睡眠呼吸暂停综合征与高血压

睡眠呼吸暂停综合征(SAS)是一种常见的睡眠障碍性疾病,占睡眠阻碍性疾病的1/3~1/2。据报道,全世界SAS患病率男性约4%,女性约2%,而65岁以上老人患病率高达20~40%〔1〕。成人SAS分为3型,其中以阻塞性睡眠呼吸暂停综合征(OSAS)最常见,占80~90%。OSAS临床表现为,由于睡眠时多种病因引起的上气道狭窄或阻塞,导致打鼾并伴有呼吸暂停和呼吸表浅,夜间反复发生低氧血症、高碳酸血症和睡眠结构紊乱,致使白天嗜睡、心肺脑血管并发症乃至多脏器损害,严重影响患者生活质量和寿命〔2〕。1SAS定义、相关术语、分型、分度及诊断SAS是指每晚7h的睡…     

睡眠呼吸暂停综合征与高血压

目的 研究睡眠呼吸暂停综合征（SAS）对24h血压的影响。方法 同步进行24h动态血压和多导睡眠检查,选择未用药或停服血管活性药2周患56例,按呼吸紊乱指数（AHI）分为正常、轻度SAS和中重度SAS三组,比较AHI与24h血压参数的关系。结果 多元回归显示,AHI与白天收缩压、舒张压（P＜0．05,P＜0．001）、夜间收缩压、舒张压（P＜0．001,P＜0．001）及夜间血压下降百分数显相关（P＜0．001,P＜0．05）。协方差分析结果显示,AHI增加,白天血压升高,与正常组和轻度SAS组相比,中重度SAS组夜间血压下降百分数减少（P＜0．05）。结论 SAS可能是高血压病的危险因素之一,并独立于年龄和体重。在中、重度SAS患中,出现血压生理节律的改变,这些改变与SAS患心脑血管发病率和死亡率增加有关。     

睡眠呼吸暂停综合征与高血压治疗

目的　观察合并睡眠呼吸暂停综合征 (SAS)的高血压病患者 ,常规药物降压治疗及呼吸道正压通气治疗对血压的影响。方法　按照睡眠资料和 2 4h血压资料 ,分为单纯高血压组与合并SAS高血压组 ,观察常规降压药物治疗 4周后 2 4h血压变化及呼吸道正压通气治疗对合并SAS的高血压患者 2 4h血压影响。结果　 2 7例单纯高血压患者 ,常规药物降压治疗 4周后 ,2 4h平均收缩压、舒张压、夜间收缩压、舒张压均明显下降 (P <0 0 1)。 2 5例合并SAS的高血压患者 2 4h平均收缩压、舒张压、夜间舒张压有所下降 (P <0 0 5 ) ,但仍高于正常值 ,而夜间收缩压无明显变化。其中 19例合并SAS高血压患者加用一夜正压通气治疗后 ,2 4h平均血压进一步下降 ,夜间收缩压和舒张压明显降低 (P <0 0 1,P <0 0 1)。结论　合并有SAS的高血压患者多为难治性 ,单纯降压药物治疗效果欠佳 ,需要同时应用正压通气进行治疗。     

阻塞性睡眠呼吸暂停综合征与高血压

阻塞性睡眠呼吸暂停综合征（OSAS）是指睡眠时上气道塌陷阻塞引起的以睡眠过程中反复出现呼吸暂停和或低通气,导致反复低氧血症和高碳酸血症,伴打鼾、睡眠结构紊乱、白天嗜睡为特征的睡眠呼吸紊乱性疾病。长期暴露于这种疾病,可引起高血压、脑卒中、冠心病、心律失常、糖耐量异常、认知功能障碍等,OSAS多与肥胖、脂质代谢紊乱、高血压等并存,     

阻塞性睡眠呼吸暂停综合征与高血压

目的　探讨阻塞性睡眠呼吸暂停综合征 (OSAS)与高血压的关系。方法　 82例患者行整夜多导睡眠图监测及睡前、醒后血压测定 ,呼吸暂停低通气指数 (AHI)≥ 5为 OSAS组 ,AHI<5为对照组 ,比较两组睡眠呼吸参数和睡眠前、后血压改变。结果　OSAS组醒后血压 14 9.5 3± 18.2 3/ 99.0 4± 11.35 mm Hg比睡前血压 131.78± 16 .95 / 87.4 8± 12 .2 mm Hg明显升高 (P<0 .0 5 ) ,较对照组睡前血压 112 .5± 10 .6 5 / 75 .6 1± 8.2 6 mm Hg明显升高 (P<0 .0 5 )。OSAS组最低氧饱和度 (Sa O2 % ) 6 1.2 5± 17.6 8较对照组83.5 9± 5 .87明显降低 (P<0 .0 5 )。OSAS组中有 31例 (5 4 .4 % )确诊为高血压病。结论　OSAS引起的夜间低氧血症可能是部分高血压病原因之一。     

睡眠呼吸暂停综合征与高血压

睡眠呼吸暂停是指睡眠中反复出现呼吸浅慢或无呼吸状态,呼吸暂停则为1次呼吸浅慢或是无呼吸超过10s.睡眠呼吸暂停是一种常见的呼吸障碍性疾病,临床可以观察到响亮而不规则的鼾声,夜间低氧血症、日间嗜睡等症状.多数为阻塞性睡眠呼吸暂停综合征(obstructive sleep apnea,OSA).OSA常可引起多种心血管系统疾病,如高血压、卒中、急性心肌梗死等.目前研究表明,OSA是独立于超重、性别、年龄及吸烟之外另一新的高血压危险因素,并越来越受到人们的关注[1].The Joint National Committee (JNC) 7会议报告中,OSA被明确列为高血压的病因之一.近年来,国内外学者均在OSA与高血压的相关性及可能的发病机制等方面进行了大量深入研究,现就OSA与高血压相关性内容综述如下.     

阻塞性睡眠呼吸暂停综合征与高血压

阻塞性睡眠呼吸暂停综合征(OSAS)是一种临床常见疾病,在临床中往往被忽视,未予充分重视。目前,OSAS和高血压发病率明显增高,流行病学研究表明二者合并的发病率远远超过单一发病率。越来越多的证据支持OSAS可导致高血压。本文对OSAS与高血压的相关性、OSAS相关高血压的特点、OSAS相关高血压病理生理学机制的最新进展、OSAS的治疗策略以及治疗OSAS对血压的影响等方面进行了综述。     

睡眠呼吸暂停综合征的临床表现

睡眠呼吸暂停综合征是一种具有潜在危险性的疾病,临床表现形式多种多样,可以累及多个脏器功能。本文就其常见临床表现及多器官损害进行了综述,希望引起临床医生的足够重视。     

睡眠呼吸暂停综合征的临床表现

睡眠呼吸暂停综合征是一种具有潜在危险性的疾病,临床表现形式多种多样,可以累及多个脏器功能。本就其常见临床表现及多器官损害进行了综述,希望引起临床医生的足够重视。     

睡眠呼吸暂停综合征与隐蔽性高血压

目的 探讨睡眠呼吸暂停综合征(SAS)患者中隐蔽性高血压(MH)的患病情况.方法 选取171例在华北煤炭医学院附属开滦医院睡眠监测室进行检查的偶测血压正常受试者,实施多导睡眠监测并同步进行24 h动态血压监测,次日晨起后采空腹肘静脉血行血生化检查.按睡眠呼吸暂停低通气指数(AHI)＜5和AHI≥5分为非SAS组和SAS组,比较两组MH的患病情况,并分析SAS组中MH和非MH的相关指标、MH相关因素.结果 1)SAS组101例中有54例MH患者,患病率为53 5%,非SAS组70例中有14例MH患者,患病率为20%,差异有非常显著意义(P<0 01).2)SAS组中MH组与非MH组比较,年龄较轻;体质量指数较高;吸烟和饮酒者较多;日间平均心率较高;最长呼吸暂停持续时间较长;血氧饱和度较低,但差异均无统计学意义(P>0 05).3)MH相关因素单因素logistic回归分析显示:SAS、体质量指数、吸烟和饮酒是MH的危险因素.结论 SAS是MH的危险因素,且独立于体质量指数、吸烟和饮酒之外.     

老年人心力衰竭伴睡眠呼吸暂停综合征的心律失常分析

目的对充血性心力衰竭(CHF)伴睡眠呼吸暂停综合征(SAS)患者出现各种心律失常的情况及其对CHF的影响进行初步探讨。方法72例确诊为CHF伴SAS患者,依据多导睡眠图和动态心电图检测分析,以睡眠呼吸暂停低通气指数(AHI)15作为界值,AHI>15者为CHF伴SAS组(A组),36例;AHI≤15者为对照组(B组),36例。结果A组心律失常的发生率明显高于B组(P<0·05),在夜间睡眠状态下心律失常,尤其是室性心律失常差异更为明显。结论CHF伴SAS患者较不伴SAS的CHF患者更易出现各种心律失常而加重CHF,严重者可导致睡眠状态下的猝死,临床上在控制CHF的同时亦应重视对SAS的及时干预。     

冠心病合并睡眠呼吸暂停综合征患者的临床特点

目的:了解冠心病合并睡眠呼吸暂停综合征患者的发生率,并探讨其临床特点。方法:对2004年11月-2005年2月入住我中心行冠状动脉造影的患者,进行多导睡眠呼吸监测,并对其临床症状进行分析。结果:175例患者接受检查入选,冠状动脉造影确诊冠心病患者135例,其中合并睡眠呼吸暂停综合征62．2％(84／135);非冠心病患者40例,其中合并睡眠呼吸暂停综合征40％(16／40),P<0．005。冠心病合并睡眠呼吸暂停综合征与冠心病不合并睡眠呼吸暂停综合征两组之间嗜睡评分、腰臀比、夜间胸痛或憋醒、夜尿增多、晨起口干有明显差别,P< 0．05。Logistic回归分析显示体重指数、夜尿增多、夜间胸痛或憋醒是冠心病患者合并睡眠呼吸暂停综合征的危险因素。结论:冠心病合并睡眠呼吸暂停综合征发病率高,应对冠心病患者进行睡眠呼吸监测,尤其夜间反复发作胸痛憋气、夜尿增多、肥胖的患者应进行睡眠呼吸监测,尽早进行诊断及治疗。     

Impact of Continuous Positive Airway Pressure Therapy on Blood Pressure in Patients with Obstructive Sleep Apnea Hypopnea: A Meta-analysis of Randomized Controlled Trials

Patients with untreated obstructive sleep apnea hypopnea (OSAH) are predisposed to developing hypertension, and therapy with continuous positive airway pressure (CPAP) may reduce blood pressure (BP). The purpose of this study was to assess the impact of CPAP therapy on BP in patients with OSAH. We performed a comprehensive literature search up to July 2006 [Medline, PubMed, EMBASE, Cochrane Database of Systematic Reviews (CDSR), Cochrane controlled trials register (CCTR), and Database of Abstract and Reviews of Effect (DARE)] to identify clinical studies and systemic reviews that examined the impact of CPAP on BP. Studies were included if they (1) were randomized controlled trials with an appropriate control group, (2) included systolic and diastolic BP measurements before and after CPAP/control in patients with OSAH, and (3) contained adequate data to perform a meta-analysis. To calculate pooled results, studies were weighted by inverse variances, with either a fixed or a random effects model used depending on the presence of heterogeneity (assessed with Q test). Ten studies met our inclusion criteria (587 patients): three studies were crossover (149 patients) and seven were parallel in design. Seven studies (421 patients) used 24-h ambulatory BP and three used one-time measurements. Two studies were of patients with heart failure (41 patients). Overall, the effects of CPAP were modest and not statistically significant; CPAP (compared to control) reduced systolic BP (SBP) by 1.38 mmHg (95% CI: 3.6 to −0.88, p = 0.23) and diastolic BP (DBP) by 1.52 mmHg (CI: 3.1 to −0.07; p = 0.06). Six of the trials studied more severe OSAH (mean AHI > 30/h, 313 patients); in these six trials, CPAP reduced SBP by 3.03 mmHg (CI 6.7 to −0.61; p = 0.10) and DBP by 2.03 mmHg (CI: 4.1 to −0.002; p = 0.05). There was a trend for SBP reduction to be associated with CPAP compliance. In unselected patients with sleep apnea, CPAP has very modest effects on BP. However, we cannot exclude the possibility that certain subgroups of patients may have more robust responses—this may include patients with more severe OSAH or difficult-to-control hypertension. Future randomized controlled trials in this area should potentially concentrate on these subgroups of patients. Dr. Ayas has received research funding from Respironics Inc., a maker of CPAP equipment.     

Changes in Depressive Symptoms after Continuous Positive Airway Pressure Treatment for Obstructive Sleep Apnea

It is generally believed that obstructive sleep apnea (OSA) causes depression in some patients, yet it is unknown whether this depression is an actual clinical phenomenon or purely a result of overlapping somatic/physical symptoms shared by both disorders. The present study investigated changes in both somatic and affective/cognitive symptoms of depression associated with the introduction of continuous positive airway pressure (CPAP) treatment for OSA. Participants were 39 outpatients (35 males, 4 females) with no current or past mental health problems, diagnosed with OSA in a hospital sleep disorders clinic. The Beck Depression Inventory (BDI) was administered prior to treatment and again 3 months after CPAP. Total BDI scores improved after CPAP, independent of objectively monitored CPAP compliance rates. Both somatic and affective/ cognitive symptoms of depression improved in a similar manner after treatment. Our findings suggest that depressive symptoms experienced by OSA patients are not solely the result of physical OSA symptoms but include a mood component as well. We introduce a hypothetical model to conceptualize the relationship between OSA and depression.     

心力衰竭合并睡眠呼吸暂停发生情况和临床特点

目的:了解心力衰竭(心衰)患者合并睡眠呼吸暂停发生情况和临床特点。方法:对符合入选标准的126例心衰患者以睡眠呼吸暂停低通气指数(AHI)≥10为界值,分为心衰合并睡眠呼吸暂停组和心衰不合并睡眠呼吸暂停组,进行病史采集及多普勒超声心动图、睡眠呼吸监测等。结果:90例心衰合并睡眠呼吸暂停组中有32例(36％)为心衰合并阻塞性睡眠呼吸暂停,58例(64％)为心衰合并中枢性睡眠呼吸暂停。心衰合并睡眠呼吸暂停组较不合并睡眠呼吸暂停组睡眠呼吸暂停低通气指数、血氧饱和度、低氧指数和鼾声指数均有显著性差异(P<0．05-0．001)。结论:心衰患者合并睡眠呼吸暂停较常见,肥胖、习惯性打鼾、高血压病史和夜尿次数增多者易合并睡眠呼吸暂停。习惯性打鼾、高血压病史和夜尿次数增多是心力衰竭患者合并睡眠呼吸暂停的独立危险因素。     

Continuous Positive Airway Pressure and Obstructive Sleep Apnea in an Hispanic Population

Objectives: We sought to explore the relationship between the diagnosis of hypertension and obstructive sleep apnea (OSA) in a Hispanic population, describe the effect of continuous positive airway pressure (CPAP) on blood pressure regulation, and assess the effect of CPAP on quality of life. Design: A retrospective, recall interview study. Participants: Patients enrolled at the Home Oxygen Program of the San Juan V.A. Medical Center with the diagnosis of OSA and treatment with CPAP. Measurements: The Calgary Sleep Apnea Quality of Life Index was administered to all patients after informed consent. Information regarding co-morbid conditions and fluctuations in blood pressure and anthropometric variables were obtained on a follow-up evaluation. Results: After excluding for the use of antihypertensive medications, weight, and age, a 10% decrease in mean arterial pressure (MAP) from 100 mm Hg to 92 mm Hg was observed in an average of 40 months of therapy (p < 0.05). With the Calgary Quality of Life Index, 67% of the patients reported an extreme improvement in their quality of life. Compliance with CPAP therapy correlated with improved quality of life (r = 0.33, p < 0.015). Conclusions: In this pilot study, there appears to be a correlation between our intervention and decline of blood pressure, independent of body weight, age, or medication usage. CPAP treatment is an effective modality in improving symptoms and quality of life.     

原发性高血压患者非杓型血压与睡眠呼吸暂停综合征的关系

目的探讨睡眠呼吸暂停综合征(SAS)是否与原发性高血压患者非杓型血压有关,及睡眠结构特点和对降压药物的反应.方法门诊轻中度原发性高血压患者用药前或停服降压药2周后,同步进行24小时动态血压和夜间多导睡眠检查,选出非杓型和杓型血压者各15例为研究组和对照组,比较呼吸紊乱指数、睡眠结构和对药物降压治疗反应的差异.结果研究组和对照组在呼吸紊乱指数(P＜0.001)、微觉醒次数(P＜0.05)、深浅睡眠期(P＜0.01,P＜0.05)方面有显著性差异,研究组对单纯药物降压没有明显效果.结论SAS引起患者微觉醒次数增多,形成片断睡眠,是非杓型血压原因之一,单纯药物治疗不能改善这些患者增高的血压.     

伴及不伴OSA高血压患者的血压变异性和OSA相关性研究

目的研究伴或不伴睡眠呼吸暂停(obstructive sleep apnea,OSA)高血压患者的血压变异性和OSA的相关性。方法纳入阴虚阳亢型轻中度高血压患者90例,对患者行便携式睡眠仪监测、24h动态血压(ABPM)监测。观察患者血压的均值、变异性,及昼夜节律和OSA的关系;采用多元逐步回归法分析OSA和血压的关系。结果与不伴OSA的高血压患者相比,伴OSA患者的血压变异性和非杓型血压发生率明显增高,夜间血压下降率明显降低(P<0.05);其中夜间平均收缩压、24h收缩压血压标准差与睡眠呼吸暂停低通气指数(apnea hypopnea index,AHI)呈正相关,夜间收缩压下降率和AHI呈负相关(P<0.05)。结论伴OSA患者的血压变异性增高,昼夜节律紊乱。     

持续气道正压通气对重度阻塞性睡眠呼吸暂停低通气综合征合并高血压患者血压及血清瘦素水平的影响研究

目的探讨持续气道正压通气(CPAP)对重度阻塞性睡眠呼吸暂停低通气综合征(OSAHS)合并高血压患者血压及血清瘦素水平的影响。方法选取我院2011年3月—2014年3月收治的资料完整的重度OSAHS合并高血压患者98例,采用随机数字表法分为对照组40例和治疗组58例。对照组患者给予常规降压药物治疗,治疗组患者在常规降压药物治疗基础上给予CPAP。观察两组患者治疗前、治疗6个月后夜间收缩压、夜间舒张压、24 h平均收缩压、24 h平均舒张压、呼吸暂停低通气指数(AHI)、最低动脉血氧饱和度(SaO2)、最长呼吸暂停时间、血清瘦素水平。结果组间比较:两组患者治疗前夜间收缩压、夜间舒张压、24 h平均收缩压、24 h平均舒张压、AHI、最低SaO2、最长呼吸暂停时间及血清瘦素水平比较,差异均无统计学意义(P0.05);治疗组患者治疗后夜间收缩压、夜间舒张压、24 h平均收缩压、24 h平均舒张压、AHI及血清瘦素水平低于对照组,最低SaO2高于对照组,最长呼吸暂停时间短于对照组(P0.05)。组内比较:对照组患者治疗后24 h平均收缩压、24 h平均舒张压较治疗前降低(P0.05),而治疗前后夜间收缩压、夜间舒张压、AHI、最低SaO2、最长呼吸暂停时间及血清瘦素水平比较,差异均无统计学意义(P0.05);治疗组患者治疗后夜间收缩压、夜间舒张压、24 h平均收缩压、24 h平均舒张压、AHI及血清瘦素水平均较治疗前降低,最低SaO2较治疗前升高,最长呼吸暂停时间较治疗前缩短(P0.05)。直线相关分析结果显示,重度OSAHS合并高血压患者治疗后24 h平均收缩压与AHI呈正相关(r=0.587,P0.05),与最低SaO2呈负相关(r=-0.519,P0.05),与血清瘦素水平呈正相关(r=0.497,P0.05)。结论在常规降压药物治疗基础上联合CAPA治疗可有效减少重度OSAHS合并高血压患者夜间间歇性低氧血症,降低交感神经兴奋性及血清瘦素水平,进而使其血压降低,有利于更好地控制血压。     

睡眠呼吸暂停综合征与隐蔽性高血压

目的探讨睡眠呼吸暂停综合征(SAS)患者中隐蔽性高血压(MH)的患病情况。方法选取171例在华北煤炭医学院附属开滦医院睡眠监测室进行检查的偶测血压正常受试者,实施多导睡眠监测并同步进行24 h动态血压监测,次日晨起后采空腹肘静脉血行血生化检查。按睡眠呼吸暂停低通气指数(AHI)<5和 AHI≥5分为非 SAS 组和 SAS 组,比较两组 MH 的患病情况,并分析 SAS 组中 MH 和非 MH 的相关指标、MH 相关因素。结果1)SAS 组101例中有54例 MH 患者,患病率为53.5%,非 SAS 组70例中有14例 MH 患者,患病率为20%,差异有非常显著意义(P<0.01)。2)SAS 组中 MH 组与非 MH 组比较,年龄较轻;体质量指数较高;吸烟和饮酒者较多;日间平均心率较高;最长呼吸暂停持续时间较长;血氧饱和度较低,但差异均无统计学意义(P>0.05)。3)MH 相关因素单因素 logistic 回归分析显示:SAS、体质量指数、吸烟和饮酒是 MH 的危险因素。结论SAS 是 MH 的危险因素,且独立于体质量指数、吸烟和饮酒之外。