Obstructive sleep apnea as a potential risk factor for aortic disease

Obstructive sleep apnea (OSA) is not only a cause of hypertension; it also possibly affects the pathogenesis and progression of aortic disease because an inspiratory effort-induced increase in negative intrathoracic pressure generates mechanical stress on the aortic wall. The objective of the present study was to examine the incidence by location of OSA as a complication in patients with aortic aneurysm and patients with aortic dissection (AD). An overnight sleep study was conducted in the following study groups: the aortic disease group (n?=?95) consisting of patients with thoracic aortic aneurysm (TAA, n?=?32), patients with abdominal aortic aneurysm (AAA, n?=?36), and patients with AD (n?=?27); and a control group (n?=?32), consisting of patients with coronary risk factors who were matched with the aortic disease group for age, gender, and body mass index (BMI). The 3% oxygen desaturation index (ODI) was significantly higher in all the TAA, AAA, and AD groups (P?=?0.045, P?=?0.003, and P?=?0.005, respectively) than in the control group. The incidence of moderate to severe OSA [apnea hypopnea index (AHI) ??15 events/h] was significantly higher in the first three groups (P?=?0.026, P?=?0.001, P?=?0.003, respectively) than in the control group, while no significant difference was found between the TAA group and the AAA group with respect to these variables. Furthermore, no significant differences were found between the thoracic AD subgroup and the abdominal AD subgroup with respect to AHI and 3% ODI, as well as with respect to the incidences of moderate to severe OSA. Patients with TAA, patients with AAA, and patients with AD showed high incidences of moderate to severe OSA. Although this result suggests that OSA may be one of risks for aortic disease, unelucidated mechanism(s) other than negative intrathoracic pressure may be involved in the pathogenesis of aortic disease.     

Obstructive sleep apnea as a risk factor for coronary events or cardiovascular death

Purpose  

This study aims to determine whether obstructive sleep apnea independently increases the risk of coronary events, including death from cardiovascular causes.     

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阻塞性睡眠呼吸暂停综合征(obstructive sleep apneasyndrome,OSAS)是由于睡眠中周期性上气道塌陷,导致呼吸暂停和(或)通气不足,引起复杂多变的低氧血症、高碳酸血症、跨胸压的异常改变及频繁的微觉醒,影响到全身多个系统或器官,其中最为突出和严重的是心脑血管并发症。因此,OS     

High risk for sleep apnea in the Berlin questionnaire and coronary artery disease

Introduction  

Obstructive sleep apnea (OSA) affects up to 30% of the adult population and is a risk factor for coronary artery disease (CAD). The diagnostic process, involving polysomnography, may be complex. Berlin questionnaire (BQ) is a validated and economical screening tool.     

Obstructive sleep apnea and cardiovascular disease

Obstructive sleep apnea (OSA) is a common disorder associated with an increased risk of cardiovascular disease and stroke. As it is strongly associated with known cardiovascular risk factors, including obesity, insulin resistance, and dyslipidemia, OSA is an independent risk factor for hypertension and has also been implicated in the pathogenesis of congestive cardiac failure, pulmonary hypertension, arrhythmias, and atherosclerosis. Obesity is strongly linked to an increased risk of OSA, and weight loss can reduce the severity of OSA. The current standard treatment for OSA-nasal continuous positive airway pressure (CPAP)-eliminates apnea and the ensuing acute hemodynamic changes during sleep. Long-term CPAP treatment studies have shown a reduction in nocturnal cardiac ischemic episodes and improvements in daytime blood pressure levels and left ventricular function. Despite the availability of effective therapy, OSA remains an underdiagnosed and undertreated condition. A lack of physician awareness is one of the primary reasons for this deficit in diagnosis and treatment.     

阻塞性睡眠呼吸暂停与心血管疾病

本文分析关于阻塞性睡眠呼吸暂停与心血管疾病之间的关系、发生发展机制的最新进展,阐述对阻塞性睡眠呼吸暂停合并心血管疾病的患者行经鼻气道持续正压通气治疗能给患者心血管疾病的治疗、预后、康复和生活质量带来益处.本篇综述的目的 在于引起医务工作者对阻塞性呼吸暂停与心血管疾病的关系的重视,从而服务于临床.     

Obstructive sleep apnea and cardiovascular disease

Obstructive sleep apnea (OSA) is a sleep-disordered breathing condition, which is increasingly being recognized as having wide-ranging pathophysiological effects on multiple organ systems. Although multiple factors affect the incidence and severity of OSA, male sex and obesity seem to play an influential role. The apnea-ventilation cycle, characterized by abnormalities in gas exchange, exaggerated respiratory effort and frequent arousals, has been shown to have deleterious effects on circulatory hemodynamics, the autonomic milieu, hormonal balance, inflammatory and coagulation cascades, endothelial function, and the redox state, with potential cardiovascular significance. Consequently, OSA is being increasingly implicated in a multitude of cardiovascular diseases (CVD) such as hypertension, congestive heart failure, atrial fibrillation, stroke, coronary artery disease, pulmonary hypertension, and metabolic syndrome. The strength of association for individual CVD is varied, and outcomes of clinical studies are conflicting. In addition, obesity, which is closely linked to both OSA and CVD, makes it harder to ascertain the independent role of OSA on CVD. Although available evidence is inconclusive, there is an increasing recognition of the direct role for OSA in CVD. Similarly, although several studies have demonstrated the cardiovascular benefits of OSA treatment, further studies are needed to confirm this.     

Obstructive sleep apnea and self-reported functional impairment in revascularized patients with coronary artery disease in the RICCADSA trial

Sleep and Breathing - Daytime sleepiness, a frequent symptom of obstructive sleep apnea (OSA), can impact functional status. In patients with coronary artery disease (CAD) and concomitant OSA, the...     

Familial premature coronary artery disease mortality and obstructive sleep apnea

BACKGROUND: Obstructive sleep apnea (OSA) is linked to both coronary artery disease (CAD) and sudden death, but any causal role remains unclear. A family history of premature CAD and related mortality is an independent risk factor for the development of CAD. We hypothesized that OSA is associated with a family history of premature mortality from ischemic heart disease. METHODS: We prospectively studied 588 subjects who underwent polysomnography from May 2000 to June 2004. Demographics, comorbidities, family history of cardiovascular disease, and the ages and causes of death for 10 strata of family members were recorded for all subjects. We excluded those subjects with known causes of premature cardiac death, such as hypertrophic cardiomyopathy and long-QT syndrome. OSA was defined by American Academy of Sleep Medicine criteria (ie, apnea-hypopnea index >or= 5). Premature CAD mortality was defined as death due to ischemic heart disease or sudden cardiac death before 55 years of age (men) or 65 years of age (women). RESULTS: Polysomnography confirmed OSA in 316 subjects and excluded it in 202 subjects. The unadjusted odds ratio (OR) for OSA and a family history of premature CAD mortality was 2.11 (95% confidence interval [CI], 1.10 to 4.31; p = 0.031). After adjusting for each subject's sex, body mass index, and history of CAD, there was a significant and independent association between OSA and family history of premature CAD mortality (OR, 2.13; 95% CI, 1.04 to 4.66; p = 0.046). CONCLUSIONS: Regardless of their own CAD status, people with OSA are more likely than those without OSA to have a family history of premature CAD mortality.     

Obstructive sleep apnea syndrome and chronic kidney disease: a new cardiorenal risk factor

Clinical and experimental studies revealed that sleep apnea might be an insidious risk factor for the progression of kidney disease and development of cardiovascular events by exacerbating well-known risk factors, namely hypertension, type 2 diabetes mellitus and obesity. Furthermore, sleep apnea also has a negative impact on endothelial function. Therefore, sleep apnea might be defined as a new cardiorenal risk factor. In this review, we aimed to summarize the evidences supporting the complex inter-relations between sleep apnea and development and progression of chronic kidney disease.     

Obstructive sleep apnea

Purpose

Attempts to understand the causes of cognitive impairment in obstructive sleep apnea (OSA) are complicated by the overlap among clinical and demographic factors that may impact cognition. The goal of the current study was to isolate the contribution of hypoxemia to cognitive impairment in OSA.

Methods

Two groups of 20 patients with newly diagnosed OSA were compared. The groups differed on severity of hypoxemia but not other demographic (e.g., age, gender, education, estimated premorbid IQ) or clinical (e.g., sleep related respiratory disturbances, daytime sleepiness, depressive symptoms) variables. Participants completed polysonmography and cognitive assessment.

Results

We compared patients with high and low hypoxemia on measures of memory, attention, executive functioning, and motor coordination using independent sample t-tests. The high hypoxemia group performed significantly better on immediate recall (Hopkins Verbal Learning Test — Revised; t?=??2.50, p?<?0.02) than the low hypoxemia group. No group differences were observed on other neuropsychological measures.

Conclusions

This study is one of the first to compare the cognitive performance of patients with high and low hypoxemia after controlling for demographic factors and aspects of OSA severity that could confound the relationship. In our carefully matched sample, we observed an unexpected advantage of higher hypoxemia on memory. These preliminary findings are discussed in the context of basic science literature on the protective effects of adaptation to intermittent hypoxemia. Our data suggest that the association between hypoxemia and cognition may not straightforward. Future research targeting the effects of hypoxemia on cognition controlling for other clinical factors in large groups of patients with OSA will be important.     

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

This chapter provides an account of obstructive sleep apnea that is designed for clinicians. Current ideas about the mechanism of upper airway obstruction are reviewed, and the clinical features are discussed in a manner intended to facilitate the clinical assessment of such patients. Various forms of treatment are reviewed, with major emphasis given to the use of nasal positive airway pressure, a form of therapy developed by the authors.     

Aortic pressure augmentation as a marker of cardiovascular risk in obstructive sleep apnea syndrome

Obstructive sleep apnea syndrome (OSAS) is associated with increases in cardiovascular morbidity and mortality. Vascular changes in individuals with OSAS have not been fully elucidated, however. The possible impact of OSAS on the extent of aortic pressure augmentation (AG), an indicator of cardiovascular risk, was investigated. Forty-five consecutive male patients aged 35 to 78 years (56.0+/-9.6 years) who were referred to the sleep clinic of Nagoya University Hospital for screening and treatment of OSAS and 71 age-matched healthy men were enrolled in the study. AG was derived from the pressure waveform measured at the radial artery by applanation tonometry. The number of apnea and hypopnea episodes per hour (apnea-hypopnea index [AHI]) was determined by standard polysomnography. AG was significantly greater in OSAS patients than in controls (9.0+/-4.1 vs. 6.4+/-3.4 mmHg, p<0.001), and it was significantly reduced in 19 OSAS patients treated with continuous positive airway pressure. AG was also significantly correlated with the AHI (r=0.562, p<0.001) and age (r=0.356, p=0.016) but not with the serum concentrations of low and high density lipoprotein-cholesterol, triglyceride, or glycosylated hemoglobin. Stepwise multiple regression analysis revealed that the AHI was the most significant contributing factor to the increased AG in OSAS patients (beta=0.109, r=0.530, p<0.001). OSAS may thus have an adverse effect on vascular function that can be ameliorated by appropriate treatment.     

睡眠呼吸暂停低通气综合征与冠状动脉粥样硬化性心脏病关系探讨

阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者中冠状动脉粥样硬化性心脏病(CAD)的发病率增高,心肌缺血事件发生频繁,CAD合并OSAHS患者预后较差,OSAHS是独立于年龄、性别、体质量指数影响CAD的发病和进展的因素.OSAHS患者全身的炎性和氧化应激反应、血液流变学改变、血液动力学改变参与了CAD的发病和进展,它们之间的确切发病机制、遗传、治疗和预后将成为今后的研究热点.     

Severity of obstructive sleep apnea and extension of coronary artery disease

Sleep and Breathing - Obstructive sleep apnea (OSA) is highly prevalent among patients with coronary artery disease (CAD). The relationship between the severity of OSA and the severity of CAD has...     

Independent association between obstructive sleep apnea and subclinical coronary artery disease

BACKGROUND: Obstructive sleep apnea (OSA) is associated with coronary risk factors, but it is unknown if OSA is associated with development of coronary disease. We evaluated the association between OSA and the presence of subclinical coronary disease assessed by coronary artery calcification (CAC). METHODS: Consecutive patients with no history of coronary disease who underwent electron-beam CT within 3 years of polysomnography between March 1991 and December 2003 were included. OSA was defined by an apnea-hypopnea index (AHI) > or = 5 events per hour, and patients were grouped by quartiles of AHI severity. Logistic regression modeled the association between OSA severity and presence of CAC. RESULTS: There were 202 patients (70% male; median age, 50 years; mean body mass index, 32 kg/m(2); 8% diabetic; 9% current smokers; 60% hypercholesterolemic; and 47% hypertensive). OSA was present in 76%. CAC was present in 67% of OSA patients and 31% of non-OSA patients (p < 0.001). Median CAC scores (Agatston units) were 9 in OSA patients and 0 in non-OSA patients (p < 0.001). Median CAC score was higher as OSA severity increased (p for trend by AHI quartile < 0.001). With multivariate adjustment, the odds ratio for CAC increased with OSA severity. Using the first AHI quartile as reference, the adjusted odds ratios for the second, third, and fourth quartiles were 2.1 (p = 0.12), 2.4 (p = 0.06), and 3.3 (p = 0.03), respectively. CONCLUSIONS: In patients without clinical coronary disease, the presence and severity of OSA is independently associated with the presence and extent of CAC. OSA identifies patients at risk for coronary disease and may represent a highly prevalent modifiable risk factor.