阻塞性睡眠呼吸暂停低通气综合征与心律失常

阻塞性睡眠呼吸暂停低通气综合征（OSAHS）是一种睡眠过程中反复出现的以呼吸暂停、睡眠结构紊乱及低氧血症等为特征的疾病.大量的临床研究证明0SAHS与高血压、代谢综合征、冠心病、心力衰竭、脑卒中以及心律失常等疾病密切相关,现通过系统综述,探讨分析了OSAHS与多种心律失常发生的关系,归纳总结其发生机制及心电学特点,并对OSAHS及其合并症的治疗进展进行相关讨论.     

阻塞性睡眠呼吸暂停患者的心律失常特点及与体位变化的关系

为了观察阻塞性睡眠呼吸暂停（ＯＳＡ）患者的心律失常特点以及睡眠体位对心律失常的影响,对２１例经五官科确诊的ＯＳＡ患者进行２４ｈ动态心电图监测。清醒状态下６例（２８．６％）偶发房性早搏、室性早搏,睡眠中２１例（１００％）均出现心律失常。心律失常特征为：随憋气加重出现传导阻滞、停搏、逸搏及早搏、短阵心动过速;呼吸恢复时,窦性心律突然加速伴早搏、心动过速。侧卧位时心律失常消失或改善（７６．７％ｖｓ３３．３％）。结论：迷走－交感神经失衡是引起ＯＳＡ患者发生心律失常的主要原因之一。     

Intima-Media Thickness in Patients With Obstructive Sleep Apnea Without Comorbidities

Background

Obstructive sleep apnea (OSA) is associated with elevated risk of cardiovascular events. The early stages of vascular complications can be visualized by means of ultrasound. Intima-media thickness (IMT) correlates with the presence of risk factors of cardiovascular diseases such as hypertension, diabetes, tobacco smoking, or hyperlipidemia. However, little is known whether OSA itself may be the cause of IMT thickening.

Methods

The study group was composed of 28 patients (6 women, 22 men; mean age = 53.8 years, mean BMI = 27.1 kg/m², mean AHI = 22.4/h) with OSA who had no comorbidities. The control group consisted of 28 healthy subjects (6 women, 22 men; mean age = 53.9 years; mean BMI = 27.5 kg/m²). In both groups IMT was assessed in common carotid arteries with the use of ultrasonography. Additionally, in patients with OSA, pulse wave velocity, echocardiography, 24-h automated blood pressure monitoring, clinical signs and symptoms, and blood tests were performed to investigate possible correlations with IMT.

Results

Median IMT was 0.41 mm in OSA patients and 0.46 mm in the control group (p = 0.087). Echocardiography revealed left ventricle hypertrophy in 21 %, systolic disorders in 8 %, and diastolic disorders in 57 % of the patients. In a large majority of patients, pulse wave velocity was found to be normal. IMT correlated with age (r = 0.446, p = 0.017), total cholesterol (r = 0.518, p = 0.005), daytime systolic blood pressure (r = 0.422, p = 0.025), pulse pressure 24 h and daytime (r = 0.424, p = 0.027 and r = 0.449, p = 0.019), early mitral flow/atrial mitral flow (E/A) (r = ?0.429, p = 0.023), and posterior wall diameter (PWD) (r = 0.417, p = 0.270).

Conclusion

In a relatively nonobese group of patients, no significant differences were found in the intima-media thickness between OSA patients without concomitant cardiovascular diseases and healthy controls. This may lead to the conclusion that IMT does not reflect increased risk of cardiovascular events in patients with isolated OSA.     

Cardiac Sympathetic Hyperactivity in Patients with Chronic Obstructive Pulmonary Disease and Obstructive Sleep Apnea

Obstructive sleep apnea (OSA) and chronic obstructive pulmonary disease (COPD) coexist in 0.5–1% of the general population. Both OSA and COPD are associated with increased sympathetic nervous activity, and patients affected by both disorders have higher risk for increased morbidity and mortality as compared with patients with COPD or OSA alone.

We tested the hypothesis that patients with COPD and OSA (Overlap syndrome) have higher sympathetic and lower parasympathetic modulation of heart rate variability (HRV) in comparison with patients suffering from COPD or OSA alone.

HRV indices in the frequency domain were evaluated from daytime electrocardiographic recordings in 14 patients with both severe OSA (apnea–hypopnea index ≥ 30) and mild-to-moderate COPD and compared with those with OSA (n = 24) or COPD (n = 16) alone.

We found that, in the Overlap syndrome group, high-frequency (HF, 0.4–0.15 Hz) power was significantly lower (0.18 nu vs 0.34 nu in OSA and 0.44 nu in COPD patients, p < 0.01) and low-frequency (LF, 0.15–0.05 Hz) power was significantly greater (0.82 nu vs 0.66 nu in OSA and 0.57 nu in COPD patients, p < 0.01) compared with COPD and OSA groups. Patients with both OSA and COPD had higher LF/HF ratio as compared with patients in OSA and COPD groups (4.5 [5.9] vs 1.9 [2.6] and 1.3 [1.3], respectively, p < 0.01). For the Overlap syndrome group, there was a significant direct relationship between LF/HF ratio and residual volume (r² = 0.62, p = 0.007).

These findings show that patients with both OSA and COPD have higher sympathetic modulation of heart rate compared with those with OSA or COPD alone. Furthermore, the findings provide a potential mechanism for the increased morbidity and mortality reported in patients suffering from both disorders, suggesting new therapeutic perspectives in Overlap syndrome.     

Excessive Daytime Sleepiness and Obstructive Sleep Apnea in Patients With Sarcoidosis

BackgroundSystemic symptoms are common in sarcoidosis and are associated with a decreased quality of life. Excessive daytime sleepiness (EDS) often is associated with obstructive sleep apnea (OSA) but may be a systemic symptom independently associated with sarcoidosis. The aim of this study was to assess the relationship between sarcoidosis and EDS.MethodsIn a retrospective analysis, we used Epworth Sleepiness Scale scores to compare sleepiness in 62 patients with sarcoidosis with 1,005 adults without sarcoidosis referred for polysomnography for suspicion of OSA. Linear regression models controlled for covariates. In a subgroup analysis of patients with sarcoidosis, sleepiness scores and polysomnograms were compared between those with normal and those with abnormal pulmonary function based on total lung capacity.ResultsEDS was more common in patients with sarcoidosis than in those without, and sarcoidosis remained an independent predictor of increased sleepiness after controlling for covariates. Compared with control patients referred for polysomnography, fewer patients with sarcoidosis had clinically significant OSA. However, among patients with sarcoidosis, OSA was more severe in those with abnormal lung function.ConclusionsSarcoidosis is independently associated with EDS. Sleepiness may contribute to the morbidity of sarcoidosis and should be followed even after treating for potentially coexisting OSA or depression. Abnormal lung function in sarcoidosis may contribute to OSA, although the mechanisms for this are not known.     

阻塞性睡眠呼吸暂停的治疗进展

谈阻塞性睡眠呼吸暂停（obstructive sleep apnea,OSA）的治疗,首先需要明确的是OSA治疗的目的。OSA是多种原因造成睡眠中上气道不同程度的狭窄或阻塞,而引发的以睡眠打鼾、呼吸暂停和日间嗜睡等症状为主的一个综合征。问题发生在上气道,引发的合并症确遍及全身,对机体的损害涉及心脑血管、呼吸、消化、血液、泌尿生殖和代谢等多个系统。     

阻塞性睡眠呼吸暂停综合征的冠心病患者室性期前收缩的临床意义

目的:分析室性期前收缩(VPC)频率及交感活性在患有阻塞性睡眠呼吸暂停综合征的冠心病患者中的意义.方法:125例患有阻塞性呼吸暂停综合征的冠心病患者,均行多导睡眠图检查,将患者按呼吸暂停低通气指数(AHI)进行分组,睡眠阶段分为清醒期、入睡期、浅睡期、中度或深度睡眠期和快速眼球运动期.并对患者心率震荡参数进行测量对比.结果:VPC频率受睡眠阶段(清醒期、浅睡期及快速眼球运动期,F=5.8,P<0.01)及AHI(F=8.7,P<0.01)影响;在严重阻塞性呼吸暂停综合征患者,快速眼球运动期VPC频率较清醒期为高(P=0.01),相反,轻、中等阻塞性呼吸暂停综合征患者VPC频率较低,且没有睡眠阶段依赖性(P≥0.05).血氧失饱和持续间期与AHI呈正相关(r2=0.71,P<0.01),且在快速眼球运动期较非快速眼球运动期为长(P<0.01),在快速眼球运动期心率震荡参数斜率与血氧失饱和持续间期呈负相关(r2=0.06,P=0.01).结论:快速眼球运动期VPC出现频率高.     

阻塞性睡眠呼吸暂停低通气综合征患者心血管疾病相关因子血清水平的变化分析

目的:探讨无心血管疾病的阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者心血管疾病相关因子血清自细胞介素-18、白细胞介素-1β、白细胞介素-10、可溶性CD40配体(sCD40L)、胰岛素样生长因子-2(IGF-2)与OSAHS病情严重程度的相关性.方法:采用酶联免疫吸附法(ELISA)测定无心血管疾病及其并发症的56例OSAHS患者[OSAHS组,根据呼吸暂停低通气指数(AHI)和夜间最低氧饱和度(SaO2min)将OSAHS分为轻、中、重度者]、10例单纯鼾症患者(鼾症组)及30例单纯肥胖者(对照组)血清相关因子水平,采用方差分析、Sperman's相关分析等统计方法,比较各组之间的差异,分析各因子浓度与多导睡眠监测(PSG)参数的相关性.结果:白细胞介素-1β:OSAHS组及鼾症组、对照组之间差异无统计学意义(P>0.05).白细胞介素-18:OSAHS组重度者与对照组、鼾症组、轻度者和中度者比较明显升高(P<0.01);中度者与对照组、鼾症组比较明显升高,差异均有统计学意义(P<0.05-0.01).白细胞介素-10:OSAHS组重度者与对照组、鼾症组、轻度者和中度者比较明显降低(P<0.01);中度者与对照组、鼾症组比较明显降低(P<0.01);轻度者与对照组、鼾症组比较明显降低(P<0.01).胰岛素样生长因子-2:OSAHS组重度者与对照组、鼾症组、轻度者和中度者比较明显升高(P<0.01);中度者与对照组、鼾症组、轻度者比较明显升高(P<0.01).可溶性CD40配体:OSAHS组重度者与对照组、鼾症组和轻度者比较明显升高,(P<0.05～0.01),中度者与对照组比较明显升高(P<0.01).白细胞介素-18的血清浓度与呼吸暂停低通气指数及最长呼吸暂停时间呈正相关(r=4.873,r=1.863,P均<0.0001);白细胞介素-10与白细胞介素-18相反,它与呼吸暂停低通气指数及最长呼吸暂停时间呈负相关(r=-0.906,r=-0.608,P均<0.0001);可溶性CD40配体也与OSAHS呈正相关(r=0.039,P=0.001);胰岛素样生长因子-2的浓度与呼吸暂停低通气指数呈正相关(r=0.261,P=0.016),与夜间最低氧饱和度呈负相关(r=-5.147,P<0.001).结论:无心血管疾病及其并发症的OSAHS患者血清中心血管疾病相关因子已经出现了与OSAHS病情严重程度相关的平衡失调,这种紊乱可能是OSAHS易发生心血管并发症的原因之一.