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Vascular inflammation and sleep disordered breathing in a community-based cohort

机译:基于社区的队列中的血管炎症和睡眠呼吸障碍

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Study Objectives: Sleep disordered breathing is associated with cardiovascular disease. The pathophysiologic mechanisms remain unclear, but enhanced vascular inflammation is implicated. We sought to evaluate the association of sleep disordered breathing with biomarkers of inflammation. Design: Crosssectional, observational. Setting: Community-based. Participants: There were 900 participants from the Framingham Heart Study site of the Sleep Heart Health Study (52% females, mean age 60 y, 23% ethnic minorities). Interventions: None. Measurements: We assessed circulating levels of nine inflammatory biomarkers in relation to polysomnographically-derived apnea-hypopnea index and hypoxemia index (% sleep time with oxyhemoglobin saturation < 90%). Multivariable models were adjusted for demographics, smoking, cardiovascular diseases, diabetes, and other potential confounders, without and with adjustment for body mass index. Results: With multivariable adjustment not including body mass index, the apnea-hypopnea index was associated with C-reactive protein, inter-leukin-6, fibrinogen, intercellular adhesion molecule-1, and P-selectin levels and hypoxemia index was associated with C-reactive protein, interleu-kin-6, and fibrinogen levels. After adjustment for body mass index, only the association of interleukin-6 with sleep disordered breathing remained significant: the adjusted mean serum interleukin-6 level was 2.93, 3.14, 3.34, and 4.62 pg/mL, respectively, in participants with apnea-hypopnea index < 5, 5-14.9, 15-29.9, and ≥ 30 events/h (P = 0.01 for trend) and 2.97, 3.01, 3.35, and 4.85 pg/mL, respectively, in participants with hypoxemia index < 0.5, 0.5-4.9, 5-9.9, and ≥ 10% of sleep time (P = 0.02 for trend). Conclusions: In a community-based sample, sleep disordered breathing is associated with higher levels of interleukin-6, a marker of myocardial infarction risk and mortality. Adiposity may mediate the increased levels of C-reactive protein, fibrinogen, intercellular adhesion molecule-1, and P-selectin observed in sleep disordered breathing.
机译:研究目标:睡眠呼吸障碍与心血管疾病有关。病理生理机制仍不清楚,但牵连血管发炎。我们试图评估睡眠呼吸障碍与炎症生物标志物的关联。设计:横截面观察。地点:基于社区。参与者:睡眠心脏健康研究的Framingham心脏研究站点有900名参与者(52%的女性,平均年龄60岁,23%的少数民族)。干预措施:无。测量:我们根据多导睡眠图得出的呼吸暂停低通气指数和低氧血症指数(氧合血红蛋白饱和度<90%的睡眠时间百分比)评估了9种炎性生物标志物的循环水平。调整了人口,吸烟,心血管疾病,糖尿病和其他潜在混杂因素的多变量模型,而没有调整体重指数。结果:通过多变量调整(不包括体重指数),呼吸暂停低通气指数与C反应蛋白,白介素6,纤维蛋白原,细胞间粘附分子-1和P选择素水平相关,而低氧血症指数与C相关-反应蛋白,白介素6和纤维蛋白原水平。调整体重指数后,只有白细胞介素6与睡眠呼吸障碍的关联仍然很明显:呼吸暂停低通气参与者的调整后平均血清白细胞介素6水平分别为2.93、3.14、3.34和4.62 pg / mL。低氧血症参与者的指数<5、5-14.9、15-29.9和≥30个事件/小时(趋势P = 0.01)和2.97、3.01、3.35和4.85 pg / mL,分别在低氧血症指数<0.5、0.5-睡眠时间的4.9、5-9.9和≥10%(趋势P = 0.02)。结论:在一个社区样本中,睡眠呼吸障碍与较高水平的白细胞介素6有关,白细胞介素6是心肌梗塞风险和死亡率的标志。肥胖可能会介导在睡眠呼吸障碍中观察到的C反应蛋白,纤维蛋白原,细胞间粘附分子1和P选择素水平升高。

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