CPAP Is Not Needed in Every Sleep Apnea Patient Awaiting Bariatric Surgery.

BACKGROUND: Obstructive sleep apnea (OSA) patients are at high risk of postoperative complications following bariatric surgery. The aim of our study was to compare peri- and postoperative outcomes in OSA patients awaiting laparoscopic bariatric surgery who were prescribed CPAP treatment or not before surgery using nocturnal home oximetry and capillary blood gas measurements. METHODS: Data on 1094 eligible patients were analyzed. In accordance with our algorithm, those with ODI < 25/h and pCO2 < 45 mmHg (358 mild/moderate apnea and 447 non-apneic) underwent surgery without previous treatment, whereas those with an ODI ≥ 25/h (n = 289) were prescribed CPAP. We compared peri- and postoperative outcomes in treated and untreated patients. RESULTS: Treated patients were significantly older with a higher body mass index and a higher percentage of men than non-apneic and untreated OSA. Hypertension and diabetes were significantly more prevalent in the treated and untreated OSA patients than in the non-apneic. Regarding the occurrence of cardiopulmonary complications, the incidence of cardiac arrhythmia was higher in the treated patients than in the non-apneic and the untreated OSA (2.4%; 0.6 and 0.5%, p = 0.03). The slightly longer length of hospital stay seen in treated patients compared to those of other groups (2.8 ± 1.7; 2.6 ± 2.1 and 2.6 ± 1.8 days, p = 0.03) was no longer observed after adjusting for age and BMI. CONCLUSIONS: There is no risk increase for complications following bariatric surgery in untreated patients presenting mild/moderate OSA identified by a noninvasive screening algorithm.

Ventilatory support or respiratory muscle training as adjuncts to exercise in obese CPAP-treated patients with obstructive sleep apnoea: a randomised controlled trial.

BACKGROUND: Obstructive sleep apnoea (OSA) and obesity are interdependent chronic diseases sharing reduced exercise tolerance and high cardiovascular risk. INTERVENTION: A 3-month intervention with innovative training modalities would further improve functional capacity and cardiovascular health than usual cycle exercise training in already continuous positive airway pressure (CPAP)-treated obese patients with OSA. METHODS: Fifty three patients (35

How to approach sleep disordered breathing in heart failure patients.

Sleep disordered breathing (SDB) is a major public health problem and is highly prevalent in patients with heart failure (HF) disease. In these patients, a thorough pre-test probability evaluation and appropriate selection of overnight sleep study should be performed before treatment evaluation. A high index of suspicion for SDB should exist when an HF patient presents with the associated clinical features or risk factors for SDB. With a high index of suspicion, polysomnography (PSG), as a gold standard, is able to confirm or rule out the disease; however, portable monitoring devices may also be appropriate and represent more cost effective diagnosis strategies to confirm the diagnosis in adequately selected patients among a HF cohort. The choice of treatment largely depends on the type and severity of SDB demonstrated by validated sleep recording. The treatment of OSA in HF with CPAP is well established, while the optimal treatment of CSA still to be defined.

Nonalcoholic fatty liver disease, nocturnal hypoxia, and endothelial function in patients with sleep apnea.

BACKGROUND: Nocturnal hypoxia, the hallmark of OSA, is a potential contributing factor for nonalcoholic fatty liver disease (NAFLD). NAFLD severity and its implication in OSA-related endothelial dysfunction have not been investigated in a large, unselected OSA population, including nonobese subjects. METHODS: Noninvasive blood tests (SteatoTest, NashTest, and FibroTest) were used to evaluate steatosis, nonalcoholic steatohepatitis (NASH), and fibrosis in a large cohort of patients with OSA. In the same group, endothelial function and its links with NAFLD severity were assessed. RESULTS: Of the 226 subjects included who were referred for suspicion of OSA (men, 55%; median age, 56 years; median BMI, 34.2 kg/m2 [33% with BMI<30 kg/m2]), 61.5% exhibited moderate or severe steatosis. By multivariate analysis, independent factors for liver steatosis were, as expected, triglyceride levels (P<.0001) and insulin resistance (P=.0004) as well as nocturnal cumulative time spent<90% of oxygen saturation (CT90) (P=.01). Thirty-eight percent had borderline or possible NASH (N1 or N2 with NashTest). CT90 was significantly associated with borderline or possible NASH (P=.035) in univariate but not in multivariate analysis. The dose-response relationship between the severity of nocturnal hypoxia and liver injury was established only in morbid obesity and not in lean. Multivariate models showed that steatosis was independently associated with endothelial dysfunction after adjustment for confounders. CONCLUSIONS: In a large, unselected OSA population, the severity of nocturnal hypoxia was independently associated with steatosis. Preexisting obesity exacerbated the effects of nocturnal hypoxemia. NAFLD is a potential mechanism of endothelial dysfunction in OSA.

Chronic intermittent hypoxia is a major trigger for non-alcoholic fatty liver disease in morbid obese.

BACKGROUND & AIMS: Morbid obesity is frequently associated with low grade systemic inflammation, increased macrophage accumulation in adipose tissue (AT), obstructive sleep apnea (OSA), and nonalcoholic fatty liver disease (NAFLD). It has been suggested that chronic intermittent hypoxia (CIH) resulting from OSA could be an independent factor for early stage of NAFLD in addition to other well-recognized factors (dyslipidemia or insulin resistance). Moreover, macrophage accumulation in AT is associated with local hypoxia in fat tissue. We hypothesized that the association between CIH and morbid obesity could exert additional specific deleterious effects both in the liver and adipose tissues. METHODS: One hundred and one morbidly obese subjects were prospectively recruited and underwent bariatric surgery during which a liver needle biopsy as well as surgical subcutaneous and omental AT biopsies were obtained. Oxygen desaturation index (ODI) quantified the severity of nocturnal CIH. RESULTS: Histopathologic analysis of liver biopsies demonstrated that NAFLD lesions (ballooning of hepatocytes, lobular inflammation), NAFLD activity score (NAS), and fibrosis were significantly more severe in patients with the highest ODI tertile (p values ≤0.001 for all hepatic lesions). In multivariate analysis, after adjustment for age, obesity, and insulin resistance status, CIH remained independently associated with hepatic fibrosis, fibroinflammation, and NAS. By contrast, no association was found between CIH, macrophage accumulation, and adipocytes size in both subcutaneous and omental adipose tissue. CONCLUSIONS: In morbidly obese patients, CIH was strongly associated with more severe liver injuries but did not worsen obesity induced macrophage accumulation in adipose tissue depots.

Increased aortic root size is associated with nocturnal hypoxia and diastolic blood pressure in obstructive sleep apnea.

STUDY OBJECTIVES: Obstructive sleep apnea (OSA) is known as a major cardiovascular risk factor, and high prevalence of OSA has been reported in patients with thoracic aortic dissection. The aim of our study was to assess the relationship between OSA, its vascular consequences, and aortic root size. DESIGN/PATIENTS: 156 newly diagnosed apneic patients free of cardiovascular disease and medication were included. Patients underwent cardiac ultrasound for measuring aortic root diameter, polysomnography, office and 24-h ambulatory blood pressure (BP) measurements, baroreflex sensitivity (BRS), and arterial stiffness evaluation by carotid-to-femoral pulse wave velocity (PWV). MEASUREMENTS AND RESULTS: In univariate analysis, greater aortic root size was associated with older age (P = 0.03) and severity of OSA as expressed by mean nocturnal oxygen saturation (SpO2) (P = 0.015). Moreover, greater aortic root size was associated with higher diastolic BP, measured both clinically (P = 0.0005) or by 24-h ambulatory BP monitoring (P = 0.02), and PWV (P = 0.03). Mean nocturnal SpO(2) was correlated with BRS (P = 0.0008), thus potentially influencing BP values and arterial stiffness. In multivariate stepwise regression analysis, diastolic BP was the only significant factor for aortic root size (P = 0.0003). CONCLUSIONS: In OSA patients, nocturnal hypoxemia decreased BRS and increased diastolic BP, which was the main factor influencing aortic root size.