Oflaz Huseyin, Cuhadaroglu Caglar, Pamukcu Burak, Meric Mehmet, Ece Turhan, Kasikcioglu Erdem, Koylan Nevres
Department of Cardiology, Faculty of Medicine, Istanbul University, Istanbul, Turkey.
Respiration. 2006;73(6):751-6. doi: 10.1159/000094183. Epub 2006 Jun 22.
Obstructive sleep apnea syndrome (OSAS) influences endothelial function and causes hypertension.
Our aim was to evaluate the role of endothelial dysfunction in the pathogenesis of hypertension in OSAS.
Twenty-three patients with OSAS but without hypertension and 15 healthy normotensive subjects were investigated. The presence or absence of OSAS was evaluated with a sleep study. Endothelial function was investigated with brachial artery ultrasound examination.
Baseline characteristics were equivalent between the two groups. Minimal oxygen saturation and apnea-hypopnea indexes in the OSAS and control groups were 62.9 +/- 16.5 versus 94.9 +/- 1.1% (p < 0.0001) and 53.1 +/- 20.3 versus 3.8 +/- 0.9 (p < 0.0001), respectively. There was not statistically significant difference between basal brachial artery diameters measured in the morning and in the evening in all groups. Flow-mediated dilation (FMD) values measured in the morning were lower than those measured in the evening in both OSAS patients and the control group: FMD of OSAS patients was 6.04 +/- 3.18% in the morning and 10.38 +/- 4.23% in the evening hours (p = 0.001), and FMD of control subjects was 10.9 +/- 2.6% in the morning and 13.9 +/- 2.32 in the evening hours (p = 0.002). Differences in FMD values measured both in the morning and evening hours in OSAS patients were lower compared with those in control subjects (p < 0.0001 in the morning hours and p = 0.003 in the evening hours).
We detected a prominent diurnal deterioration in endothelial function in normotensive OSAS patients compared with healthy subjects. This deterioration may occur due to ongoing hypoxemia during the night and it may be a possible cause of hypertension and atherosclerotic cardiovascular diseases in patients with OSAS.
阻塞性睡眠呼吸暂停综合征（OSAS）会影响内皮功能并导致高血压。
我们的目的是评估内皮功能障碍在OSAS患者高血压发病机制中的作用。
对23例患有OSAS但无高血压的患者和15名健康的血压正常受试者进行了研究。通过睡眠研究评估是否存在OSAS。通过肱动脉超声检查研究内皮功能。
两组的基线特征相当。OSAS组和对照组的最低氧饱和度及呼吸暂停低通气指数分别为62.9±16.5对94.9±1.1%（p<0.0001）和53.1±20.3对3.8±0.9（p<0.0001）。所有组中，早晨和晚上测量的基础肱动脉直径之间无统计学显著差异。OSAS患者和对照组中，早晨测量的血流介导的血管舒张（FMD）值均低于晚上测量的值：OSAS患者早晨的FMD为6.04±3.18%，晚上为10.38±4.23%（p=0.001），对照组受试者早晨的FMD为10.9±2.6%，晚上为13.9±2.32（p=0.002）。与对照组相比，OSAS患者早晨和晚上测量的FMD值差异均较低（早晨p<0.0001，晚上p=0.003）。
与健康受试者相比，我们发现血压正常的OSAS患者内皮功能存在明显的昼夜恶化。这种恶化可能是由于夜间持续低氧血症所致，可能是OSAS患者高血压和动脉粥样硬化性心血管疾病的一个潜在原因。
