Obstructive sleep apnea (OSA) is an underdiagnosed condition characterized by recurrent episodes of obstruction of the upper airway leading to sleep fragmentation and intermittent hypoxia during sleep. Obesity predisposes to OSA, and the prevalence of OSA is increasing worldwide because of the ongoing epidemic of obesity. Recent evidence has shown that surrogate markers of cardiovascular risk, including sympathetic activation, systemic inflammation, and endothelial dysfunction, are significantly increased in obese patients with OSA versus those without OSA, suggesting that OSA is not simply an epiphenomenon of obesity. Moreover, findings from animal models and patients with OSA show that intermittent hypoxia exacerbates the metabolic dysfunction of obesity, augmenting insulin resistance and nonalcoholic fatty liver disease. In patients with the metabolic syndrome, the prevalence of moderate to severe OSA is very high (∼60%). In this population, OSA is independently associated with increased glucose and triglyceride levels as well as markers of inflammation, arterial stiffness, and atherosclerosis. A recent randomized, controlled, crossover study showed that effective treatment of OSA with continuous positive airway pressure for 3 months significantly reduced several components of the metabolic syndrome, including blood pressure, triglyceride levels, and visceral fat. Finally, several cohort studies have consistently shown that OSA is associated with increased cardiovascular mortality, independent of obesity. Taken together, these results support the concept that OSA exacerbates the cardiometabolic risk attributed to obesity and the metabolic syndrome. Recognition and treatment of OSA may decrease the cardiovascular risk in obese patients.

Obstructive sleep apnoea syndrome (OSAS) often coexists in patients with chronic obstructive pulmonary disease (COPD). The present prospective cohort study tested the effect of OSAS treatment with continuous positive airway pressure (CPAP) on the survival of hypoxaemic COPD patients. It was hypothesised that CPAP treatment would be associated with higher survival in patients with moderate-to-severe OSAS and hypoxaemic COPD receiving long-term oxygen therapy (LTOT).Prospective study participants attended two outpatient advanced lung disease LTOT clinics in São Paulo, Brazil, between January 1996 and July 2006. Of 603 hypoxaemic COPD patients receiving LTOT, 95 were diagnosed with moderate-to-severe OSAS. Of this OSAS group, 61 (64%) patients accepted and were adherent to CPAP treatment, and 34 did not accept or were not adherent and were considered not treated.The 5-yr survival estimate was 71% (95% confidence interval 53-83%) and 26% (12-43%) in the CPAP-treated and nontreated groups, respectively (p,0.01). After adjusting for several confounders, patients treated with CPAP showed a significantly lower risk of death (hazard ratio of death versus nontreated 0.19 (0.08-0.48)).The present study found that CPAP treatment was associated with higher survival in patients with moderate-to-severe OSAS and hypoxaemic COPD receiving LTOT.

This study was designed to evaluate the variability of the apnoea–hypopnoea index (AHI) in 20 patients with obstructive sleep apnoea–hypopnoea syndrome (OSAHS) and to determine possible relationships of this variability with other polysomnographic parameters. The subjects were recorded on four consecutive nights. The mean AHI values were not significantly altered throughout the four recording nights (P=0.67). The intraclass correlation coefficient of the AHI on the four nights was 0.92. However, the Bland and Altman plot showed that, individually, the AHI presented an important variability, which was not related to its initial value. In regard to the OSAHS severity, 50% of the patients changed the classification from the first to the subsequent nights. Thirteen of the 20 patients (65%) presented a variation in the AHI value equal or higher than 10 events h–1. When we evaluated the AHI mean values for a specific body position and sleep stage, no difference was observed among the nights. In both supine and lateral–ventral decubitus, higher AHI was observed during Stages 1 and 2 than the other stages. Additionally, the AHI during Stages 1 and 2 and REM sleep was higher on the supine than on the lateral–ventral decubitus. The AHI in OSAHS patients presented a good correlation among the four recording nights; however, a significant individual variability should be considered, especially when AHI is applied in OSAHS classification or as a criterion of therapeutic success.

Sympathetic nervous system and hypothalamic-pituitary-adrenal (HPA) axis activation may be the mechanism of this relationship. The aim of this study was to evaluate HPA axis and ambulatory blood pressure monitoring in obese men with and without OSAS and to determine whether nasal continuous positive airway pressure therapy (nCPAP) influenced responses. Twenty-four-hour ambulatory blood pressure monitoring and overnight cortisol suppression test with 0.25 mg of dexamethasone were performed in 16 obese men with OSAS and 13 obese men controls. Nine men with severe apnea were reevaluated 3 mo after nCPAP therapy. Body mass index and blood pressure of OSAS patients and obese controls were similar. In OSAS patients, the percentage of fall in systolic blood pressure at night (P ϭ 0.027) and salivary cortisol suppression postdexamethasone (P ϭ 0.038) were lower, whereas heart rate (P ϭ 0.022) was higher compared with obese controls. After nCPAP therapy, patients showed a reduction in heart rate (P ϭ 0.036) and a greater cortisol suppression after dexamethasone (P ϭ 0.001). No difference in arterial blood pressure (P ϭ 0.183) was observed after 3 mo of nCPAP therapy. Improvement in cortisol suppression was positively correlated with an improvement in apnea-hypopnea index during nCPAP therapy (r ϭ 0.799, P ϭ 0.010). In conclusion, men with OSAS present increased postdexamethasone cortisol levels and heart rate, which were recovered by nCPAP. sleep disorders; low-dose dexamethasone test; ambulatory blood pressure monitoring OBSTRUCTIVE SLEEP APNEA SYNDROME (OSAS) is receiving increased attention because it seems to be associated with a variety of long-term consequences, such as high rates of morbidity and mortality, mostly due to cardiovascular disease (23). Although obesity is the main risk factor for OSAS (39), it has been demonstrated that OSAS may increase the risk for hypertension, myocardial infarction, congestive heart failure, and stroke independently of obesity. Continuous positive airway pressure (CPAP) therapy is the treatment of choice for patients with moderate-to-severe OSAS, since it is highly effective in improving nocturnal hypoxia and sleep fragmentation, enhancing the quality of life and reducing many cardiovascular complications related to OSAS. However, the lack of acceptance and inadequate adherence to CPAP therapy remain the major causes of sleep apnea treatment failure (10,20,21,31,32).The mechanisms proposed to explain the increased cardiovascular disease in obstructive sleep apnea are under assessment. It is speculated that recurrent episodes of upper airway constriction, progressive hypoxemia, and sleep fragmentation may result in neural and metabolic changes, including activation of peripheral sympathetic activity, inflammatory pathways, and hypothalamic-pituitary-adrenal (HPA) axis, impairment of insulin sensitivity, and generation of reactive oxygen species, which could predispose to vascular damage (16,26,27,34).Sympathetic nervous system has been well demonstrated to be activated in sleep ap...

Background: Obese subjects are at increased risk of developing obstructive sleep apnea syndrome (OSAS). However, the individual role of local (i.e., upper airway-related) and general (clinical and whole-body anthropometric) characteristics in determining OSAS in obese patients is still controversial. Objectives: To contrast the clinical, anthropometric and upper airway anatomical features of obese subjects presenting or not presenting with OSAS. Methods: Thirty-seven obese (BMI ≧30 kg/m²) males with OSAS and 14 age- and gender-matched obese controls underwent clinical and anthropometric (BMI, waist-to-hip ratio and neck circumference) evaluation. In a subgroup of subjects (18 and 11 subjects, respectively), magnetic resonance imaging (MRI) during wakefulness was used to study the upper airway anatomy. Results: OSAS patients showed significantly higher BMI, waist-to-hip ratio and neck circumference as compared to controls (p < 0.05). They also referred to nonrepairing sleep, impaired attention, and previous car accidents more frequently (p < 0.05). The transversal diameter of the airways (TDAW) at the retroglossal level by MRI was found to be an independent predictor of the presence and severity of OSAS (p < 0.05). Parapharyngeal fat increase, however, was not related to OSAS. A TDAW >12 mm was especially useful to rule out severe OSAS (apnea-hypopnea index >30, negative predictive value = 88.9%, likelihood ratio for a negative test result = 0.19). Conclusions: MRI of the upper airway can be used in association with clinical and anthropometric data to identify obese males at increased risk of OSAS.