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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 relatively common in general population as well as in patients with neuromuscular disease. SDB comprises a wide spectrum of disorders varying from simple snoring to complete closure of the upper airway as seen in obstructive sleep apnoea (OSA). It includes also other disorders like prolonged hypoxemia, hypoventilation, and central sleep apnoea (CSA). Neuromuscular diseases (NMD) form a group of disorders that can cause significant reduction in the quality and span of life. The involvement of respiratory system in the context of these disorders is the most serious complication, and it is considered as the leading cause of death in those patients. NMD can affect ventilation, cough, swallowing, and phonation. The involvement of respiratory muscles makes NMD patients vulnerable to sleep-disordered breathing with a significant prevalence of SDB among such patients.

Background: Apnea of prematurity (AOP) is nearly universal among very preterm infants, but neither the apnea burden nor its clinical associations have been systematically studied in a large consecutive cohort. Methods: We analyzed continuous bedside monitor chest impedance and electrocardiographic waveforms and oxygen saturation data collected on all neonatal intensive care unit (NICU) patients <35 wk gestation from 2009 to 2014 ( n = 1,211; >50 infant-years of data). Apneas, with bradycardia and desaturation (ABDs), defined as central apnea ≥10 s associated with both bradycardia <100 bpm and oxygen desaturation <80%, were identified using a validated automated algorithm. Results: Number and duration of apnea events decreased with increasing gestational age (GA) and postmenstrual age (PMA). ABDs were more frequent in infants <31 wk GA at birth but were not more frequent in those with severe retinopathy of prematurity (ROP), bronchopulmonary dysplasia (BPD), or severe intraventricular hemorrhage (IVH) after accounting for GA. In the day before diagnosis of late-onset septicemia and necrotizing enterocolitis, ABD events were increased in some infants. Many infants continued to experience short ABD events in the week prior to discharge home. Conclusion: Frequency of apnea events is a function of GA and PMA in infants born preterm, and increased apnea is associated with acute but not with chronic pathologic conditions.

While full-night polysomnography is the gold standard for the diagnosis of obstructive sleep apnea, its limitations include a high cost and first-night effects. This study developed an algorithm for the detection of respiratory events based on impulse-radio ultra-wideband radar and verified its feasibility for the diagnosis of obstructive sleep apnea. A total of 94 subjects were enrolled in this study (23 controls and 24, 14, and 33 with mild, moderate, and severe obstructive sleep apnea, respectively). Abnormal breathing detected by impulse-radio ultra-wideband radar was defined as a drop in the peak radar signal by ≥30% from that in the pre-event baseline. We compared the abnormal breathing index obtained from impulse-radio ultra-wideband radar and apnea–hypopnea index (AHI) measured from polysomnography. There was an excellent agreement between the Abnormal Breathing Index and AHI (intraclass correlation coefficient = 0.927). The overall agreements of the impulse-radio ultra-wideband radar were 0.93 for Model 1 (AHI ≥ 5), 0.91 for Model 2 (AHI ≥ 15), and 1 for Model 3 (AHI ≥ 30). Impulse-radio ultra-wideband radar accurately detected respiratory events (apneas and hypopneas) during sleep without subject contact. Therefore, impulse-radio ultra-wideband radar may be used as a screening tool for obstructive sleep apnea.

Congenital central hypoventilation syndrome (CCHS) represents a rare genetic disorder usually caused by mutations in the homeodomain transcription factor PHOX2B. Some CCHS patients suffer mainly from deficiencies in CO2 and/or O2 respiratory chemoreflex, whereas other patients present with full apnea shortly after birth. Our goal was to identify the neuropathological mechanisms of apneic presentations in CCHS. In the developing murine neuroepithelium, Phox2b is expressed in three discrete progenitor domains across the dorsal‐ventral axis, with different domains responsible for producing unique autonomic or visceral motor neurons. Restricting the expression of mutant Phox2b to the ventral visceral motor neuron domain induces marked newborn apnea together with a significant loss of visceral motor neurons, RTN ablation, and preBötzinger complex dysfunction. This finding suggests that the observed apnea develops through non‐cell autonomous developmental mechanisms. Mutant Phox2b expression in dorsal rhombencephalic neurons did not generate significant respiratory dysfunction, but did result in subtle metabolic thermoregulatory deficiencies. We confirm the expression of a novel murine Phox2b splice variant which shares exons 1 and 2 with the more widely studied Phox2b splice variant, but which differs in exon 3 where most CCHS mutations occur. We also show that mutant Phox2b expression in the visceral motor neuron progenitor domain increases cell proliferation at the expense of visceral motor neuron development. We propose that visceral motor neurons may function as organizers of brainstem respiratory neuron development, and that disruptions in their development result in secondary/non‐cell autonomous maldevelopment of key brainstem respiratory neurons.

The most appropriate physiological signals to develop simplified as well as accurate screening tests for obstructive sleep apnoea (OSA) remain unknown. This study aimed at assessing whether joint analysis of at-home oximetry and airflow recordings by means of machine-learning algorithms leads to a significant diagnostic performance increase compared to single-channel approaches. Consecutive patients showing moderate-to-high clinical suspicion of OSA were involved. The apnoea-hypopnoea index (AHI) from unsupervised polysomnography was the gold standard. Oximetry and airflow from at-home polysomnography were parameterised by means of 38 time, frequency, and non-linear variables. Complementarity between both signals was exhaustively inspected via automated feature selection. Regression support vector machines were used to estimate the AHI from single-channel and dual-channel approaches. A total of 239 patients successfully completed at-home polysomnography. The optimum joint model reached 0.93 (95%CI 0.90–0.95) intra-class correlation coefficient between estimated and actual AHI. Overall performance of the dual-channel approach (kappa: 0.71; 4-class accuracy: 81.3%) significantly outperformed individual oximetry (kappa: 0.61; 4-class accuracy: 75.0%) and airflow (kappa: 0.42; 4-class accuracy: 61.5%). According to our findings, oximetry alone was able to reach notably high accuracy, particularly to confirm severe cases of the disease. Nevertheless, oximetry and airflow showed high complementarity leading to a remarkable performance increase compared to single-channel approaches. Consequently, their joint analysis via machine learning enables accurate abbreviated screening of OSA at home.

Sleep related disordered breathing (SDB) in pediatric Prader-Willi Syndrome is gaining increased attention due to the possible association of growth hormone therapy, SDB and sudden death. However data on the patterns of SDB and their management, particularly in infants in this population, is lacking. The aim of this study was to 1) describe patterns of SDB in growth hormone naive infants with PWS and the management of these disorders in our institution 2) Compare the patterns of sleep disorders between infants and children with PWS. Polysomnograms of infants and children (0-18 years of age) with Prader-Willi Syndrome were reviewed. Age, sex, anthropometrics, sleep architecture, obstructive and central apnea indices and oxygen saturations were recorded. Data of infants with central sleep apnea treated with oxygen were analyzed to evaluate the efficacy of this treatment. The main outcome measures were obstructive and central apnea indices on a polysomnogram. Data of 44 patients, 23 under 2 years of age and 21 older children were included. Infants when compared with older children were more likely to experience central sleep apnea (43% vs. 5%; p = 0.003). In older children obstructive was significantly more prevalent than central sleep apnea. Supplemental oxygen was used to treat 9/23 infants with central sleep apnea. Oxygen therapy resulted in a significant decrease in the median central apnea index from 14 (5,68) to 1 (0,6; p = 0.008) events/hour and an improvement in the oxygen saturation nadir from 70% (52, 92) to 81% (64, 95; p = 0.080). Central sleep apnea with associated oxygen desaturations is more prevalent in infants compared with older children with Prader-Willi Syndrome. Supplemental oxygen was efficacious in treating central sleep apnea in infants. Routine sleep surveillance for all children with Prader-Willi Syndrome and treatment with oxygen for central sleep apnea should be considered.

Obstructive sleep apnea-hypopnea syndrome (OSAHS) is one of the most common sleep disorders affecting nearly one billion of the global adult population, making it a major public health issue. Even if in-lab polysomnography (PSG) remains the gold standard to diagnose OSAHS, there is a growing interest to develop new solutions with more convenient at home devices enhanced with AI-based algorithms for the detection of sleep apnea. This retrospective study aimed to assess the performances of a new method based on nocturnal long-term electrocardiogram signal to detect apneas and hypopneas, in patients who performed attended in-lab PSG. After assessing the quality of the ECG signal, the new method automatically detected apneas and hypopneas using dedicated machine learning algorithm. The agreement between the new ECG-based detection method and the standard interpretation of PSG by a sleep clinician was determined in a blind manner. Eighty-five exams were included into the study with a mean bias between the proposed method and the scorer of 3.5 apneas-hypopneas/hour (/h) (95% CI -48.1 to 55.1). At a threshold of 15/h, sensibility and specificity were 93.3% and 66.7% respectively, and positive and negative predictive values were 87.5% and 80%, respectively. The proposed method using nocturnal long-term electrocardiogram signals showed very high performances to detect apneas and hypopneas. Its implementation in a simple ECG-based device would offer a promising opportunity for preliminary evaluation of patients suspected or at-risk of OSAHS.

Obstructive sleep apnea (OSA) is associated with an increased prevalence of aortic aneurysm, but the impact of OSA on the subclinical damage of large thoracic vessels remains controversial. Short sleep duration and poor sleep quality has been reported to be related with higher arterial stiffness. In the current study, we aimed to investigate the association of sleep disturbance and sleep apnea with the size of the ascending aorta (AA), descending thoracic aorta (DTA), and main pulmonary artery (MPA). One hundred and fifty-five newly diagnosed OSA patients free of cardiovascular disease and medication were included. In-laboratory polysomnography (PSG) and chest computed tomography (CT) scanning were performed. The sleep duration was defined as total sleep time (TST) as recorded during overnight PSG, with TST < 6 h defined as short sleep duration. Sleep latency (SL), sleep efficiency (SE) and wake after sleep onset (WASO) were used to assess the objective sleep quality, and the Epworth Sleepiness Scale (ESS) was used to assess EDS (excessive daytime sleepiness). The diameter of AA was positively associated with age ( B  = 0.199, P  < 0.001) and diastolic blood pressure (DBP) ( B  = 0.103, P  < 0.001), and was negatively associated with mean pulse oxygen saturation (SpO 2 mean) ( B  = − 0.176, P  = 0.022). The diameter of DTA was positively associated with age ( B  = 0.112, P  < 0.001), body mass index (BMI) ( B  = 0.184, P  = 0.041), and DBP ( B  = 0.033, P  = 0.024), and was negatively associated with TST ( B  = − 0.006, P  = 0.023). Neither nocturnal hypoxia nor TST were associated with the diameter of MPA or the ratio of MPA to AA (PA/A). The aortic or MPA measurements were not associated with SL, SE, WASO or ESS. In patients with OSA, nocturnal hypoxia and sleep duration were associated with the diameter of AA and DTA, respectively. It is suggested that sleep apnea and sleep disturbance may exert effects on the remodeling and enlargement of thoracic large vessels through distinctive mechanisms.

Based on the fact that erythropoietin (Epo) administration in rodents protects against spatial learning and cognitive deficits induced by chronic intermittent hypoxia (CIH)-mediated oxidative damage, here we tested the hypothesis that Epo in the brain protects against cardiorespiratory disorders and oxidative stress induced by CIH in adult mice. Adult control and transgenic mice overexpressing Epo in the brain only (Tg21) were exposed to CIH (21%-10% O2-10 cycles/hour-8 hours/day-7 days) or room air. After CIH exposure, we used the tail cuff method to measure arterial pressure, and whole-body plethysmography to assess the frequency of apneic episodes at rest, minute ventilation, and ventilatory responses to hypoxia and hypercapnia. Finally, the activity of pro-oxidant (XO-xanthine oxidase, and NADPH) and antioxidant (super oxide dismutase) enzymes was evaluated in the cerebral cortex and brainstem. Exposure of control mice to CIH significantly increased the heart rate and arterial pressure, the number of apneic events, and the ventilatory response to hypoxia and hypercapnia. Furthermore, CIH increased the ratio of pro-oxidant to antioxidant enzymes in cortex and brainstem tissues. Both physiological and molecular changes induced by CIH were prevented in transgenic Tg21 mice. We conclude that the neuroprotective effect of Epo prevents oxidative damage in the brain and cardiorespiratory disorders induced by CIH. Considering that Epo is used in clinics to treat chronic kidney disease and stroke, our data show convincing evidence suggesting that Epo may be a promising alternative drug to treat sleep-disorder breathing.