Effect of nasal valve dilation on effective CPAP level in obstructive sleep apnea

Nasal problems are frequent at high continuous positive airway pressure (CPAP). We hypothesized that a reduction of the nasal resistance reduces CPAP and investigated the effect of a nasal valve dilator (Nozovent) on CPAP in patients with obstructive sleep apnea. In a randomized cross-over design Nozovent was inserted in 38 patients during one of two nights using AutoSet T. CPAP differences > 1 cm H2O were considered as clinically relevant. With Nozovent the median CPAP pressure was reduced from 8.6 cm H2O to 8.0 H2O (P = 0.023) in all patients, but the number of patients with a reduction of CPAP by 1 cm H2O was not significant. The median CPAP level among 20 patients requiring a CPAP level of above 9 cm H2O was reduced from 10.3 to 9.1 cm H2O, P < 0.05. A clinical improvement with Nozovent was seen in 10 of 20 patients requiring a pressure of above 9 cm H2O compared with 4 of 18 patients who needed lower pressures, P = 0.025. Nozovent reduces the CPAP level 1 cm H2O in 50% of patients requiring a high pressure (> 9 cm H2O). Future studies should identify possible patients benefiting from a nasal dilator during CPAP therapy.     

Effect of nasal-valve dilation on obstructive sleep apnea

OBJECTIVE: Nasal-valve dilation reduces nasal resistance and increases air flow. It is possible that this mechanism prevents hypopharyngeal collapse and sleep apneas. We investigated the effect of a plastic device (Nozovent; Prevancure AB; V?stra Fr?lunda, Sweden)-which dilates the nasal valve-on patients with obstructive sleep apnea (OSA). DESIGN: Prospective interventional study. SUBJECTS: Twenty-six consecutive patients with OSA were included (22 men; mean +/- SD age, 54.8+/-11.3 years; respiratory disturbance index [RDI], 34.4+/-18.5 events/h; body mass index, 31.6+/-5.7 kg/m(2)). INTERVENTION: The nasal dilator was inserted during sleep into the nares and fitted to exert a dilating force on the nasal valves by means of its elasticity. MEASUREMENTS: Polysomnographic studies were performed before and after 1 month of treatment. A responder is defined as one with a reduction in RDI to < 50% of the baseline value and RDI of < or =10 events/h during treatment. RESULTS: Five patients dropped out. As a result, only 21 patients were analyzed. Four patients responded, and 17 patients were nonresponders. In the whole population, neither the mean values for respiration during sleep nor sleep staging changed significantly with the device. CONCLUSIONS: The investigated nasal dilator had no effect on sleep-related breathing disorders in patients with moderate to severe OSA. The reduction in nasal resistance does not prevent hypopharyngeal obstruction.     

Operative timing for absent pulmonary valve with obstructive sleep apnea

Congenital absence of the pulmonary valve appears to have a prolonged fate, despite substantial regurgitation, thus the optimal timing of surgical correction remains unclear. A 53-year-old man with isolated pulmonary regurgitation accompanied by obstructive sleep apnea developed progressive heart failure after reopening of the foramen ovale. Closure of the interatrial shunt and pulmonary valve replacement with a 25-mm mechanical prosthesis relieved his refractory left heart failure.     

Effect of supine knee position on obstructive sleep apnea

We previously reported a case of a middle-aged man whose obstructive sleep apnea (OSA) was virtually eliminated when he slept in the supine "knees up" position. In this study, we attempt to replicate this phenomenon in a group of volunteers with previously diagnosed OSA. Results indicated no significant improvement in OSA when sleeping supine knees up. Examination of distribution of within subjects' change [calculated as Respiratory Disturbance Index (RDI) in the "knees down" position vs RDI in the knees up position] indicated a trend for improvement in the latter (p=0.12, two-tailed probability). These results suggest that knee position is unlikely to be a robust intervention for OSA though they allow for the possibility that some patients may have a moderation of their condition by such a manipulation.     

睡眠呼吸暂停低通气综合征问卷对阻塞性睡眠呼吸暂停综合征诊断价值

目的 评价阻塞性睡眠呼吸暂停低通气综合征(OSAHS)的流行病学调查表筛查价值.方法 疑似OSAHS的987例患者为研究对象,按照中华医学会呼吸病学分会睡眠学组睡眠呼吸暂停低通气综合征流行病学调查表进行问卷并行多导睡眠监测.将此问卷表进行量化评分,用克隆巴赫信度系数(α系数)进行信度计算,将各相关因素做方差分析及x2检验,筛选出有统计学意义的因素最后做Logistic回归分析.以鼾声中度以上的打鼾及体质量指数≥25 kg/m2为高危,反之为低危,进行敏感性,特异性,假阳性,假阴性,阳性似然比,阴性似然比,阳性预测值等.结果 疑似OSAHS患者987例,其中男800例(81.05％),女187例(18.95％),年龄18～80岁,平均(47±12)岁,平均体质量指数(29±5) kg/m2.＞60岁者156例(15.81％),≤60岁者831例(84.19％).克隆巴赫信度系数(Cronbach'salpha)是0.803,假阳性者20,假阴性者142,真阳性者742,真阴性者83,问卷的敏感性是83.94％,特异性是80.58％,假阳性率19.42％,假阴性率16.06％,阳性似然比4.32,阴性似然比0.20,阳性预测值0.97,阴性预测值0.37,正确率83.59％.结论 该睡眠调查表对OSAHS筛查具有一定意义,可用于临床OSAHS的初筛,尤其适合在社区和基层医院中推广使用.     

Quantitation of mitral valve tenting in ischemic mitral regurgitation by transthoracic real-time three-dimensional echocardiography

OBJECTIVES: We sought to investigate the geometric changes of the mitral leaflets and annulus, clarify the maximum tenting site of the leaflets, and quantify the valve tenting in ischemic mitral regurgitation (MR) using three-dimensional (3D) echocardiography. BACKGROUND: Although the understanding of the mechanisms of ischemic MR has advanced recently, the geometric changes of the mitral leaflets and annulus have been assessed by two-dimensional echocardiography in the clinical setting, despite the unique configuration of the leaflets and annulus. METHODS: Utilizing real-time 3D echocardiography, we obtained transthoracic volumetric images in 12 patients with ischemic MR presenting with global left ventricular dysfunction and in 10 controls. Original software was used to crop the 3D data into 18 radial planes, and we marked the mitral annulus and leaflets in each plane in mid-systole. The 3D images of the leaflets and annulus were reconstructed for the quantitative measurements. RESULTS: In ischemic MR, the annulus flattened with apparent tenting of the leaflets. Maximum and mean tenting length were longer and tenting volume was larger in ischemic MR than control subjects (maximum tenting length: 9.8 +/- 2.0 mm vs. 3.1 +/- 1.2 mm, p < 0.0001, mean tenting length: 3.7 +/- 0.9 mm vs. 0.7 +/- 0.5 mm, p < 0.0001, tenting volume: 4.09 +/- 1.22 ml vs. 0.45 +/- 0.29 ml, p < 0.0001). The maximum tenting site was located in anterior leaflet in all patients. CONCLUSIONS: We clearly demonstrated 3D geometric deformity of the mitral leaflets and annulus in ischemic MR using novel software for creating images by 3D echocardiography. This technique will be helpful in making a proper decision for the surgical strategy in each patient.     

OSAHS对血管内皮功能变化的影响

目的探讨OSAHS对血管内皮功能变化的影响。方法选取OSAHS患者80例(OSAHS组),分为轻度15例,中度41例,重度24例,体检肥胖者30例(对照组),检测血清ET-1、NO、ADM水平。结果 OSAHS组NO低于对照组(P0.05),ET-1、ADM高于对照组(P0.05),中度、重度患者NO高于轻度(P0.05),重度高于中度(P0.05),ET-1、ADM中度及重度低于轻度(P0.05),重度低于中度(P0.05);治疗后AHI、ET-1、ADM下降(P0.05),SaO2、NO升高(P0.05);OSAHS患者NO与AHI存在负相关(P0.05),ET-1、ADM与AHI存在正相关(P0.05)。结论 OSAHS中重度患者明显存在血管内皮功能受损。     

阻塞性睡眠呼吸暂停对冠状动脉粥样硬化斑块的影响

目的 探讨阻塞性睡眠呼吸暂停(OSAS)对冠状动脉粥样硬化斑块的影响.方法 126例老年冠心病(CAD)患者根据多导睡眠仪监测结果,分为OSAS合并CAD组(62例)、无OSAS组(64例).所有患者常规清晨空腹卧位取静脉血测定测定胆固醇(TC)、三酰甘油(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、血常规白细胞计数、中性粒细胞分类及血清(hs-CRP)水平.根据冠状动脉造影术、64层螺旋CT检查结果记录OSAS合并CAD组、无OSAS组冠状动脉病变、Gensini评分及粥样硬化斑块情况.结果 CAD合并OSAS组TC、TG、LDL-C分别为(5.76+0.85)mmol/L、(3.37±0.97)mmol/L、(3.65±0.58)mmol/L,HDL-C为(1.06±0.20)mmol/L,无OSAS组TC、TG、LDL-C分别为(4.26±0.78)mmol/L、(1.72±0.54)mmol/L、(2.91±0.58)mmol/L,HDL-C为(1.13±0.14)mmol/L,CAD合并OSAS组TC、TG、LDL-C均高于无OSAS组(t值分别为2.959、3.556、2.165,P<0.05),HDL-C低于无OSAS组(t=2.545,P<0.05);OSAS合并CAD组患者血白细胞数、中性粒细胞百分比及hs-CRP水平较无OSAS组明显增高(P<0.05);OSAS合并CAD组冠状动脉多支病变发生率为51%,Gensini积分为(23.6±20.7)分,冠状动脉软斑块为(67.6+9.7)个,无OSAS组分别为30%,(18.9±19.4)分,(39.3±9.4)个,两组比较差异有统计学意义(t值分别为5.39,2.048,19.001,P<0.05).结论 OSAS和冠状动脉粥样硬化性心脏病密切相关,促进冠状动脉粥样硬化斑块的形成.     

阻塞性睡眠呼吸暂停低通气综合征对心脏的影响

目的:探讨阻塞性睡眠呼吸暂停低通气综合征(OSAHS)对心血管事件的影响。方法:对237例OSAHS患者与228例健康者的心率变异性(HRV)、24h动态心电图及超声心动图进行对比分析。结果:对照组与OSAHS组间比较,HRV各指标差异有统计学意义(P<0.01);室性期前收缩、房室传导阻滞、窦性停搏发生次数差异有统计学意义(P<0.01);左室质量及质量指数差异有统计学意义(P<0.01)。结论:OSAHS可引起严重的HRV、心律失常及左室质量增加。     

Effect of musculoskeletal pain on sleep architecture in patients with obstructive sleep apnea

Rationale

Obstructive sleep apnea and chronic musculoskeletal pain both affect sleep. Sleep architecture of patients suffering from both is largely unknown.

Objectives

This study seeks to define the sleep architecture of patients with chronic musculoskeletal pain and obstructive sleep apnea.

Methods

Patients with obstructive sleep apnea diagnosed by sleep study during the past 3 years were included. Patients with clinical documentation of chronic musculoskeletal pain constituted cases, while others were classified as controls.

Measurements

Demographics, clinical factors affecting sleep, medications affecting sleep, Epworth sleepiness scores, and polysomnographic parameters; total sleep time, sleep efficiency, sleep stages, rapid eye movement (REM) sleep onset, apnea–hypopnea index, arousal index, and periodic leg movements were recorded.

Results

There were 393 subjects: 200 cases (obstructive sleep apnea and chronic musculoskeletal pain) and 193 controls (obstructive sleep apnea alone). There was significant difference in total sleep time (274.5?±?62.5 vs. 302.2?±?60.1 min, p?=?0.0001), sleep efficiency (73.54?±?15.8 vs. 78.76?±?14.3 %, p?=?0.0003), and REM sleep onset (148.18?±?80.5 vs. 124.8?±?70.9 min, p?=?0.006). Subgroup analysis within the obstructive sleep apnea with chronic musculoskeletal pain group revealed that subjects had better total sleep time and sleep efficiency if they were on REM sleep affecting medications (suppressants and stimulants). Those on REM sleep suppressants slept 25.7 min longer and had 6.4 % more efficient sleep than those not on REM suppressants (p?=?0.0034 and p?=?0.0037).

Conclusion

Patients with obstructive sleep apnea and chronic musculoskeletal pain sleep not only significantly less but also with inferior sleep quality. Their REM sleep is also less in duration and its onset is delayed. Despite low TST and SE, these patients may not exhibit sleepiness.     

Pathogenesis of obstructive sleep apnea

Obstructive sleep apnea is a fairly common disorder with significant adverse health consequences. However, the pathogenetic mechanisms remain incompletely understood. Upper airway (UA) patency is determined by several neuromuscular and nonneuromuscular factors including (1) UA dilating muscle activity, (2) the collapsing transmural pressure generated during inspiration, (3) changes in caudal traction, (4) vasomotor tone, and (5) mucosal adhesive forces. This review addresses the effect of sleep on UA function and how these factors conspire to cause UA obstruction.     

Pathophysiology of obstructive sleep apnea

The pharyngeal muscles are essential for effective lung ventilation because they help maintain an open upper airspace for the unhindered passage of air into the lungs. Sleep, especially rapid-eye-movement sleep, however, causes fundamental modifications of pharyngeal muscle tone and reflex responses that in normal individuals lead to airway narrowing and hypoventilation. In individuals with already anatomically narrow upper airways, these effects of sleep predispose them to inspiratory flow limitation (hypopneas), airway closure, and obstructive sleep apnea. Obstructive sleep apnea is a common disorder affecting at least 2% to 4% of North American adults and is associated with serious clinical, social, and economic consequences. This review addresses the physiology and pathophysiology of obstructive sleep apnea, hypopneas, and snoring, that is, the full spectrum of the most common sleep-related breathing events involving the upper airway. Specifically, the anatomical features of the upper airway that are important to its mechanical properties and degree of collapsibility are reviewed. The sites of airway narrowing and closure and the implications for common treatments strategies are also discussed. This article also focuses on the neuromuscular control mechanisms operating in wakefulness and sleep that influence pharyngeal muscle tone and upper airway collapsibility. The effects of sleep on the reflex mechanisms that normally operate to protect the upper airspace from suction collapse during breathing are also addressed. Throughout this review, these mechanisms are discussed with an emphasis on understanding the physiology and pathophysiology of sleep-disordered breathing and obstructive sleep apnea.     

Effect of obstructive sleep apnea on the response to hypertension therapy

Obstructive sleep apnea (OSA) often precedes cardiovascular disease, partly due to treatment resistant hypertension. The nocturnal apneas of OSA trigger increased sympathetic nervous discharge during both sleep and wakefulness. Apneas also trigger cardiac release of the endogenous diuretic atrial natriuretic peptide. We hypothesized that treatment of the excess sympathetic nervous activity of OSA with a β₁ blocker would lower 24 h blood pressure (BP) more than diuretic therapy. Subjects with OSA associated hypertension received 2 weeks of placebo followed by the β₁ blocker nebivolol or hydrochlorothiazide (HCTZ) for 6 weeks in a blinded crossover study. BP, baroreflex sensitivity (BRS), heart rate variability (HRV), arterial reactivity, and stiffness were measured after placebo and each treatment. The β₁ blocker lowered clinic BP by ?11/?8 mmHg, more than the ?3/?1 effect of HCTZ (P < 0.01). The β₁ blocker lowered 24 h diastolic blood pressure (DBP) more than HCTZ. Although given at bedtime, neither drug increased BP dipping. Nebivolol increased HRV in the high-frequency band. Nebivolol did not alter BRS while HCTZ significantly diminished BRS compared to nebivolol (P < 0.01). Nebivolol increased flow-mediated brachial artery dilation when compared to HCTZ and slowed pulse wave velocity, indicating a decrease in arterial stiffness.

Diuretic therapy failed to lower BP in OSA subjects and this might account for the frequent association of OSA with treatment resistant hypertension. However, blockade of the excess sympathetic nervous activity of OSA with a β₁ blocker lowered both clinic and 24 h DBP.     

阻塞性睡眠呼吸暂停对高血压患者血管内皮影响研究

目的 回顾性分析高血压合并阻塞性睡眠呼吸暂停综合征(OSAS)患者的预后及影响因素.方法 对2004年1月至2007年10月江苏省省级机关医院确诊的高血压病患者共168例,通过电话和门诊随访,随访时间中位数35个月.根据多导睡眠仪监测结果 分为:高血压合并OSAS(OSAS+)组和高血压不合并OSAS(OSAS-)组.所有患者均通过彩色多普勒超声测定肱动脉血流介导的舒张功能(FMD),并测定与高血压预后相关的血清生化指标.随访患者心血管死亡、心绞痛或心肌梗死、脑卒中等事件.结果 OSAS+组患者血清超敏C反应蛋白(hsCRP)水平高于OSAS-组,(2.49±2.65)mmol/Lvs(1.73±1.76)mmol/L(P<0.05),FMD值低于OSAS-组,(6.20±3.40)%vs(8.39±3.86)0A(P<0.05).OSAS+组患者总事件发生率高于OSAS-组(28.8%A vs 13.7%,P=0.016).Logistic多因素回归分析显示:FMD主要损伤因素排名首位是OSAS(OR=2.89,P=0.003),其次是血清hsCRP(OR=1.23,P=0.044);FMD、血清hsCRP及尿酸成为高血压患者预后的影响因子(OR=1.7,1.7,3.5,P=0.03,0.00,0.01).结论 OSAS影响高血压患者血管内皮功能,使总的事件(心脑血管原因导致的死亡、心绞痛或心肌梗死和脑卒中)发生率增加.OSAS可能主要通过损伤血管内皮功能间接影响高血压患者的预后.     

Hypertension and obstructive sleep apnea

Obstructive sleep apnea is a common disorder that is often unrecognized and underappreciated. Emerging evidence suggests that there is a causal link between obstructive sleep apnea and hypertension. This relationship appears to be independent of other comorbidities that have been previously linked to hypertension, such as obesity. The majority of studies support the contention that alleviation of sleep disordered breathing has a clinically significant beneficial impact on decreasing both nighttime and daytime blood pressure. A pathophysiologic basis for patients with sleep apnea having an increased risk for hypertension is not fully elucidated. However, there is consistent evidence that autonomic mechanisms are implicated. Sympathetic activation along with humoral responses to repetitive episodes of hypoxemia and apnea over the longer term may cause vasoconstriction, endothelial dysfunction, and possibly hypertension. Patients with sleep apnea are often obese and may be predisposed to weight gain. Hence, obesity may further contribute to hypertension in this patient population.     

Myxedema and obstructive sleep apnea

Three cases of hypersomnolence, snoring and documented sleep apnea are reported. All three patients were profoundly myxedematous, both clinically and biochemically. Polygraphic studies during sleep documented the presence of repetitive episodes of obstructive sleep apnea in all three patients. These were accompanied by arterial oxygen desaturation. After becoming euthyroid following the administration of the l-thyroxine all patients underwent a repeat evaluation in the sleep laboratory. These studies revealed nearly complete resolution of obstructive sleep apnea in all patients. In addition, several sleep parameters showed marked improvement. These data strongly suggest that the presence of profound daytime sleepiness in hypothyroid patients could be indicative of a potentially lethal complication of myxedema, obstructive sleep apnea.     

Coagulability in obstructive sleep apnea

BACKGROUND:

Obstructive sleep apnea (OSA) is a common disorder that affects both quality of life and cardiovascular health. The causal link between OSA and cardiovascular morbidity/mortality remains elusive. One possible explanation is that repeated episodes of nocturnal hypoxia lead to a hypercoagulable state that predisposes patients to thrombotic events. There is evidence supporting a wide array of hematological changes that affect hemostasis (eg, increased hematocrit, blood viscosity, platelet activation, clotting factors and decreased fibrinolytic activity).

OBJECTIVE:

To provide a comprehensive review of the current evidence associating OSA with increased coagulability, and to highlight areas for future research.

METHODS:

Keyword searches in Ovid Medline were used to identify relevant articles; all references in the articles were searched for relevant titles. The Web of Science was used to identify articles citing the relevant articles found using the Ovid Medline search. All original peer-reviewed articles, meta-analyses and systematic reviews regarding the pertinent topics between 1990 and present were selected for review.

RESULTS:

Hematocrit, blood viscosity, certain clotting factors, tissue factor, platelet activity and whole blood coagulability are increased in patients with OSA, while fibrinolysis is impaired.

CONCLUSION:

There is considerable evidence that OSA is associated with a procoagulant state. Several factors are involved in the procoagulant state associated with OSA. There is a need for adequately powered clinical studies involving well-matched control groups to address potential confounding variables, and to accurately delineate the individual factors involved in the procoagulant state associated with OSA and their response to treatment.