Influence of apolipoprotein E, smoking, and alcohol intake on carotid atherosclerosis -: National heart, lung, and blood institute family heart study
Influence of apolipoprotein E, smoking, and alcohol intake on carotid atherosclerosis -: National heart, lung, and blood institute family heart study
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DOI：
10.1161/01.str.0000014325.54063.1a
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发表时间：
2002-05-01
期刊：
影响因子：
8.3
通讯作者：
Ellison, RC
中科院分区：
文献类型：
--
作者：
Djoussé, L;Myers, RH;Ellison, RC
载脂蛋白E（apoE）亚型和生活方式因素在冠心病的发生发展中起重要作用。载脂蛋白E和颈动脉粥样硬化的关联仍然存在争议。方法，我们调查了载脂蛋白E，吸烟，饮酒，和他们的相互作用与颈动脉粥样硬化对544个人无冠心病的国家心脏，肺，血液研究所（NHLBI）家庭心脏研究的关系。通过高分辨率ultrason.Results-subjects在apoE 4组的颈动脉粥样硬化病变检测血压较低，高密度脂蛋白胆固醇较低，低密度脂蛋白胆固醇较高。在多变量logistic回归模型中，apoE亚型和饮酒与颈动脉粥样硬化的患病率无显著相关性（趋势分别为P=0.94和0.98）。相反，与从不吸烟的人相比，颈动脉粥样硬化的患病率比值比为1.7 [95%置信区间（CI），1.1至2.7]，2.8（95% CI，1.2 - 6.2）和1.9（95% CI，0.7至5.5）分别为既往吸烟者，目前吸烟者1至20支/天，目前吸烟者>20支/天（趋势P=0.0018）。我们没有发现apoE和饮酒之间相互作用的证据。我们的数据表明，apoE等位基因<$（4）和吸烟对颈动脉粥样硬化有协同作用：优势比为1.7（95% CI，0.8 - 3.6）单独吸烟，1.0（95% CI，0.6 - 1.8），单用地塞米松（4），3.7（95%可信区间，1.1 ~ 3.6），与apoE等位基因<$（4）和吸烟的联合存在有关。吸烟而非饮酒或ApoE与颈动脉粥样硬化几率增加相关。我们的数据表明apoE等位基因<$4和吸烟对颈动脉粥样硬化有协同作用。
Background-Apolipoprotein E (apoE) isoforms and lifestyle factors play an important role in the development of coronary heart disease. The association of apoE and carotid atherosclerosis remains controversial.Methods-We investigated the relation of apoE, cigarette smoking, alcohol drinking, and their interaction with carotid atherosclerosis on 544 individuals free of coronary heart disease in the National Heart, Lung, and Blood Institute (NHLBI) Family Heart Study. Atherosclerotic lesions of the carotid arteries were detected through high-resolution ultrasound.Results-Subjects in the apoE4 group had lower blood pressure, lower high-density lipoprotein cholesterol, and higher low-density lipoprotein cholesterol. In a multivariate logistic regression model, apoE isoforms and alcohol consumption were not significantly associated with the prevalence odds of carotid atherosclerosis (P=0.94 and 0.98, respectively, for trend). In contrast, compared with those who never smoked, the prevalence odds ratios for carotid atherosclerosis were 1.7 [95% confidence interval (CI), 1.1 to 2.7], 2.8 (95% CI, 1.2 to 6.2), and 1.9 (95% CI, 0.7 to 5.5) for former smokers, current smokers of 1 to 20 cigarettes per day, and current smokers of >20 cigarettes day, respectively (P=0.0018 for trend). We did not find evidence of an interaction between apoE and alcohol consumption. Our data suggested a synergistic effect between the apoE allele epsilon(4) and smoking on carotid atherosclerosis: odds ratios were 1.7 (95% CI, 0.8 to 3.6) for smoking alone, 1.0 (95% CI, 0.6 to 1.8) for epsilon(4) alone, and 3.7 (95% CI, 1.1 to 3.6) for the joint presence of the apoE allele epsilon(4) and smoking.Conclusions-Smoking but not alcohol consumption or ApoE is associated with an increased odds of carotid atherosclerosis. Our data suggest a synergistic effect between the apoE allele epsilon(4) and smoking on carotid atherosclerosis.