Explore the vast range of titles available.

Abstract Study Objectives Sleep-disordered breathing (SDB) is prevalent among children and is associated with adverse health outcomes. Worldwide, approximately 250 million individuals reside at altitudes higher than 2000 meters above sea level (masl). The effect of chronic high-altitude exposure on children with SDB is unknown. This study aims to determine the impact of altitude on sleep study outcomes in children with SDB dwelling at high altitude. Methods A single-center crossover study was performed to compare results of high-altitude home polysomnography (H-PSG) with lower altitude laboratory polysomnography (L-PSG) in school-age children dwelling at high altitude with symptoms consistent with SDB. The primary outcome was apnea-hypopnea index (AHI), with secondary outcomes including obstructive AHI; central AHI; and measures of oxygenation, sleep quality, and pulse rate. Results Twelve participants were enrolled, with 10 included in the final analysis. Median altitude was 1644 masl on L-PSG and 2531 masl on H-PSG. Median AHI was 2.40 on L-PSG and 10.95 on H-PSG. Both obstructive and central respiratory events accounted for the difference in AHI. Oxygenation and sleep fragmentation were worse and pulse rate higher on H-PSG compared to L-PSG. Conclusions These findings reveal a clinically substantial impact of altitude on respiratory, sleep, and cardiovascular outcomes in children with SDB who dwell at high altitude. Within this population, L-PSG underestimates obstructive sleep apnea and central sleep apnea compared to H-PSG. Given the shortage of high-altitude pediatric sleep laboratories, these results suggest a role for home sleep apnea testing for children residing at high altitude.

Sleep-disordered breathing (SDB) is common in individuals with established cardiovascular disease (CVD), particularly those with heart failure (HF). There are two main types of SDB, central sleep apnoea (CSA) and obstructive sleep apnoea (OSA) which frequently overlap as mixed SDB. Investigating for SDB could be considered in patients with excessive daytime sleepiness, male sex, high body mass index, low ejection fraction, atrial fibrillation (AF), in patients with no dipping blood pressure pattern, recurrent paroxysms of nocturnal dyspnoea or when an apnoea is witnessed. Excessive daytime sleepiness is less likely to be reported by patients with HF than by the general population. In patients with CVD and OSA, continuous positive airway pressure (CPAP) ventilation for over 4 hours daily reduced the risk of major adverse cardiovascular events, but there was no reduction in mortality. In patients with AF and OSA treated with AF ablation, CPAP use was associated with a reduced risk of recurrence of AF. In patients with HF and OSA, small studies have demonstrated that CPAP improves symptoms, brain natriuretic peptide levels and ejection fraction, but data on survival are lacking. Treatment remains unclear in patients with HF and CSA. The presence of CSA may be a defensive adaptive response to HF, and effectively treating CSA as demonstrated in a randomised clinical trial of adaptive servo-ventilation caused more harm than benefit when compared to optimal medical therapy. Thus, the focus of treating CSA should remain on improving the underlying HF by optimising medical therapy and, if indicated, cardiac resynchronisation therapy.

Excess adiposity is a reversible etiologic risk factor for obstructive sleep apnea. In this trial, tirzepatide reduced the apnea–hypopnea index of participants with obstructive sleep apnea and obesity.

This randomized trial showed no effect of early adenotonsillectomy, as compared with watchful waiting, on the primary outcome of attention and executive functioning in children with obstructive sleep apnea. Many secondary outcomes favored early surgery. The childhood obstructive sleep apnea syndrome is associated with numerous adverse health outcomes, including cognitive and behavioral deficits. 1 The most commonly identified risk factor for the childhood obstructive sleep apnea syndrome is adenotonsillar hypertrophy. Thus, the primary treatment is adenotonsillectomy, which accounts for more than 500,000 procedures annually in the United States alone. 2 Nevertheless, there has been no controlled study evaluating the benefits and risks of adenotonsillectomy, as compared with watchful waiting, for the management of the obstructive sleep apnea syndrome. The Childhood Adenotonsillectomy Trial (CHAT) was designed to evaluate the efficacy of early adenotonsillectomy versus watchful waiting with supportive . . .

Abstract Study Objectives This study aimed to evaluate and compare the effects of high and low-intensity expiratory muscle strength training (EMST) on disease severity, systemic inflammation, oxidative stress, respiratory muscle strength, exercise capacity, symptoms, daytime sleepiness, fatigue severity, and sleep quality in male patients with obstructive sleep apnea syndrome (OSAS). Methods Thirty-one male patients diagnosed with moderate OSAS were included in this double-blind, randomized, parallel study. Patients were randomized into two groups: High-EMST and Low-EMST groups. EMST was used at home 7 days/week, once a day, for 25 breaths, 12 weeks. Respiratory muscle strength was measured using a mouth pressure device. Disease severity (Apnea–Hypopnea Index [AHI]) and, respiratory sleep events by polysomnography, total oxidant level(TOS), total antioxidant level(TAS), oxidative stress index (OSI), C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-10 (IL-10) levels by blood serum were evaluated. Results The percentage of AHI change in the high-EMST group(50.8%) was significantly higher than in the low-EMST group(6.3%; p = .002, d = 1.31). In general, as MEP increased by one unit, AHI decreased by 0.149 points (b = −0.149; CR = −3.065; p = .002), and as AHI increased by one unit, ODI increased by 0.746 points (b = 0.746; CR = 10.604; p < .001). TOS, OSI, TNF-α and IL-6 levels decreased at similar rates in both groups. Conclusions EMST significantly reduces systemic inflammation and oxidative stress while improving expiratory muscle strength in male patients with moderate OSAS. High-EMST is more effective in enhancing the severity of disease than low-EMST. EMST is a practical, effective, and promising treatment for pulmonary rehabilitation in patients with moderate OSAS. Clinical Trials Effect of EMST systemic inflammation and oxidative stress in patients with moderate OSAS, https://clinicaltrials.gov/study/NCT05242406, with the number NCT05242406. Graphical Abstract Graphical Abstract

Sleep apnoea, one of the most common chronic diseases, is a risk factor for ischaemic stroke, stroke recurrence, and poor functional recovery after stroke. More than half of stroke survivors present with sleep apnoea during the acute phase after stroke, with obstructive sleep apnoea being the most common subtype. Following a stroke, sleep apnoea frequency and severity might decrease over time, but moderate to severe sleep apnoea is nevertheless present in up to a third of patients in the chronic phase after an ischaemic stroke. Over the past few decades evidence suggests that treatment for sleep apnoea is feasible during the acute phase of stroke and might favourably affect recovery and long-term outcomes. Nevertheless, sleep apnoea still remains underdiagnosed and untreated in many cases, due to challenges in the detection and prediction of post-stroke sleep apnoea, uncertainty as to the optimal timing for its diagnosis, and a scarcity of clear treatment guidelines (ie, uncertainty on when to treat and the optimal treatment strategy). Moreover, the pathophysiology of sleep apnoea associated with stroke, the proportion of stroke survivors with obstructive and central sleep apnoea, and the temporal evolution of sleep apnoea subtypes following stroke remain to be clarified. To address these shortcomings, the management of sleep apnoea associated with stroke should be integrated into a multidisciplinary diagnostic, treatment, and follow-up strategy.

The effect of continuous positive airway pressure (CPAP) on mediators of cardiovascular disease and depression in women with obstructive sleep apnea (OSA) is unknown. We aimed to assess the effect of CPAP therapy on a variety of biomarkers of inflammation, antioxidant activity, and depression in women with OSA. We conducted a multicenter, randomized controlled trial in 247 women diagnosed with moderate-to-severe OSA (apnea-hypopnea index [AHI] ≥ 15). Women were randomized to CPAP (n = 120) or conservative treatment (n = 127) for 12 weeks. Changes in tumor necrosis factor α (TNFα), interleukin 6 (IL-6), C-reactive protein (CRP), intercellular adhesion molecule 1 (ICAM-1), catalase (CAT), superoxide dismutase (SOD), and brain-derived neurotrophic factor (BDNF) were assessed. Additional analyses were conducted in subgroups of clinical interest. Women had a median (25th-75th percentiles) age of 58 (51-65) years, body mass index 33.5 (29.0-38.3) kg/m2, and AHI 33.3 (22.8-49.3). No differences were found between groups in the baseline levels of the biomarkers. After 12 weeks of follow-up, there were no changes between groups in any of the biomarkers assessed. These results did not change when the analyses were restricted to sleepy women or to those with severe OSA. In women with CPAP use at least 5 hours per night, only TNFα levels decreased compared to the control group (-0.29 ± 1.1 vs -0.06 ± 0.53, intergroup difference -0.23 [95% CI = -0.03 to -0.50]; p = 0.043). Twelve weeks of CPAP therapy does not improve biomarkers of inflammation, antioxidant activity, or depression compared to conservative treatment in women with moderate-to-severe OSA. NCT02047071.

Background: Obesity is strongly associated with prevalence of obstructive sleep apnea (OSA), and weight loss has been shown to reduce disease severity. Objective: To investigate whether liraglutide 3.0 mg reduces OSA severity compared with placebo using the primary end point of change in apnea–hypopnea index (AHI) after 32 weeks. Liraglutide’s weight loss efficacy was also examined. Subjects/Methods: In this randomized, double-blind trial, non-diabetic participants with obesity who had moderate (AHI 15–29.9 events h −1 ) or severe (AHI ⩾30 events h −1 ) OSA and were unwilling/unable to use continuous positive airway pressure therapy were randomized for 32 weeks to liraglutide 3.0 mg ( n =180) or placebo ( n =179), both as adjunct to diet (500 kcal day −1 deficit) and exercise. Baseline characteristics were similar between groups (mean age 48.5 years, males 71.9%, AHI 49.2 events h −1 , severe OSA 67.1%, body weight 117.6 kg, body mass index 39.1 kg m −2 , prediabetes 63.2%, HbA 1c 5.7%). Results: After 32 weeks, the mean reduction in AHI was greater with liraglutide than with placebo (−12.2 vs −6.1 events h −1 , estimated treatment difference: −6.1 events h −1 (95% confidence interval (CI), −11.0 to −1.2), P =0.0150). Liraglutide produced greater mean percentage weight loss compared with placebo (−5.7% vs −1.6%, estimated treatment difference: −4.2% (95% CI, −5.2 to −3.1%), P <0.0001). A statistically significant association between the degree of weight loss and improvement in OSA end points ( P <0.01, all) was demonstrated post hoc . Greater reductions in glycated hemoglobin (HbA 1c ) and systolic blood pressure (SBP) were seen with liraglutide versus placebo (both P <0.001). The safety profile of liraglutide 3.0 mg was similar to that seen with doses ⩽1.8 mg. Conclusions: As an adjunct to diet and exercise, liraglutide 3.0 mg was generally well tolerated and produced significantly greater reductions than placebo in AHI, body weight, SBP and HbA 1c in participants with obesity and moderate/severe OSA. The results confirm that weight loss improves OSA-related parameters.

Short sleep duration and decreased sleep quality are emerging risk factors for obesity and its associated morbidities. Chronotype, an attribute that reflects individual preferences in the timing of sleep and other behaviors, is a continuum from morningness to eveningness. The importance of chronotype in relation to obesity is mostly unknown. Evening types tend to have unhealthy eating habits and suffer from psychological problems more frequently than Morning types, thus we hypothesized that eveningness may affect health parameters in a cohort of obese individuals reporting sleeping less than 6.5 hours per night. BASELINE DATA FROM OBESE (BMI: 38.5±6.4 kg/m(2)) and short sleeping (5.8±0.8 h/night by actigraphy) participants (n = 119) of the Sleep Extension Study were analyzed (www.ClinicalTrials.gov, identifier NCT00261898). Assessments included the Horne and Ostberg Morningness-Eveningness questionnaire, a three-day dietary intake diary, a 14-day sleep diary, 14 days of actigraphy, and measurements of sleep apnea. Twenty-four hour urinary free cortisol, 24 h urinary norepinephrine and epinephrine levels, morning plasma ACTH and serum cortisol, fasting glucose and insulin, and lipid parameters were determined. Eveningness was associated with eating later in the day on both working and non-working days. Progression towards eveningness was associated with an increase in BMI, resting heart rate, food portion size, and a decrease in the number of eating occasions and HDL-cholesterol. Evening types had overtly higher 24 h urinary epinephrine and morning plasma ACTH levels, and higher morning resting heart rate than Morning types. In addition, Evening types more often had sleep apnea, independent of BMI or neck circumference. Eveningness was associated with eating later and a tendency towards fewer and larger meals and lower HDL-cholesterol levels. In addition, Evening types had more sleep apnea and higher stress hormones. Thus, eveningness in obese, chronically sleep-deprived individuals compounds the cardiovascular risk associated with obesity.

In this study, continuous positive airway pressure plus weight loss was no better than either one alone in reducing C-reactive protein levels in patients with obstructive sleep apnea, but improvements were seen in insulin resistance, triglyceride levels, and blood pressure. Available clinical data derived largely from observational studies link obstructive sleep apnea 1 to proatherosclerotic risk factors, including insulin resistance, 2 dyslipidemia, hypertension, 3 and inflammation. 4 Obesity and obstructive sleep apnea are strongly associated. 5 – 8 Like obstructive sleep apnea, obesity is linked to insulin resistance, 6 dyslipidemia, 9 hypertension, 9 , 10 and inflammation. 10 However, the relative causal roles that obstructive sleep apnea and obesity play in these abnormalities is unclear. 6 , 11 , 12 The interrelationships between obesity and obstructive sleep apnea are complex and bidirectional, and they cannot be confidently discerned in observational studies. Randomized trials have shown the beneficial effects of weight loss on cardiovascular risk . . .