Longitudinal association of sleep-disordered breathing and nondipping of nocturnal blood pressure in the Wisconsin Sleep Cohort Study

Longitudinal association of sleep-disordered breathing and nondipping of nocturnal blood pressure in the Wisconsin Sleep Cohort Study
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DOI:
10.1093/sleep/31.6.795
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发表时间:
2008-06-01
期刊:
影响因子:
5.6
通讯作者:
Stubbs, Maryan
Stubbs, Maryan
中科院分区:
医学2区
文献类型:
--
作者:
Hla, Khin Mae;Young, Terry;Stubbs, Maryan

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研究目的:睡眠呼吸障碍(SDB)和正常夜间血压(BP)降低(非下降)的减弱之间的关系仅在横断面上进行了研究。本研究的目的是调查SDB是否与nondiping.Methods前瞻性相关:SDB和事件nondiping之间的纵向关联进行了检查,在一个子样本的328名成年人参加了威斯康星州睡眠队列研究谁完成了2个或更多的24小时动态血压研究平均7.2年的后续行动。通过基线实验室多导睡眠描记仪确定的SDB由呼吸暂停低通气指数(AHI)类别定义。收缩压和舒张压非下降定义为收缩压和舒张压睡眠-觉醒血压比值> 0.9。所有模型均调整了年龄,性别,体重指数在基线和随访,吸烟,饮酒,高血压,睡眠时间,随访时间的长度,和抗高血压药物use.Results:有一个剂量反应增加的机会发展收缩期非下降的参与者与SDB。基线AHI 5-< 15和AHI 15与AHI < 5相比,收缩压未下降事件的调整优势比(95%置信区间)分别为3.1(1.3-7.7)和4.4(1.2-16.3)(P趋势= 0.006)。调整后的优势比相应SDB类别的舒张期非倾斜事件(95%置信区间)无统计学显著性:2.0(0.8-5.6)和1.3(0.2-7.1).结论:我们的纵向研究发现,在基线时具有SDB严重程度的人群中,基础样本提供的证据与因果关系一致。夜间收缩压不下降可能是SDB导致心血管疾病增加的一种机制。
Study Objectives: The association of sleep-disordered breathing (SDB) and blunting of normal nocturnal lowering of blood pressure (BP) (nondipping) has only been examined cross-sectionally. The purpose of this study is to investigate whether SDB is prospectively associated with nondipping.Methods: The longitudinal association between SDB and incident nondipping was examined in a subsample of 328 adults enrolled in the Wisconsin Sleep Cohort Study who completed 2 or more 24-hour ambulatory BP studies over an average of 7.2 years of follow-up. SDB identified by baseline in-laboratory polysomnography was defined by apnea-hypopnea index (AHI) categories. Systolic and diastolic nondipping was defined by systolic and diastolic sleep-wake BP ratios > 0.9. All models were adjusted for age, sex, body mass index at baseline and follow-up, smoking, alcohol consumption, hypertension, sleep time, length of follow-up time, and antihypertensive medication use.Results: There was a dose-response increased odds of developing systolic nondipping in participants with SDB. The adjusted odds ratios (95% confidence interval) of incident systolic nondipping for baseline AHI 5 to < 15 and AHI 15, versus AHI < 5, were 3.1 (1.3-7.7) and 4.4 (1.2-16.3), respectively (P trend = 0.006). The adjusted odds ratios (95% confidence interval) of incident diastolic nondipping for corresponding SDB categories were not statistically significant: 2.0 (0.8-5.6) and 1.3 (0.2-7.1).Conclusions: Our longitudinal findings of a dose-response increase in development of systolic nondipping of BP with severity of SDB at baseline in a population-based sample provide evidence consistent with a causal link. Nocturnal systolic nondipping may be a mechanism by which SDB contributes to increased cardiovascular disease.