Alcohol Intake, Myocardial Infarction, Biochemical Risk Factors, and Alcohol Dehydrogenase Genotypes
Alcohol Intake, Myocardial Infarction, Biochemical Risk Factors, and Alcohol Dehydrogenase Genotypes
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DOI：
10.1161/circgenetics.109.873604
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发表时间：
2009-10-01
影响因子：
--
通讯作者：
Nordestgaard, Borge G.
中科院分区：
文献类型：
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作者：
Tolstrup, Janne S.;Gronbaek, Morten;Nordestgaard, Borge G.
背景：与不饮酒者相比，轻度至中度饮酒者发生心肌梗死的风险较低。我们测试了酒精摄入量与心肌梗死风险和危险因素之间的关联，以及这些关联是否被酒精脱氢酶的变化所改变。方法和结果：我们使用了哥本哈根城市心脏研究中来自丹麦普通人群的9584名男性和女性的信息。1991 ~ 2007年随访期间，共发生心肌梗死663例。我们观察到，增加酒精摄入量与心肌梗死风险降低、低密度脂蛋白胆固醇和纤维蛋白原降低、舒张压和收缩压以及高密度脂蛋白胆固醇升高以及u型非空腹甘油三酯升高有关。相比之下，ADH1B和ADH1C基因型与心肌梗死风险或任何心血管生化危险因素无关，并且没有迹象表明酒精摄入量与心肌梗死之间以及酒精摄入量与危险因素之间的关联因基因型而改变。结论：增加酒精摄入量与心肌梗死风险降低、低密度脂蛋白胆固醇和纤维蛋白原降低、舒张压和收缩压、高密度脂蛋白胆固醇升高、u型非空腹甘油三酯升高有关。这些关联不受ADH1B和ADH1C基因型的影响。（中国心血管病杂志，2009;2:507-514）
Background-The risk of myocardial infarction is lower among light-to-moderate alcohol drinkers compared with abstainers. We tested associations between alcohol intake and risk of myocardial infarction and risk factors and whether these associations are modified by variations in alcohol dehydrogenases.Methods and Results-We used information on 9584 men and women from the Danish general population in the Copenhagen City Heart Study. During follow-up, from 1991 to 2007, 663 incident cases of myocardial infarction occurred. We observed that increasing alcohol intake was associated with decreasing risk of myocardial infarction, decreasing low-density lipoprotein cholesterol and fibrinogen, increasing diastolic and systolic blood pressure and high-density lipoprotein cholesterol, and with U-shaped nonfasting triglycerides. In contrast, ADH1B and ADH1C genotypes were not associated with risk of myocardial infarction or with any of the cardiovascular biochemical risk factors, and there was no indication that associations between alcohol intake and myocardial infarction and between alcohol intake and risk factors were modified by genotypes.Conclusions-Increasing alcohol intake is associated with decreasing risk of myocardial infarction, decreasing low-density lipoprotein cholesterol and fibrinogen, increasing diastolic and systolic blood pressure and high-density lipoprotein cholesterol, and U-shaped nonfasting triglycerides. These associations were not modified by ADH1B and ADH1C are genotypes. (Circ Cardiovasc Genet. 2009;2:507-514.)