genotype epsilon 2/3 was > 2:1. The mechanism of the observed association between the epsilon 2/3 genotype and carotid atherosclerosis is unknown, but it is likely due to the known effects of the E2 isoform in causing delayed clearance of triglyceride-rich lipoproteins.
authors.affiliation: Human Genetics Center, University of Texas Health Science Center, Houston 77225, USA.
authors.forename: M
authors.initials: M
authors.lastname: de Andrade
authors.forename: I
authors.initials: I
authors.lastname: Thandi
authors.forename: S
authors.initials: S
authors.lastname: Brown
authors.forename: A
authors.initials: A
authors.lastname: Gotto
authors.forename: W
authors.initials: W
authors.lastname: Patsch
authors.forename: E
authors.initials: E
authors.lastname: Boerwinkle
mesh_terms: D000328:Adult; D001057:Apolipoproteins E / Q000235:genetics*; D001161:Arteriosclerosis / Q000453:epidemiology / Q000209:etiology*; D002339:Carotid Arteries / Q000473:pathology*; D016022:Case-Control Studies; D015331:Cohort Studies; D004224:Diterpenes; D005215:Fasting; D005260:Female; D006801:Humans; D008019:Life Style; D008055:Lipids / Q000097:blood; D008074:Lipoproteins / Q000097:blood; D008297:Male; D008954:Models, Biological; D015337:Multicenter Studies as Topic; D011110:Polymorphism, Genetic; D015995:Prevalence; D012044:Regression Analysis; D000084562:Retinyl Esters; D014801:Vitamin A / Q000031:analogs & derivatives / Q000097:blood
chemical_list: D001057:Apolipoproteins E; D004224:Diterpenes; D008055:Lipids; D008074:Lipoproteins; D000084562:Retinyl Esters; D014801:Vitamin A; C014794:retinol palmitate