阻塞性睡眠呼吸暂停综合征与难治性高血压

阻塞性睡眠呼吸暂停综合征(OSAS)与难治性高血压关系密切,它可通过交感神经兴奋增强、内皮功能损伤、肾素-血管紧张素-醛固酮系统紊乱等机制引起血压增高,而且临床表现有自己的特点。因此,对于难治性高血压患者应注意有无OSAS以及是否给予了相应治疗。     

Obstructive sleep apnea and resistant hypertension: a case-control study

BACKGROUND: Obstructive sleep apnea syndrome (OSAS) has been linked to resistant hypertension, but the magnitude of this association and its independence of confounding have not been established. METHODS: Case patients were 63 patients with resistant hypertension (BP >or= 140/90 mm Hg using at least three BP-lowering drugs, including a diuretic), and control subjects were 63 patients with controlled BP receiving drug treatment. The primary outcome was the frequency of OSAS (apnea-hypopnea index [AHI] >or= 10 episodes per hour) determined with a portable home monitor. The comparison of AHI episodes in patients truly normotensive, truly hypertensive, and in patients with white coat or masked hypertension, based on BP determined at office and by ambulatory BP monitoring (ABPM) was a secondary outcome. RESULTS: Case patients and control subjects were well matched for confounding factors. OSAS was present in 45 case patients (71%) and in 24 control subjects (38%) [p < 0.001]. In a logistic regression model, OSAS was strongly and independently associated with resistant hypertension (odds ratio, 4.8; 95% confidence interval, 2.0 to 11.7). The AHI of case patients with normal BP in ABPM (white coat hypertension) and control subjects with abnormal BP in ABPM (masked hypertension) was intermediate between the AHI of individuals with normal and abnormal BP measures in both settings (p < 0.001). CONCLUSIONS: The magnitude and independence of the risk of OSAS for resistant hypertension strengthen the concept that OSAS is a risk factor for resistant hypertension. Comorbid OSAS should be considered in patients with resistant hypertension.     

Obstructive sleep apnea as a cause of neurogenic hypertension

Abnormalities in neural circulatory control may contribute importantly to the hypertensive state. The sympathetic nervous system in particular is a key mechanism for increasing blood pressure. Patients with obstructive sleep apnea have increased sympathetic activity. Obesity or other coexisting disease states do not explain the heightened sympathetic drive. This review examines the evidence linking sleep apnea with hypertension and the possible role of excessive sympathetic drive as a mediator of higher blood pressure in sleep apnea. Abnormalities in reflex circulatory control that could act to increase sympathetic activity in sleep apnea are also discussed.     

Obstructive sleep apnea and hypertension

There is growing evidence of a causal relationship between obstructive sleep apnea (OSA) and hypertension. Untreated OSA may have direct and deleterious effects on cardiovascular function and structure through several mechanisms, including sympathetic activation, oxidative stress, inflammation, and endothelial dysfunction. OSA may contribute to or augment elevated blood pressure levels in a large proportion of the hypertensive patient population. It is important to consider OSA in the differential diagnosis of hypertensive patients who are obese. OSA should be especially considered in those hypertensive patients who respond poorly to combination therapy with antihypertensive medications.     

Obstructive sleep apnea and hypertension

There has long been a recognized link between obstructive sleep apnea (OSA) and the cardiovascular system, no aspect of which has been more studied than blood pressure. Research in OSA has not only demonstrated dysregulation of homeostatic cardiovascular mechanisms but also has furthered our understanding of blood pressure regulatory control. Acute nocturnal blood pressure elevations associated with disordered breathing events have been reproduced from a number of observational studies, the accrual of which has also made an increasing argument for the importance of OSA in the pathogenesis of diurnal hypertension, as suggested by the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7), which implicated OSA as a secondary cause of hypertension. Accumulating data from randomized controlled treatment trials in OSA, particularly with continuous positive airway pressure, though sometimes inconsistent, suggest a potential role in blood pressure reduction. Further research is needed to better clarify indications for OSA treatment as well as its role as an adjunct to other antihypertensive treatments.     

Obstructive sleep apnea is independently associated with insulin resistance

Epidemiological studies have implicated obstructive sleep apnea (OSA) as an independent comorbid factor in cardiovascular and cerebrovascular diseases. It is postulated that recurrent episodes of occlusion of upper airways during sleep result in pathophysiological changes that may predispose to vascular diseases. Insulin resistance is a known risk factor for atherosclerosis, and we postulate that OSA represents a stress that promotes insulin resistance, hence atherogenesis. This study investigated the relationship between sleep-disordered breathing and insulin resistance, indicated by fasting serum insulin level and insulin resistance index based on the homeostasis model assessment method (HOMA-IR). A total of 270 consecutive subjects (197 male) who were referred for polysomnography and who did not have known diabetes mellitus were included, and 185 were documented to have OSA defined as an apnea-hypopnea index (AHI) > or =5. OSA subjects were more insulin resistant, as indicated by higher levels of fasting serum insulin (p = 0.001) and HOMA-IR (p < 0.001); they were also older and more obese. Stepwise multiple linear regression analysis showed that obesity was the major determinant of insulin resistance but sleep-disordered breathing parameters (AHI and minimum oxygen saturation) were also independent determinants of insulin resistance (fasting insulin: AHI, p = 0.02, minimum O(2), p = 0.041; HOMA-IR: AHI, p = 0.044, minimum O(2), p = 0.022); this association between OSA and insulin resistance was seen in both obese and nonobese subjects. Each additional apnea or hypopnea per sleep hour increased the fasting insulin level and HOMA-IR by about 0.5%. Further analysis of the relationship of insulin resistance and hypertension confirmed that insulin resistance was a significant factor for hypertension in this cohort. Our findings suggest that OSA is independently associated with insulin resistance, and its role in the atherogenic potential of sleep disordered breathing is worthy of further exploration.     

阻塞性睡眠呼吸暂停低通气综合征与高血压

阻塞性睡眠呼吸暂停低通气综合征(OSAHS)是普遍的睡眠呼吸失调,常与肥胖相伴随,发病呈增加趋势。近期研究表明,无论是否存在其它心血管病的危险因素,OSAHS都可促进高血压的发病,并增加其治疗的难度。本文就OSAHS在高血压发病中的作用机制与防治展望作一综述。     

Obstructive sleep apnea is common in patients with interstitial lung disease

Purpose

The incidence of obstructive sleep apnea (OSA) in interstitial lung disease (ILD) has been reported at different frequencies in several studies. The aims of our study were to evaluate the frequency of OSA in ILD and to analyze the relationship between polysomnography (PSG) findings and pulmonary function, disease severity, parenchymal involvement, and Epworth Sleepiness Scale (ESS) scores.

Methods

ILD patients with parenchymal involvement were evaluated. The disease severity was assessed using an index consisting of body mass index (BMI), carbon monoxide diffusion capacity, the Modified Medical Research Council dyspnea scale, and the 6-min walking distance. All of the patients had lung function, chest X-ray, PSG, ESS scoring, and an upper airway examination. Patients with a BMI?≥?30 or significant upper airway pathologies were excluded.

Results

Of 62 patients, 50 patients comprised the study group (14 male, 36 female; mean age 54?±?12.35 years, mean BMI 25.9?±?3.44 kg/m²) with diagnoses of idiopathic pulmonary fibrosis (IPF; n?=?17), stage II–III sarcoidosis (n?=?15), or scleroderma (n?=?18). The frequency of OSA was 68 %. The mean apnea–hypopnea index (AHI) was 11.4?±?12.5. OSA was more common in IPF patients (p?=?0.009). The frequency of rapid eye movement-related sleep apnea was 52.9 %. The frequency of OSA was higher in patients with a disease severity index ≥3 (p?=?0.04). The oxygen desaturation index and the AHI were higher in patients with diffuse radiological involvement (p?=?0.007 and p?=?0.043, respectively).

Conclusions

OSA is common in ILD. PSG or at minimum nocturnal oximetry should be performed, particularly in patients with functionally and radiologically severe disease.     

快速眼动睡眠期的阻塞型呼吸暂停与高血压

快速眼动(REM)睡眠期阻塞型睡眠呼吸暂停(OSA)是指发生在REM期的阻塞型睡眠呼吸暂停综合征,由于REM期交感神经活性异常增高,因此发生在此期的OSA可以使交感神经活性更高,心血管功能更不稳定。目前认为REM-OSA很可能是OSA相关高血压发生的主要原因,并且也可能是目前OSA相关高血压用持续正压通气(CPAP)治疗效果不明显的重要原因。临床工作中应重视对REM-OSA的诊断和治疗,这对OSA相关高血压的防治具有重要意义。     

Obstructive sleep apnea and hypertension: from correlative to causative relationship

Sleep-disordered breathing, manifested by repetitive episodes of partial or complete cessation of breathing during sleep associated with brief arousal and autonomic activation, is estimated to affect as many as 4% of adult men and 2% of adult women. Studies conducted during the 1980s revealed a strong association between sleep-disordered breathing and hypertension. The results of these early studies, which relied on relatively small samples of patients, have been confirmed in recent years by large-scale epidemiologic studies that are controlled for all possible confounding factors. This paper reviews the evidence suggesting a causative relationship between hypertension and disordered breathing in sleep. The authors discuss the possible underlying mechanisms of the two entities and address the clinical implications of this relationship. They conclude by recommending a proactive approach to the diagnosis of breathing disorders in sleep, in order to prevent the cardiovascular sequelae of this syndrome.     

Obstructive sleep apnea and hypertension: Mechanisms,evaluation, and management

Obstructive sleep apnea (OSA) is a recognized cause of secondary hypertension. OSA episodes produce surges in systolic and diastolic pressure that keep mean blood pressure levels elevated at night. In many patients, blood pressure remains elevated during the daytime, when breathing is normal. Contributors to this diurnal pattern of hypertension include sympathetic nervous system overactivity and alterations in vascular function and structure caused by oxidant stress and inflammation. Treatment of OSA with nasal continuous positive airway pressure (CPAP) abolishes apneas, thereby preventing intermittent arterial pressure surges and restoring the nocturnal “dipping” pattern. CPAP treatment also has modest beneficial effects on daytime blood pressure. Because even small decreases in arterial pressure can contribute to reducing cardiovascular risk, screening for OSA is an essential element of evaluating patients with hypertension.     

Obstructive sleep apnea, cardiovascular disease, and pulmonary hypertension

With the growing epidemic of obesity in an aging population, obstructive sleep apnea (OSA) is increasingly encountered in clinical practice. Given the acute cardiopulmonary stressors consequent to repetitive upper airway collapse, as well as evidence for cardiovascular homeostatic dysregulation in subjects with sleep apnea, there is ample biologic plausibility that OSA imparts increased cardiovascular risk, independent of comorbid disease. Indeed, observational studies have suggested strong associations with multiple disorders, such as systemic hypertension, heart failure, cardiac arrhythmias, and pulmonary hypertension. Further data in the form of longitudinal cohort studies and randomized controlled trials are accruing to add to the body of evidence. This review examines pathophysiologic mechanisms and explores current concepts regarding the impact of OSA and its treatment on selected clinical disease states.