RELATION OF APOLIPOPROTEIN E PHENOTYPE TO MYOCARDIAL-INFARCTION AND MORTALITY FROM CORONARY-ARTERY DISEASE

RELATION OF APOLIPOPROTEIN E PHENOTYPE TO MYOCARDIAL-INFARCTION AND MORTALITY FROM CORONARY-ARTERY DISEASE
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DOI:
10.1016/0002-9149(93)90732-r
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发表时间:
1993-01-15
影响因子:
2.8
通讯作者:
NEATON, JD
NEATON, JD
中科院分区:
医学3区
文献类型:
--
作者:
EICHNER, JE;KULLER, LH;NEATON, JD

文献摘要

被引文献

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载脂蛋白E多态性是低密度脂蛋白(LDL)胆固醇的遗传决定因素。其作为冠状动脉疾病(CAD)的危险因素的地位,无论是通过与LDL胆固醇水平的因果关系还是独立的,都不太清楚。来自多危险因素干预试验的数据被用来检查载脂蛋白E表型对冠状动脉事件风险的影响。在12,866名随机参与者中,有619名在巢式病例对照设计中进行了研究。CAD死亡(93例)和非致命性心肌梗死(113例)与412例对照组相匹配。白色人群载脂蛋白E等位基因频率(ε 2 = 0.06,ε 3 = 0.79和ε 4 = 0.15)与其他非选择性白色美国人群非常相似,载脂蛋白E与总胆固醇和LDL胆固醇的关系与其他研究中观察到的结果基本相似,ε 2等位基因与较低的总胆固醇和LDL胆固醇相关,ε 4等位基因与较高的总胆固醇和LDL胆固醇相关。患者和对照组的等位基因频率是不一样的。ε 4的存在与CAD风险增加相关,这在致死性病例中最为明显。试验期间LDL胆固醇随时间的变化与载脂蛋白E表型之间没有关系。
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 (epsilon2 = 0.06, epsilon3 = 0.79, and epsilon4 = 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 epsilon2 allele being associated with lower and the epsilon4 allele with higher total and LDL cholesterol. Allele frequencies were not the same for patients and control subjects. The presence of epsilon4 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.