Impact of the Metabolic Syndrome on Mortality is Modified by Objective Short Sleep Duration.
Impact of the Metabolic Syndrome on Mortality is Modified by Objective Short Sleep Duration.
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DOI：
10.1161/jaha.117.005479
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发表时间：
2017-05-17
影响因子：
5.4
通讯作者：
Bixler EO
中科院分区：
文献类型：
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作者：
Fernandez-Mendoza J;He F;LaGrotte C;Vgontzas AN;Liao D;Bixler EO
研究客观睡眠时间是否是代谢综合征（MetS）对全因死亡率和心血管疾病/脑血管疾病死亡率影响的效应调节因子。我们在宾夕法尼亚州立大学成人队列研究中解决了这个问题，这是一个随机的一般人群样本，共有1344名男性和女性（48.8±14.2岁），他们在睡眠实验室接受了研究，随访时间为16.6±4.2年。MetS定义为存在3种或以上肥胖（≥30 kg/m2）、总胆固醇（≥200 mg/dL）、甘油三酯（≥150 mg/dL）、空腹血糖（≥100 mg/dL）和血压（≥130/85 mm Hg）升高。多导睡眠图睡眠持续时间被分为有临床意义的类别。在1344名参与者中，22.0%的人在随访期间死亡。我们使用控制多个潜在混杂因素的考克斯比例风险模型检验代谢综合征和多导睡眠持续时间对死亡率的相互作用（P<0.05）。与代谢综合征相关的全因和心血管疾病/脑血管疾病死亡率的风险比（95% CI）在睡眠≥6小时的个体中为1.29（0.89-1.87）和1.49（0.75-2.97），在睡眠<6小时的个体中为1.99（1.53-2.59）和2.10（1.39-3.16）。有趣的是，这种效应改变主要是由MetS的血压升高和葡萄糖失调组分驱动的。与代谢综合征相关的死亡风险在睡眠时间短的人中增加。代谢综合征患者的睡眠时间短可能与更大的中枢自主神经和代谢功能障碍有关。未来的临床试验应该检查延长睡眠是否能改善MetS患者的预后。
To examine whether objective sleep duration is an effect modifier of the impact of metabolic syndrome (MetS) on all‐cause and cardiovascular disease/cerebrovascular mortality. We addressed this question in the Penn State Adult Cohort, a random, general population sample of 1344 men and women (48.8±14.2 years) who were studied in the sleep laboratory and followed up for 16.6±4.2 years. MetS was defined by the presence of 3 or more of obesity (≥30 kg/m2), elevated total cholesterol (≥200 mg/dL), triglycerides (≥150 mg/dL), fasting glucose (≥100 mg/dL), and blood pressure (≥130/85 mm Hg). Polysomnographic sleep duration was classified into clinically meaningful categories. Among the 1344 participants, 22.0% of them died during the follow‐up. We tested the interaction between MetS and polysomnographic sleep duration on mortality using Cox proportional hazard models controlling for multiple potential confounders (P<0.05). The hazard ratios (95% CI) of all‐cause and cardiovascular disease/cerebrovascular mortality associated with MetS were 1.29 (0.89–1.87) and 1.49 (0.75–2.97) for individuals who slept ≥6 hours and 1.99 (1.53–2.59) and 2.10 (1.39–3.16) for individuals who slept <6 hours. Interestingly, this effect modification was primarily driven by the elevated blood pressure and glucose dysregulation components of MetS. The risk of mortality associated with MetS is increased in those with short sleep duration. Short sleep in individuals with MetS may be linked to greater central autonomic and metabolic dysfunction. Future clinical trials should examine whether lengthening sleep improves the prognosis of individuals with MetS.