Kraiczi H, Caidahl K, Samuelsson A, Peker Y, Hedner J
Department of Pulmonary Medicine, Sahlgrenska University Hospital, Gothenburg, Sweden.
Chest. 2001 Apr;119(4):1085-91. doi: 10.1378/chest.119.4.1085.
To investigate whether a dose-effect relationship exists between the severity of obstructive sleep apnea (OSA) and subclinical indicators of myocardial or vascular dysfunction.
Cross-sectional study using correlation analysis.
Twenty subjects referred to our sleep laboratory for screening or therapy of OSA but without regular medication and without known cardiovascular disease.
Severity of OSA was quantified by polysomnography. Moreover, nocturnal excretion of norepinephrine was determined. Left ventricular (LV) myocardial function was assessed with Doppler echocardiography. Using ultrasonographic measurements, endothelium-dependent and endothelium-independent conduit artery dilation were measured as flow-mediated and glyceryltrinitrate-induced changes in brachial artery diameter.
Worsening nocturnal hypoxemia, measured as nocturnal oxygen saturation nadir or percentage of sleep time spent in hypoxemia (< 90% hemoglobin oxygen saturation), predicted increased interventricular septum thickness (corrected for age and body mass index), prolonged isovolumetric relaxation time, decreased ratio between peak early and late mitral flow velocities, as well as reduced endothelium-dependent dilatory capacity of the brachial artery (all relationships corrected for cofactor age and with p < 0.05) were observed. Associations between these cardiovascular function markers and nocturnal excretion of norepinephrine followed the same trend, but relations with interventricular septum thickness and flow-mediated artery dilation missed significance (p = 0.064 and p = 0.061, respectively). LV posterior wall thickness, measures of LV systolic function, early mitral flow deceleration time, and endothelium-independent artery dilation were not significantly related to the degree of nocturnal hypoxemia or norepinephrine excretion. None of the correlations with apnea-hypopnea index were statistically significant.
The severity of apnea-related hypoxemia is associated with a gradual deterioration of LV diastolic function as well as large-artery endothelial function.
探讨阻塞性睡眠呼吸暂停(OSA)的严重程度与心肌或血管功能障碍的亚临床指标之间是否存在剂量效应关系。
采用相关性分析的横断面研究。
20名因OSA筛查或治疗转诊至我们睡眠实验室的受试者,他们未规律用药且无已知心血管疾病。
通过多导睡眠图对OSA严重程度进行量化。此外,测定夜间去甲肾上腺素排泄量。采用多普勒超声心动图评估左心室(LV)心肌功能。通过超声测量,以内皮依赖性和非内皮依赖性的导管动脉扩张来衡量,即肱动脉直径因血流介导和硝酸甘油诱导的变化。
以夜间氧饱和度最低点或低氧血症(血红蛋白氧饱和度<90%)睡眠时长百分比衡量的夜间低氧血症加重,预示着室间隔厚度增加(校正年龄和体重指数)、等容舒张时间延长、二尖瓣血流速度早期峰值与晚期峰值之比降低,以及肱动脉内皮依赖性扩张能力降低(所有关系均校正了年龄等因素,p<0.05)。这些心血管功能标志物与夜间去甲肾上腺素排泄之间的关联遵循相同趋势,但与室间隔厚度和血流介导的动脉扩张的关系未达到显著水平(分别为p = 0.064和p = 0.061)。左心室后壁厚度、左心室收缩功能指标、二尖瓣血流早期减速时间和非内皮依赖性动脉扩张与夜间低氧血症程度或去甲肾上腺素排泄无显著相关性。与呼吸暂停低通气指数的所有相关性均无统计学意义。
与呼吸暂停相关的低氧血症严重程度与左心室舒张功能以及大动脉内皮功能的逐渐恶化相关。