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PurposeTo investigate the prevalence of treatment-emergent central sleep apnea (TECSA) in individuals with obstructive sleep apnea syndrome (OSAS) during continuous positive airway pressure (CPAP) titration and assess their polysomnographic characteristics.MethodsA total of 116 patients with OSAS who underwent full-night CPAP titration at the Sleep Laboratory of Adana City Research and Education Hospital from September 2017 to January 2018 were recruited for the study. The patients’ polysomnographic data related to respiratory events and sleep stages were reviewed in a retrospective manner.ResultsWhile on CPAP titration, 20 of the 116 patients developed central sleep apnea (CSA). The prevalence of TECSA in the patients with OSAS was 17.2%, being separately determined as 16.3% and 2.2% for the male and female patients, respectively. In the baseline PSG, the groups did not statistically significantly differ in relation to the apnea hypopnea index (AHI), central apnea index (CAI), arousal index (AI), or oxygen desaturation index (ODI). However, the TECSA group had a significantly higher mean oxygen saturation value compared to the non-TECSA group (p = 0.01). The total AHI, CAI, and AI values of the TECSA group were significantly higher during the whole CPAP titration compared to the non-TECSA group. No significant difference was observed in the comparison of the two groups in relation to the titration pressure and ODI.ConclusionTECSA is a phenomenon that can occur with obstructive sleep apnea treatment and mostly regress spontaneously following appropriate CPAP treatment. TECSA is observed at different rates of prevalence. In this study, the prevalence of TECSA was higher than previously reported.

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.

Considerable progress has been made over the last several decades in our understanding of the pathophysiology of both central and obstructive sleep apnea. Central sleep apnea, in its various forms, is generally the product of an unstable ventilatory control system (high loop gain) with increased controller gain (high hypercapnic responsiveness) generally being the cause. High plant gain can contribute under certain circumstances (hypercapnic patients). On the other hand, obstructive sleep apnea can develop as the result of a variety of physiologic characteristics. The combinations of these may vary considerably between patients. Most obstructive apnea patients have an anatomically small upper airway with augmented pharyngeal dilator muscle activation maintaining airway patency awake, but not asleep. However, individual variability in several phenotypic characteristics may ultimately determine who develops apnea and how severe the apnea will be. These include: (1) upper airway anatomy, (2) the ability of upper airway dilator muscles to respond to rising intrapharyngeal negative pressure and increasing Co(2) during sleep, (3) arousal threshold in response to respiratory stimulation, and (4) loop gain (ventilatory control instability). As a result, patients may respond to different therapeutic approaches based on the predominant abnormality leading to the sleep-disordered breathing.

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.

Abstract Medication-induced central sleep apnea (CSA) is one of the eight categories of causes of CSA but in the absence of awareness and careful history may be misclassified as primary CSA. While opioids are a well-known cause of respiratory depression and CSA, non-opioid medications including sodium oxybate, baclofen, valproic acid, gabapentin, and ticagrelor are less well-recognized. Opioids-induced respiratory depression and CSA are mediated primarily by µ-opioid receptors, which are abundant in the pontomedullary centers involved in breathing. The non-opioid medications, sodium oxybate, baclofen, valproic acid, and gabapentin, act upon brainstem gamma-aminobutyric acid (GABA) receptors, which co-colonize with µ-opioid receptors and mediate CSA. The pattern of ataxic breathing associated with these medications is like that induced by opioids on polysomnogram. Finally, ticagrelor also causes periodic breathing and CSA by increasing central chemosensitivity and ventilatory response to carbon dioxide. Given the potential consequences of CSA and the association between some of these medications with mortality, it is critical to recognize these adverse drug reactions, particularly because discontinuation of the offending agents has been shown to eliminate CSA.

Study objectivesTo assess the accuracy of WatchPAT (WP—Itamar-Medical, Caesarea, Israel) enhanced with a novel systolic upstroke analysis coupled with respiratory movement analysis derived from a dedicated snoring and body position (SBP) sensor, to enable automated algorithmic differentiation between central sleep apnea (CSA) and obstructive sleep apnea (OSA) compared with simultaneous in-lab sleep studies with polysomnography (PSG).MethodsEighty-four patients with suspected sleep-disordered breathing (SDB) underwent simultaneous WP and PSG studies in 11 sleep centers. PSG scoring was blinded to the automatically analyzed WP data.ResultsOverall WP apnea-hypopnea index (AHI; mean ± SD) was 25.2 ± 21.3 (range 0.2–101) versus PSG AHI 24.4 ± 21.2 (range 0–110) (p = 0.514), and correlation was 0.87 (p < 0.001). Using a threshold of AHI ≥ 15, the sensitivity and specificity of WP versus PSG for diagnosing sleep apnea were 85% and 70% respectively and agreement was 79% (kappa = 0.867). WP central AHI (AHIc) was 4.2 ± 7.7 (range 0–38) versus PSG AHIc 5.9 ± 11.8 (range 0–63) (p = 0.034), while correlation was 0.90 (p < 0.001). Using a threshold of AHI ≥ 15, the sensitivity and specificity of WP versus PSG for diagnosing CSA were 67% and 100% respectively with agreement of 95% (kappa = 0.774), and receiver operator characteristic (ROC) area under the curve of 0.866, (p < 0.01). Using a threshold of AHI ≥ 10 showed comparable overall sleep apnea and CSA diagnostic accuracies.ConclusionsThese findings show that WP can accurately detect overall AHI and effectively differentiate between CSA and OSA.

Background Congenital Central Hypoventilation Syndrome (CCHS) is a rare condition characterized by an alveolar hypoventilation due to a deficient autonomic central control of ventilation and a global autonomic dysfunction. Paired-like homeobox 2B (PHOX2B) mutations are found in most of the patients with CCHS. In recent years, the condition has evolved from a life-threatening neonatal onset disorder to include broader and milder clinical presentations, affecting children, adults and families. Genes other than PHOX2B have been found responsible for CCHS in rare cases and there are as yet other unknown genes that may account for the disease. At present, management relies on lifelong ventilatory support and close follow up of dysautonomic progression. Body This paper provides a state-of-the-art comprehensive description of CCHS and of the components of diagnostic evaluation and multi-disciplinary management, as well as considerations for future research. Conclusion Awareness and knowledge of the diagnosis and management of this rare disease should be brought to a large health community including adult physicians and health carers.

Sleep-disordered breathing in neuromuscular diseases is due to an exaggerated reduction in lung volumes during supine sleep, a compromised physiologic adaptation to sleep, and specific features of the diseases that may promote upper airway collapse or heart failure. The normal decrease in the rib cage contribution to the tidal volume during phasic REM sleep becomes a critical vulnerability, resulting in saw-tooth oxygen desaturation possibly representing the earliest manifestation of respiratory muscle weakness. Hypoventilation can occur in REM sleep and progress into non-REM sleep, with continuous desaturation and hypercarbia. Specific characteristics of neuromuscular disorders, such as pharyngeal neuropathy or weakness, macroglossia, bulbar manifestations, or low lung volumes, predispose patients to the development of obstructive events. Central sleep-disordered breathing can occur with associated cardiomyopathy (e.g., dystrophies) or from instability in the control of breathing due to diaphragm weakness. Mitigating factors such as recruitment of accessory respiratory muscles, reduction in REM sleep, and loss of normal REM atonia in some individuals may partially protect against sleep-disordered breathing. Noninvasive ventilation, a standard-of-care management option for sleep-disordered breathing, can itself trigger specific sleep-disordered breathing events including air leaks, patient-ventilator asynchrony, central sleep apnea, and glottic closure. These events increase arousals, reduce adherence, and impair sleep architecture. Polysomnography plays an important role in addressing pitfalls in the diagnosis of sleep-disordered breathing in neuromuscular diseases, identifying sleep-disordered breathing triggered by noninvasive ventilation, and optimizing noninvasive ventilation settings.

To evaluate long-term efficacy and safety of phrenic nerve stimulation (PNS) in patients with moderate-to-severe central sleep apnea (CSA) through 3 years of therapy. Patients in the remedē System Pivotal Trial were observed every 3 months after implant until US Food and Drug Administration approval. At the time of approval and study closure, all patients completed 24 months of follow-up; 33 patients had not reached the 36-month visit. Sleep metrics (polysomnography) and echocardiographic parameters are reported at baseline, 12, 18, and 24 months, in addition to available 36-month sleep results from polygraphy. Safety was assessed through 36 months; however, analysis focused through 24 months and available 36-month results are provided. Patients were assessed at 24 (n = 109) and 36 (n = 60) months. Baseline characteristics included mean age 64 years, 91% male, and mean apnea-hypopnea index 47 events per hour. Sleep metrics (apnea-hypopnea index (AHI), central apnea index, arousal index, oxygen desaturation index, rapid eye movement sleep) remained improved through 24 and 36 months with continuous use of PNS therapy. At least 60% of patients in the treatment group achieved at least 50% reduction in AHI through 24 months. Serious adverse events (SAEs) related to the remedē System implant procedure, device, or therapy through 24 months were reported by 10% of patients, no unanticipated adverse device effects or deaths, and all events resolved. No additional related SAEs were reported between 24 and 36 months. These data suggest beneficial effects of long-term PNS in patients with CSA appear to sustain through 36 months with no new safety concerns. NCT01816776.

The prevalence and consequences of central sleep apnea (CSA) in adults are not well described. By utilizing the large Veterans Health Administration (VHA) national administrative databases, we sought to determine the incidence, clinical correlates, and impact of CSA on healthcare utilization in Veterans. Analysis of a retrospective cohort of patients with sleep disorders was performed from outpatient visits and inpatient admissions from fiscal years 2006 through 2012. The CSA group, defined by International Classification of Diseases-9, was compared with a comparison group. The number of newly diagnosed CSA cases increased fivefold during this timeframe; however, the prevalence was highly variable depending on the VHA site. The important predictors of CSA were male gender (odds ratio [OR] = 2.31, 95% confidence interval [CI]: 1.94–2.76, p < 0.0001), heart failure (HF) (OR = 1.78, 95% CI: 1.64–1.92, p < 0.0001), atrial fibrillation (OR = 1.83, 95% CI: 1.69–2.00, p < 0.0001), pulmonary hypertension (OR = 1.38, 95% CI:1.19–1.59, p < 0.0001), stroke (OR = 1.65, 95% CI: 1.50–1.82, p < 0.0001), and chronic prescription opioid use (OR = 1.99, 95% CI: 1.87–2.13, p < 0.0001). Veterans with CSA were at an increased risk for hospital admissions related to cardiovascular disorders compared with the comparison group (incidence rate ratio [IRR] = 1.50, 95% CI: 1.16–1.95, p = 0.002). Additionally, the effect of prior HF on future admissions was greater in the CSA group (IRR: 4.78, 95% CI: 3.87–5.91, p < 0.0001) compared with the comparison group (IRR = 3.32, 95% CI: 3.18–3.47, p < 0.0001). Thus, CSA in veterans is associated with cardiovascular disorders, chronic prescription opioid use, and increased admissions related to the comorbid cardiovascular disorders. Furthermore, there is a need for standardization of diagnostics methods across the VHA to accurately diagnose CSA in high-risk populations.