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首页> 外文期刊>Circulation. Genomic and precision medicine. >Prospective Study of Epigenetic Age Acceleration and Incidence of Cardiovascular Disease Outcomes in the ARIC Study (Atherosclerosis Risk in Communities)
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Prospective Study of Epigenetic Age Acceleration and Incidence of Cardiovascular Disease Outcomes in the ARIC Study (Atherosclerosis Risk in Communities)

机译:前瞻性研究表观遗传年龄的加速度心血管疾病的发病率和结果在ARIC研究(动脉粥样硬化的风险社区)

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BACKGROUND: DNA methylation-based patterns of biological aging, known as epigenetic age acceleration, are predictive of all-cause mortality, but little is known about their association with cardiovascular disease (CVD). METHODS: We estimated 2 versions of epigenetic age acceleration (Horvath and Hannum) using whole-blood samples from 2543 blacks. Linear and Cox proportional hazards regression, respectively, were used to assess the association of age acceleration with carotid intimamedia thickness (cross-sectionally) and incident cardiovascular events, including CVD mortality, myocardial infarction, fatal coronary heart disease, peripheral arterial disease, and heart failure, during a median 21-year follow-up. All models were adjusted for chronological age and traditional CVD risk factors. RESULTS: In comparison to chronological age, the 2 measures of epigenetic age acceleration were weaker, but independent, potential risk markers for subclinical atherosclerosis and most incident cardiovascular outcomes, including fatal coronary heart disease, peripheral arterial disease, and heart failure. For example, each 5-year increment of epigenetic age acceleration was associated with an average of 0.01 mm greater carotid intima-media thickness (each P<0.01), and the hazard ratios (95% confidence intervals) of fatal coronary heart disease per 5-year increment in Horvath and Hannum age acceleration were 1.17 (1.02-1.33) and 1.22 (1.04-1.44), respectively. CONCLUSIONS: In this sample of blacks, increased epigenetic age acceleration in whole blood was a potential risk marker for incident fatal coronary heart disease, peripheral arterial disease, and heart failure independently of chronological age and traditional CVD risk factors. DNA methylation-based measures of biological aging may help to identify new pathophysiological mechanisms contributing to the development of CVD.
机译:背景:DNA的methylation-based模式生物老化,被称为表观遗传的年龄加速度,是所有原因的预测死亡率,但对他们所知甚少与心血管疾病(CVD)。方法:我们估计2版本的表观遗传年龄加速度(Horvath)和所有)使用从2543年黑人遗传损伤样本。Cox比例风险回归,分别被用来评估协会年龄与颈动脉intimamedia加速度厚度(横向比较)和事件心血管疾病,包括心血管疾病死亡率,冠心病心肌梗死,致命的疾病、外周动脉疾病和心脏失败,在21年平均随访。模型调整的实足年龄传统的心血管疾病的危险因素。实足年龄相比,2措施表观遗传年龄的加速度较弱,但是独立的,潜在的风险标记亚临床动脉粥样硬化和大多数事件心血管疾病的结果,包括致命的冠状动脉心脏病,外周动脉疾病,心力衰竭。表观遗传年龄的加速度有关平均的0.01毫米大的颈动脉(每个P < 0.01),内膜-中膜厚度和风险比率(95%置信区间)的死亡冠心病每5年递增Horvath)和所有年龄加速度是1.17(1.02 - -1.33)和1.22(1.04 - -1.44),分别。结论:在这个示例的黑人,增加表观遗传年龄加速度在全血潜在风险事件的标志致命的冠状动脉心脏病,外周动脉疾病,心力衰竭的独立的实足年龄和传统的心血管疾病的危险因素。methylation-based生物老化的措施可能有助于确定新的病理生理机制的发展做出贡献CVD。

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