阻塞性睡眠呼吸暂停患者对冠状动脉造影的心血管反应

目的观察阻塞性睡眠呼吸暂停患者对冠状动脉造影这一生理和心理应激原的心血管反应。方法回顾性分析我院2003-2005年冠状动脉造影阴性并行睡眠呼吸监测的患者83例,比较合并(OSA组)和不合并阻塞性睡眠呼吸暂停患者(No-OSA组)在冠状动脉造影前、造影中和造影后血压和心率的改变。结果共74例冠状动脉造影阴性的患者入选,其中OSA组56例和No-OSA组18例。OSA组冠状动脉造影过程中收缩压升高幅度明显高于No-OSA组(CAG过程中血压升高的百分数,分别为17.6±2.5%和6.7±4.6%,P=0.047),冠状动脉造影术后舒张压恢复延迟(P=0.018)。两组患者心率对冠状动脉造影的反应没有明显差别。应激时收缩压的升高幅度与夜间血氧饱和度小于90%持续的时间呈负相关(r=-0.222,P=0.031),与嗜睡评分呈正相关(r=0.257,P=0.028)。结论阻塞性睡眠呼吸暂停患者对冠状动脉造影这一应激原的心血管反应,收缩压过度增加,舒张压恢复延迟,与夜间低氧及睡眠片段化相关,可能在阻塞性睡眠呼吸暂停合并心血管疾病中起作用。     

阻塞性睡眠呼吸暂停低通气综合征血压变化的相关性研究

目的探讨阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者的血压变化及其相关因素。方法对206例睡眠打鼾患者行多导睡眠图(PSG)监测,其中OSAHS 168例,单纯打鼾患者38例,同时对30例无睡眠打鼾者作为正常对照组行PSG检测,分别观测各组睡前、晨起血压变化,同时对OSAHS组晨起舒张压与呼吸暂停指数、低通气指数、睡眠呼吸暂停低通气指数(AHI)、夜间最低血氧饱和度(SaO_2)、夜间平均SaO_2、SaO_2低于90%时间(T90)相关性进行分析。结果正常对照组及单纯鼾症组相比睡前、晨起血压变化不明显;OSAHS各组睡前、晨起收缩压变化不明显,而舒张压晨起较睡前明显升高,晨起舒张压变化与呼吸暂停指数、低通气指数、AHI、T90成正相关,与夜间最低SaO_2成负相关。结论 OSAHS患者血压变化主要以舒张压升高为主,睡眠呼吸紊乱对于OSAHS血压升高有着重要的意义,OSAHS可能为高血压发病的独立危险因素之一。     

基于脉搏传导时间的血压监测与阻塞性睡眠呼吸暂停的相关性性

背景：阻塞性睡眠呼吸暂停（Obstructive Sleep Apnea,OSA）与高血压密切相关。基于脉冲传输时间（Pulse Transit Time,PTT）的血压监测技术能够监测逐博血压,但目前其报道的相关临床应用较少。本研究旨在阐明基于PTT的逐博血压监测（PTT-BP）在OSA患者血压监测方面的应用价值。 方法：我们回顾性分析了解放军总医院睡眠呼吸监测中心57例疑似OSA患者,使用基于PTT技术的Ⅲ级睡眠监测仪记录睡眠监测情况和同时的血压的变化情况。血压增加指数定义为睡眠监测每小时内3-30秒内血压≥12 mmHg的瞬时升高的次数。我们将监测到的血压情况与睡眠监测参数进行比较,以发现夜间血压变化与OSA疾病的相关性。 结果：最终共50例患者的数据纳入研究,确诊OSA的患者总数为42例,平均年龄53.60±11.93岁。其中男性31例,女性11例。 OSA患者的REI指数关,ODI指数,血氧饱和度低于90%的时间占比均与血压增加指数呈显著性强相关（R=0.651, 0.633,0.714,P值均＜0.001）,最低血压饱和度与血压增加指数呈负相关（R=-0.582,P＜0.001）。中重度OSA患者在夜间血压参数上均显著性的高于轻度OSA患者（P＜0.05）：包括血压增加指数,血压增加次数,平均收缩压,最高收缩压,仰卧位收缩压,仰卧位舒张压等指标。年龄＜60岁及男性这两个因素,在平均血压升高值,最大血压升高值这两个指标方面明显高于年龄≥60岁及女性的OSA患者（P＜0.05）。 结论：基于PTT的逐博血压测定能够反映OSA患者夜间的血压升高情况。OSA的病情严重程度与夜间血压升高密切相关,低于60岁的患者和OSA患者男性在血压升高方面更加明显。     

合并阻塞性睡眠呼吸暂停的高血压患者血压变异性和靶器官损害的研究

目的阻塞性睡眠呼吸暂停（OSA）引发睡眠期间血流动力学变化,增加夜间血压变异性,加重靶器官损害,但这种影响可能受年龄的干扰。方法143例多导睡眠诊断的OSA患者分为3组：〈60岁高血压组（62例）、〈60岁正常血压组（38例）和〉60岁正常血压组（43例）,全部进行24h动态血压监测,分析白天和夜间血压变化的标准差（SD）和变异系数（CV）,在排除年龄干扰因素外,判断OSA对血压变异性的影响及靶器官的损害情况。结果与〈60岁正常血压组相比,高血压组白天和夜间血压变化SD明显增加,白天收缩压18．5和10．6mmHg（P〈O．05）;白天舒张压13．8和10．6mmHg（P〈0．05）;夜间收缩压20．5和12．6mmHg（P〈0．01）;夜间舒张压17．8和12．6mmHg（P〈O．01）。血压CV也明显增加,白天收缩压0．119和0．078（P〈0．01）;白天舒张压0．139和0．118（P〈0．05）;夜间收缩压0．137和0．111（P〈0．01）;夜间舒张压0．195和0．177（P〈O．01）。与〉60岁正常血压组相比,高血压组白天和夜间血压变化SD明显增加,白天收缩压18．5和13．3mmHg（P〈O．05）;白天舒张压13．8和10．2mmHg（P〈O．05）;夜间收缩压20．5和15．2mmHg（P〈0．01）;夜间舒张压17．8和14．2mmHg（P〈0．01）。白天收缩压CV增加（0．119和0．093;P〈O．05）;夜间收缩压和舒张压CV增加（O．137和0．123;P〈0．01;0．195和0．179;P〈0．05）。与〈60岁正常血压组相比,〉60岁正常血压组白天收缩压CV增加（0．093和0．078;P〈O．05）。与〈60或〉60岁正常血压组相比,高血压组靶器官损害增加（P〈0．01）。与〈60岁正常血压组相比,〉60岁正常血压组靶器官损害也增加（P〈0．05）。结论尽管年龄可能影响血压变异性,但是OSA对血压变异性的影响明显超过年龄的作用,并加重靶器官损害。因此,对于合并OSA的老年高血压患者更应给予足够重视。     

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。     

阻塞性睡眠呼吸暂停患者的血压变化

阻塞性睡眠呼吸暂停(Obstructive Sleep Apnea,OSA)综合征是以睡眠时反复出现上气道塌陷,引起进行性低氧、高碳酸血症及酸中毒为特征。当患者清醒时,咽喉部肌肉收缩,上气道畅通,气流恢复正常。成人中OSA的发生率约为1％～3％。一些研究发现,不论OSA患者日间血压是否升高,睡眠时可反复出现阵发性血压升高。本文综述OSA与血压变化的关系,OSA引起血压改变的机理以及与OSA相关改变的后果等问题。     

阻塞性睡眠呼吸暂停低通气综合征与心律失常及高血压的相关性研究

目的:探讨阻塞性睡眠呼吸暂停低通气综合征(OSAHS)与心律失常及高血压的相关性。方法:应用多导睡眠图监测系统(PSG)行至少7h睡眠呼吸监测,长程心电图(Holter)同步记录心电动态变化,动态血压监测仪监测24h血压波动。结果:OSAHS组心律失常及高血压的发生率明显高于对照组(P0.05),病情分度越重者,其心律失常及高血压的发生率也越高(P0.05);重度OSAHS伴高血压与单纯高血压组比较,日间平均收缩压(DABPS)、日间平均舒张压(DABPD)、夜间平均收缩压(NABPS)、夜间平均舒张压(NABPD)、血压变异率水平均具有统计学差异。结论:心律失常及高血压的发生与OSAHS的严重程度相关,是导致心血管疾病及增加心血管意外的危险因素之一。     

鼻腔CPAP和鼻腔给氧治疗阻塞性睡眠呼吸暂停对比研究的初步报告

本文比较鼻腔持续气道正压通气(CPAP)和鼻腔给氧治疗轻度阻塞性睡眠呼吸暂停(OSA)患者的疗效.受试者为8例轻度OSA 患者,均为男性,平均年龄57±4.8岁;病例选择标准为呼吸暂停+呼吸不全指数(AHI)须≥5,且至少伴有下列情况之一者:①日间过度嗜睡,多次睡眠潜伏期试验(MSLT)显示平均睡眠潜伏期≤10分钟;②高血压,收缩压>150mmHg 和(或)舒张压≥95mmHg;③重度心律失常。实验方法为:第1个月8例患者于夜间随机接受鼻腔给氧或压缩空气(4L/min)治疗;第3个月所有患者均应用鼻腔CPAP,其压力为2.5～     

阻塞性睡眠呼吸暂停低通气综合征患者血浆神经肽Y水平与睡前及晨起血压的相关性

目的 探讨阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者血浆神经肽Y(NPY)浓度与患者睡前及晨起血压水平的相关性.方法 分组:肥胖OSAHS患者32例(OSAHS组)、非OSAHS肥胖者26例(单纯肥胖组)和体质量正常的健康成人27名(正常对照组).其中OSAHS组和单纯肥胖组接受多导睡眠仪(PSG)监测.血浆NPY的浓度采用酶联免疫吸附试验(ELISA)法测定.结果 OSAHS组血浆NPY浓度显著高于单纯肥胖组(P＜0.05)及正常对照组(P＜0.01).OSAHS患者睡前舒张压、晨起收缩压及舒张压比单纯肥胖组明显升高,差异有统计学意义.相关分析显示,OSAH S组血浆NPY浓度与患者睡前舒张压、晨起收缩压及舒张压呈正相关(P值分别为0.049、0.017、0.006).结论 OSAHS组NPY水平升高,NPY对OSAHS患者血压尤其晨起血压升高起到一定促进作用.     

手术治疗伴难治性高血压的阻塞性睡眠呼吸暂停低通气综合征患者的疗效

目的探讨多平面联合手术治疗阻塞性睡眠呼吸暂停低通气综合征(OSAHS)伴难治性高血压病人的疗效。方法对36例病人行多平面联合手术,术前及术后6个月、1年和2年行多道睡眠图监测(PSG)和动态血压监测,记录血压及呼吸暂停低通气指数(AHI)、SaO2<90%的时间占总睡眠时间的百分比和最低血氧饱和度(LSaO2)等,并比较手术前后服用降压药物种类的变化。结果患者夜间的AHI、SaO2<90%的时间均较手术前显著降低,LSaO2明显提高(P<0.01)。术后6个月、1年和2年所有病人的收缩压和舒张压与术前比较均明显下降(P<0.05,P<0.01),并且所有病人的收缩压和舒张压下降幅度均超过5 mmHg。术后6个月有31例病人、术后1年有33例病人、术后2年有32例病人血压恢复正常;并且平均服用药物种类下降,术前36例病人(3.62±0.62)种,术后6个月时(2.83±0.55)种,1年时(2.78±0.72)种,2年时(2.73±0.57)种,与术前相比差异均有统计学意义(P<0.05)。结论对OSAHS伴难治性高血压病人进行多平面联合手术可有效改善血压,减少降压药物的使用。     

Refractory hypertension and sleep apnoea: effect of CPAP on blood pressure and baroreflex.

This study was undertaken to determine whether abolition of obstructive sleep apnoea (OSA) by continuous positive airway pressure (CPAP) could reduce blood pressure (BP) in patients with refractory hypertension. In 11 refractory hypertensive patients with OSA, the acute effects of CPAP on nocturnal BP were studied during sleep and its longer term effects on 24-h ambulatory BP after 2 months. During a single night's application, CPAP abolished OSA and reduced systolic BP in stage 2 sleep from 138.3 +/- 6.8 to 126.0 +/- 6.3 mmHg. There was also a trend towards a reduction in average diastolic BP (from 77.7 +/- 4.5 to 72.9 +/- 4.5). CPAP usage for 2 months was accompanied by an 11.0 +/- 4.4 mmHg reduction in 24-h systolic BP. In addition, both the nocturnal and daytime components of systolic BP fell significantly by 14.4 +/- 4.4 and 9.3 +/- 3.9 mmHg, respectively. Diastolic BP was reduced significantly at night by 7.8 +/- 3.0 mmHg. In patients with refractory hypertension, acute abolition of obstructive sleep apnoea by continuous positive airway pressure reduces nocturnal blood pressure. These data also suggest that continuous positive airway pressure may reduce nocturnal and daytime systolic blood pressure chronically. Randomised trials are needed to confirm the latter results.     

Regulation of ventilation before and after sleep in patients with obstructive sleep apnoea

The objective was to examine whether abnormal breathing during sleep may affect regulation of ventilation after awakening in patients with obstructive sleep apnoea (OSAS). In 19 patients with OSA and 12 normal subjects we examined ventilatory responses to hypoxia (HVR) and to hypercapnia (HCVR) before and after sleep (BS and AS), and compared the changes in ventilatory responses with respiratory events during sleep. In the OSA group, the values of resting ventilation were significantly smaller in AS than those in BS and end-tidal partial pressure of CO2 in arterial blood (Pco2) (PETCO2) rose significantly from BS to AS. The slopes of the HVR or HCVR did not differ between BS and AS. However, both the response lines shifted downward and minute ventilation (VE)80 (VE at arterial oxygen saturation (Sao2) of 80%) in HVR and VE60 (VE at PETCO2 of 60 mmHg) in HCVR decreased significantly from BS to AS. The percentage changes of VE80 and VE60 were significantly correlated with mean Sao2, total sleep time below Sao2 of 90% and lowest Sao2 during sleep. However, in normal subjects we observed no circadian variation in their ventilatory responses. These data support the hypothesis that repeated episodes of nocturnal hypoxia and hypercapnia may modify the regulation of ventilation after awakening in patients with OSA.     

Haemodynamic responses to obstructive sleep apnoeas in premenopausal women.

OBJECTIVES: Obstructive apnoeas during sleep are associated with marked cyclical blood pressure fluctuations in men with obstructive sleep apnoea (OSA). Haemodynamic responses to OSA in women are largely unknown. We aimed to investigate haemodynamics during apnoeic events in women with OSA and to assess the influence of the menstrual cycle on these responses. DESIGN AND METHODS: Full overnight polysomnography and continuous non-invasive blood pressure monitoring was performed in 13 women with OSA during follicular and luteal phases of the menstrual cycle. Change in blood pressure (deltaBP) from pre- to post-apnoea termination was measured for each apnoeic cycle. RESULTS: Only 10 of 13 subjects ovulated. In women who ovulated, pressor responses to apnoea termination occurred in both non-rapid eye movement (NREM) and rapid eye movement (REM) sleep, but substantially increased during the luteal phase of ovulatory cycles [NREM change in mean arterial pressure (deltaMAP) 12 +/- 3 mmHg during the follicular phase and 20 +/- 3 mmHg during the luteal phase, P < 0.001; REM deltaMAP 11 +/- 3 mmHg during the follicular phase and 23 +/- 3 mmHg during the luteal phase, P < 0.001]. Sleep apnoea severity did not change during the cycle in NREM sleep, but was reduced in REM during the luteal phase. Changes in pressor responses were absent in non-ovulating subjects. CONCLUSIONS: Obstructive apnoeas in women were associated with marked blood pressure changes, similar to those previously reported in men. While respiratory events improved slightly in the luteal phase, blood pressure responses to these events increased by approximately 100%. Thus, the menstrual cycle has discordant effects on the respiratory and cardiovascular effects of OSA in women.     

Continuous positive airway pressure improves nocturnal baroreflex sensitivity of patients with heart failure and obstructive sleep apnea

OBJECTIVES: To determine the acute effects of continuous positive airway pressure (CPAP) on baroreceptor reflex sensitivity (BRS) for heart rate during sleep in congestive heart failure (CHF) patients with obstructive sleep apnea (OSA). DESIGN AND METHODS: In eight CHF patients with OSA not previously treated with CPAP, spontaneous BRS was assessed during overnight polysomnography prior to the onset of sleep, and during stage 2 non-rapid eye movement sleep (NREM) before, during and after application of CPAP. RESULTS: CPAP alleviated OSA and acutely increased the slope of BRS (median, 25%,75%) [from 3.9 (3.5, 4.8) to 6.2 (4.6, 26.2) ms/mmHg, P<0.05]. Increases in the slope of BRS persisted following withdrawal of CPAP [4.9 (4.3, 6.9) ms/mmHg, P<0.05]. CPAP also lowered heart rate (from 81.3 +/- 4.9 to 76.0 +/- 5.7 bpm, P< 0.05), an effect which persisted after its withdrawal (76.7 +/- 5.7 bpm, P < 0.05). Systolic blood pressure at the midpoint of the pressure range of BRS sequences fell while on CPAP (from 139 +/- 8 to 120 +/- 7 mmHg, P < 0.05), and remained lower following CPAP withdrawal (124 +/- 9 mmHg, P < 0.05). CONCLUSIONS: In CHF patients with OSA, CPAP increases acutely BRS during sleep, lowers heart rate and resets the operating point for BRS to a lower blood pressure. These effects of CPAP persist after its withdrawal, suggesting that nocturnal CPAP therapy may cause sustained improvement in the neural control of heart rate.     

Treatment of obstructive sleep apnoea with nasal continuous positive airway pressure in stroke.

The prevalence of obstructive sleep apnoea (OSA) following stroke is high and OSA is associated with increased morbidity, mortality and poor functional outcome. Nasal continuous positive airway pressure (nCPAP) is the treatment of choice for OSA, but its effects in stroke patients are unknown. The effectiveness and acceptance of treatment with nCPAP in 105 stroke patients with OSA, admitted to rehabilitation was prospectively investigated. Subjective wellbeing was measured with a visual analogue scale in 41 patients and 24-h blood pressure was determined in 16 patients before and after 10 days of treatment. Differences were compared between patients who did and did not accept treatment. There was an 80% reduction of respiratory events with concomitant increase in oxygen saturation and improvement in sleep architecture. No serious side-effects were noticed. Seventy-four patients (70.5%) continued treatment at home. Nonacceptance was associated with a lower functional status, as measured by the Barthel Index, and the presence of aphasia. Ten days after initiation of nCPAP, compliant users showed a clear improvement in wellbeing (differences in visual analogue scale (deltaVAS) mean+/-SD 26+/-26 mm) versus noncompliant patients (deltaVAS 2+/-25 mm, p=0.021). Only the compliant group had a reduction in mean nocturnal blood pressure (deltaBP; -8+/-7.3 mmHg versus 0.8+/-8.4 mmHg, p=0.037). Stroke patients with obstructive sleep apnoea can be treated effectively with nasal continuous positive airway pressure and show a similar improvement and primary acceptance to obstructive sleep apnoea patients without stroke. Continuous positive airway pressure acceptance is associated with improved wellbeing and decreased nocturnal blood pressure.     

Baroreflex control of heart rate during sleep in severe obstructive sleep apnoea: effects of acute CPAP.

Baroreflex control of heart rate during sleep (baroreflex sensitivity; BRS) has been shown to be depressed in obstructive sleep apnoea (OSA), and improved after treatment with continuous positive airway pressure (CPAP). Whether CPAP also acutely affects BRS during sleep in uncomplicated severe OSA is still debatable. Blood pressure was monitored during nocturnal polysomnography in 18 patients at baseline and during first-time CPAP application. Spontaneous BRS was analysed by the sequence method, and estimated as the mean sequence slope. CPAP did not acutely affect mean blood pressure or heart rate but decreased cardiovascular variability during sleep. Mean BRS increased slightly during CPAP application (from 6.5+/-2.4 to 7.5+/-2.9 ms x mmHg(-1)), mostly in response to decreasing blood pressure. The change in BRS did not correlate with changes in arterial oxygen saturation or apnoea/hypopnoea index. The small change in baroreflex control of heart rate during sleep at first application of continuous positive airway pressure in severe obstructive sleep apnoea was unrelated to the acute resolution of nocturnal hypoxaemia, and might reflect autonomic adjustments to positive intrathoracic pressure, and/or improved sleep architecture. The small increase in baroreflex control of heart rate during sleep may be of clinical relevance as it was accompanied by reduced cardiovascular variability, which is acknowledged as an independent cardiovascular risk factor.     

Circadian rhythm of blood pressure in patients with obstructive sleep apnea.

AIMS: The aims of this study were to examine the circadian variation in blood pressure (BP) in obstructive sleep apnea (OSA) and to compare this between normotensive and hypertensive subjects. METHODS: We measured 24-hour ambulatory BP (ABP) in 72 men (mean age 51 +/- 8 years), with OSA diagnosed on overnight sleep study. Measurements of BP were made at 15 min intervals for 24 h using either an Oxford Medilog ABP or Spacelabs 90207 recorder. All recordings were performed after > or = 3 week washout of anti-hypertensive drugs. The day-time monitoring period was defined as 07:00 hrs to 22:00 and night-time 22:00 to 07:00. The ratio of night:day systolic and diastolic BP was calculated. RESULTS: The patients were obese (mean body mass index 33 +/- 5 kg/m2) with a central pattern of obesity (waist:hip ratio 0.99 +/- 0.14, normal < 0.94). The mean 24-h ABP (systolic/diastolic) was 138 +/- 18/88 +/- 12 mmHg. The mean daytime ABP was 143 +/- 18/93 +/- 12 and night-time ABP 128 +/- 20/80 +/- 12 Hg. The night:day BP ratio was 0.90 +/- 0.07 (systolic) and 0.87 +/- 0.09 (diastolic) indicating that average BP was lower during the night. This pattern was similar in normotensive and hypertensive subjects. In contrast there was a significant relationship between increasing BMI and night:day blood pressure ratio (r = 0.56, p < 0.001) independent of the effects of OSA. CONCLUSION: In contrast to previous studies, men with OSA have a normal diurnal pattern of blood pressure levels. These findings suggest that any influence of OSA on BP is manifested throughout the 24-h period.     

Meta‐analysis of changes in the levels of catecholamines and blood pressure with continuous positive airway pressure therapy in obstructive sleep apnea

Stress from obstructive sleep apnea (OSA) stimulates catecholamine release consequently exacerbating hypertension. However, different studies have shown a conflicting impact of continuous positive airway pressure (CPAP) treatment in patients with OSA on catecholamine levels and blood pressure. We aimed to examine changes to catecholamine levels and blood pressure in response to CPAP treatment. We conducted a meta‐analysis of data published up to May 2020. The quality of the studies was evaluated using standard tools for assessing the risk of bias. Meta‐analysis was conducted using RevMan (v5.3) and expressed in standardized mean difference (SMD) for catecholamines and mean difference (MD) for systolic (SBP) and diastolic blood pressure (DBP). A total of 38 studies met our search criteria; they consisted of 14 randomized control trials (RCT) totaling 576 participants and 24 prospective cohort studies (PCS) of 547 participants. Mean age ranged between 41 and 62 year and body mass index between 27.2 and 35.1 kg/m². CPAP treatment reduced 24‐hour urinary noradrenaline levels both in RCT (SMD = −1.1; 95% confidence interval (CI): −1.63 to − 0.56) and in PCS (SMD = 0.38 (CI: 0.24 to 0.53). SBP was also reduced by CPAP treatment in RCT (4.8 mmHg; CI: 2.0‐7.7) and in PCS (7.5 mmHg; CI: 3.3‐11.7). DBP was similarly reduced (3.0 mmHg; CI: 1.4‐4.6) and in PCS (5.1 mmHg; CI: 2.3‐8.0). In conclusion, CPAP treatment in patients with OSA reduces catecholamine levels and blood pressure. This suggests that sympathetic activity plays an intermediary role in hypertension associated with OSA‐related stress.     

Blood pressure changes after automatic and fixed CPAP in obstructive sleep apnea: relationship with nocturnal sympathetic activity

Treatment of obstructive sleep apnea (OSA) by continuous positive airway pressure (CPAP) usually causes a reduction in blood pressure (BP), but several factors may interfere with its effects. In addition, although a high sympathetic activity is considered a major contributor to increased BP in OSA, a relationship between changes in BP and in sympathetic nervous system activity after OSA treatment is uncertain. This study was undertaken to assess if, in OSA subjects under no pharmacologic treatment, treatment by CPAP applied at variable levels by an automatic device (APAP) may be followed by a BP reduction, and if that treatment is associated with parallel changes in BP and catecholamine excretion during the sleep hours. Nine subjects underwent 24-h ambulatory BP monitoring and nocturnal urinary catecholamine determinations before OSA treatment and 2 months following OSA treatment by APAP (Somnosmart2, Weinmann, Hamburg, Germany). Eight control subjects were treated by CPAP at a fixed level. After APAP treatment, systolic blood pressure (SBP) decreased during sleep (p < 0.05), while diastolic blood pressure (DBP) decreased both during wakefulness (p < 0.05) and sleep (p < 0.02). Similar changes were observed in subjects receiving fixed CPAP. Nocturnal DBP changes were correlated with norepinephrine (in the whole sample: r = .61, p < 0.02) and normetanephrine (r = .71, p < 0.01) changes. In OSA subjects under no pharmacologic treatment, APAP reduces BP during wakefulness and sleep, similarly to CPAP. A reduction in nocturnal sympathetic activity could contribute to the reduction in DBP during sleep following OSA treatment.     

High prevalence of unrecognized sleep apnoea in drug-resistant hypertension.

OBJECTIVES: To determine the prevalence of obstructive sleep apnoea (OSA) in adult patients with drug-resistant hypertension, a common problem in a tertiary care facility. DESIGN: Cross-sectional study. SETTING: University hypertension clinic. PATIENTS AND METHODS: Adults with drug-resistant hypertension, defined as a clinic blood pressure of > or = 140/90 mmHg, while taking a sensible combination of three or more antihypertensive drugs, titrated to maximally recommended doses. Each of the 41 participants completed an overnight polysomnographic study and all but two had a 24 h ambulatory blood pressure measurement. RESULTS: Prevalence of OSA, defined as an apnoea-hypopnoea index of > or = 10 obstructive events per hour of sleep, was 83% in the 24 men and 17 women studied. Patients were generally late middle-aged (57.2 +/- 1.6 years, mean +/- SE), predominantly white (85%), obese (body mass index, 34.0 +/- 0.9 kg/m2) and taking a mean of 3.6 +/- 0.1 different antihypertensive medications daily. OSA was more prevalent in men than in women (96 versus 65%, P = 0.014) and more severe (mean apnoea-hypopnoea index of 32.2 +/- 4.5 versus 14.0 +/- 3.1 events/h, P = 0.004). There was no gender difference in body mass index or age. Women with OSA were significantly older and had a higher systolic blood pressure, lower diastolic blood pressure, wider pulse pressure and slower heart rate than women without OSA. CONCLUSIONS: The extraordinarily high prevalence of OSA in these patients supports its potential role in the pathogenesis of drug-resistant hypertension, and justifies the undertaking of a randomized controlled trial to corroborate this hypothesis.