Department of Medicine, American University of Beirut, Beirut, Lebanon.
Sleep. 2013 May 1;36(5):763-768C. doi: 10.5665/sleep.2644.
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.
Cross-sectional, observational.
Community-based.
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).
None.
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.
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, interleukin-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).
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.
睡眠呼吸障碍与心血管疾病有关。其病理生理机制尚不清楚,但血管炎症增强与之相关。我们试图评估睡眠呼吸障碍与炎症生物标志物的关系。
横断面观察性研究。
社区为基础。
该研究来自弗雷明汉心脏研究的睡眠心脏健康研究站点,共纳入 900 名参与者(52%为女性,平均年龄 60 岁,23%为少数民族)。
无。
我们评估了与多导睡眠图衍生的呼吸暂停低通气指数和低氧血症指数(%睡眠时间血氧饱和度<90%)相关的 9 种炎症生物标志物的循环水平。多变量模型调整了人口统计学因素、吸烟、心血管疾病、糖尿病和其他潜在的混杂因素,未调整和调整了体重指数。
在不包括体重指数的多变量调整中,呼吸暂停低通气指数与 C 反应蛋白、白细胞介素-6、纤维蛋白原、细胞间黏附分子-1 和 P 选择素水平相关,低氧血症指数与 C 反应蛋白、白细胞介素-6 和纤维蛋白原水平相关。调整体重指数后,只有白细胞介素-6 与睡眠呼吸障碍的相关性仍然显著:呼吸暂停低通气指数<5、5-14.9、15-29.9 和≥30 次/小时的参与者血清白细胞介素-6 水平分别为 2.93、3.14、3.34 和 4.62pg/ml(趋势 P=0.01),低氧血症指数<0.5、0.5-4.9、5-9.9 和≥10%睡眠时间的参与者分别为 2.97、3.01、3.35 和 4.85pg/ml(趋势 P=0.02)。
在社区为基础的样本中,睡眠呼吸障碍与更高水平的白细胞介素-6 相关,后者是心肌梗死风险和死亡率的标志物。肥胖可能介导了睡眠呼吸障碍中观察到的 C 反应蛋白、纤维蛋白原、细胞间黏附分子-1 和 P 选择素水平的升高。