Central sleep apnea (CSA) is a sleep-related breathing disorder characterized by repeated cessation of respiratory drive during sleep. Unlike obstructive sleep apnea, CSA is not caused by upper airway obstruction but by a dysfunction in central respiratory regulation. The prevalence of CSA is low in the general population (0.9-1.5%), but significantly higher in risk groups such as patients with heart failure (up to 50%). Pathophysiologically, CSA is marked by instability of respiratory brainstem drive, prolonged circulation time, and increased CO2 sensitivity. Cheyne-Stokes respiration, a common manifestation in heart failure patients, is associated with increased mortality. Diagnosis is primarily based on polysomnography, which allows differentiation between central and obstructive apneas, as well as sleep stages. A central apnea-hypopnea index (cAHI) ≥ 5/h is considered pathological. Additional assessments, such as echocardiography and blood gas analysis, are important for evaluating underlying conditions. Treatment focuses on treating the underlying disease, especially in heart failure patients. Device-based treatments such as continuous positive airway pressure (CPAP) and adaptive servo-ventilation (ASV) are available, although ASV is contraindicated in symptomatic heart failure patients with reduced left-ventricular ejection fraction (LV-EF) ≤ 45%. Implantable transvenous phrenic nerve stimulation is a promising new treatment option for CSA, particularly for heart failure patients who cannot receive ASV. In the case of neurological diseases and high-altitude exposure, CSA treatment needs to be individually tailored. Clinically, early identification and treatment of CSA are crucial to improve quality of life. Improvement in prognosis through CSA treatment has not yet been conclusively demonstrated, highlighting the need for further research on this topic. CSA remains a dynamic field in sleep and cardiovascular medicine with high clinical relevance.

Neuromuscular diseases are often accompanied by various types of sleep-related breathing disorders, which can exacerbate the underlying condition and are associated with a poor prognosis. Early identification is essential, and interventions such as non-invasive ventilation, oxygen therapy, and respiratory rehabilitation should be initiated promptly to mitigate disease progression and improve outcomes. Nevertheless, the rates of missed and misdiagnosed cases remain common in clinical practice. Currently, there are no standardized guidelines for the diagnosis and treatment of sleep-disordered breathing related to neuromuscular diseases in China. Therefore, based on the latest domestic and international research progress, and combined with domestic clinical diagnosis and treatment experience, the Sleep Disorder Group of Chinese Thoracic Society has brought together multidisciplinary experts to develop this expert consensus. This consensus provides a comprehensive overview of the epidemiology, clinical manifestations, diagnostic approaches, assessment strategies, and treatment of sleep-disordered breathing related to neuromuscular diseases. It formulates evidence-based recommendations to guide clinical practice, with the aim of providing standardized recommendations for their diagnosis and management.Statement 1: The neuromuscular disorders that are most frequently associated with sleep-disordered breathing include: myasthenia gravis (1A), amyotrophic lateral sclerosis (2B), post-polio syndrome (2B), myotonic dystrophy (2B), peripheral neuropathies (2C), and metabolic myopathies, among other neuromuscular conditions.Statement 2: Patients with neuromuscular disorders frequently develop multiple types of sleep-disordered breathing concurrently or sequentially, with obstructive sleep apnea (OSA) being the most prevalent manifestation. Distinct clinical manifestations of OSA are observed across different neuromuscular disease subtypes (1A).Statement 3: Neuromuscular disorders predispose to central sleep apnea (CSA), with clinical manifestations varying significantly across disease subtypes, stages of progression, and severity levels (1A).Recommendation 1: In patients with neuromuscular disorders exhibiting progressive hypercapnia or worsening hypoxemia, clinicians should investigate potential comorbid nocturnal alveolar hypoventilation and/or sleep-associated hypoxemia (1A).Recommendation 2: When sleep-disordered breathing is suspected, patients with neuromuscular disorders should be evaluated for symptoms of sleep-disordered breathing. Meanwhile, sleep monitoring, non-invasive CO2 monitoring, and related examinations should be actively performed according to the actual situation (1A). A polysomnography should be performed when there is a high clinical suspicion of sleep-disordered breathing but a negative result on a portable sleep monitor (1A).Recommendation 3: (1) Noninvasive positive pressure ventilation (NPPV) titration under polysomnography is the standard method to determine the effective treatment parameters for neuromuscular diseases with sleep-disordered breathing (1A). (2) Positive airway pressure titration in OSA patients with neuromuscular diseases should follow American Academy of Sleep Medicine (AASM) guidelines (1A). (3) For neuromuscular disorders with CSA or Cheyne-Stokes respiration, bi-level positive airway pressure (BPAP) with ST pattern is recommended (1A); When BPAP is not tolerated or accompanied by severe Cheyne-Stokes respiratory and heart failure in patients, adaptive support ventilation (ASV) should be used (2B). (4) Patients with neuromuscular disease and sleep-related alveolar hypoventilation should be treated with BPAP or variable assurance pressure support (VAPS) (1A). (5) BPAP with alternate frequency is preferred for neuromuscular disorders with "pseudo-central events" (1A).Recommendation 4: Oxygen therapy alone is not recommended for neuromuscular disease patients combined with sleep-disordered breathing (2D). Oxygen therapy with monitoring of CO2 level is recommended when non-invasive ventilation therapy cannot effectively correct hypoxemia (2C). Diaphragmatic pacing should not be routinely used in amyotrophic lateral sclerosis patients with respiratory failure (2B). Transvenous phrenic nerve stimulation is not currently applied to CSA caused by neuromuscular disorders (2D). Respiratory rehabilitation may improve respiratory muscle strength in a subset of patients with neuromuscular disorders (2B). Protiline can be used for REM-associated alveolar hypoventilation, and daytime sleepiness could be addressed with methylphenidate and modafinil (2C).Recommendation 5: Neuromuscular disease combined with sleep-disordered breathing is a chronic disease requiring patient-centered, individualized education and long-term follow-up management (1A).

Background: Sleep-disordered breathing (SDB), particularly Cheyne-Stokes respiration (CSR), is highly prevalent among patients hospitalized with acute decompensated heart failure (ADHF) and is associated with worse clinical outcomes. Sodium-glucose cotransporter-2 inhibitors (SGLT2i) have demonstrated cardiorenal benefits in heart failure, but their effects on nocturnal respiratory parameters remain underexplored. Objectives: This study aims to evaluate the impact of SGLT2i therapy on key respiratory and cardiac indices including CSR burden, oxygenation, and right heart function in patients with ADHF and reduced left ventricular ejection fraction. Methods: In this single-center prospective cohort study, 60 patients with ADHF, LVEF < 40%, and a baseline apnea-hypopnea index (AHI) > 5 were assessed before and three months after the initiation of SGLT2i therapy. Sleep respiratory parameters were measured using home polygraphy (ApneaLinkTM), while cardiac and renal indices were evaluated by echocardiography, NT-proBNP, and the estimated glomerular filtration rate (eGFR). Structural and functional echocardiographic changes were analyzed both at baseline and following the 3-month treatment period. Patient-reported outcomes were assessed using the Epworth Sleepiness Scale (ESS) and Kansas City Cardiomyopathy Questionnaire (KCCQ). Results: After 3 months of SGLT2i therapy, significant improvements were observed in daytime sleepiness (ESS: -2.68 points; p < 0.001), CSR index (-5.63 events/h; p < 0.001), AHI (-3.07 events/h; p < 0.001), ODI (-6.11 events/h; p < 0.001), and mean nocturnal SpO2 (+1.95%; p < 0.001). KCCQ scores increased by 9.16 points (p < 0.001), indicating improved quality of life. Cardiac assessments revealed reductions in NT-proBNP (-329.6 pg/mL; p < 0.001) and E/e' ratio (-1.08; p < 0.001), with no significant change in LVEF or chamber dimensions. Right ventricular function improved, as evidenced by the increased TAPSE/sPAP ratio (+0.018; p < 0.001). Renal function remained stable, with a non-significant upward trend in eGFR. Conclusions: This exploratory study suggests that SGLT2 inhibitors may be associated with the attenuation of Cheyne-Stokes respiration and an improvement in right heart function in patients with ADHF, warranting further investigation in controlled trials. These findings highlight the potential of SGLT2is to address overlapping cardio-respiratory dysfunction in this high-risk population.

Central sleep apnea (CSA) is a heterogeneous group of sleep-related breathing disorders characterized by intermittent absence of respiratory effort during sleep. CSA results from impaired neurological signaling from the respiratory centers to the respiratory muscles, leading to airflow cessation for at least 10 s. Major causes include heart failure, opioid use, central neurological disorders, and altitude exposure. This review outlines the pathophysiology of CSA, emphasizing ventilatory instability and brainstem dysfunction as key mechanisms. It details the classification of CSA subtypes, including Cheyne-Stokes respiration, high-altitude CSA, and drug-induced CSA. Clinical manifestations range from excessive daytime sleepiness to cardiovascular complications. Diagnostic approaches encompass polygraphy, polysomnography, and various laboratory tests to evaluate comorbidities. Treatment requires a multidisciplinary approach, addressing underlying conditions while utilizing positive airway pressure (PAP) therapy, adaptive servo-ventilation (ASV), supplemental oxygen, and pharmacological interventions. Newer modalities, such as phrenic nerve stimulation, offer promising outcomes for CSA management. This review underscores the necessity of an individualized, interdisciplinary strategy to improve patient outcomes in CSA.

Cheyne-Stokes respiration (CSR), a rhythmic rise and fall in ventilation often experienced by patients with heart failure during sleep, is typically accompanied by an oscillation in heart rate (HR) at the same frequency. The mechanisms responsible for this oscillation are still debated. In this study, we used the experimental model of the transient hypoxia test (i.e., a laboratory test that mimics the transient nature of the cyclic desaturations that occur during hyperpnoeic phases of CSR) to assess accurately the temporal relationship between the HR response to transient hypoxia and the tidal volume response in six heart failure patients. The same relationship was assessed during CSR using polysomnographic signals. We hypothesized that this relationship would provide important insights into the key mechanisms contributing to the HR response. During transient hypoxia, HR started to increase around the onset of tidal volume increase but continued to increase after the peak of the latter had been reached. The time delay between the two peaks (HR vs. tidal volume) was 7.9 ± 4.8 s. The same delay during hyperpnoeic phases of CSR was 1.0 ± 0.9 s. In addition, the increases in lung volume were much greater than those found in the laboratory tests. Based on the known dynamics of vagal and sympathetic control of HR, we speculate that the HR response to transient hypoxia might be attributable predominantly to the sympathetically mediated tachycardic effect of the increased central inspiratory drive, whereas the fast, vagally mediated pulmonary inflation reflex might be the predominant mechanism during CSR.

Central sleep apnea due to Cheyne-Stokes respiration is frequently described in adults with cardiac failure, but few (< 20) cases are reported in children. We report the case of a 10-year-old male with dilated cardiomyopathy and cardiac failure (left ventricular ejection fraction 36%), in whom recurrent, prolonged pauses in breathing during sleep were noted. A cardiorespiratory polygraphy sleep study was performed, which demonstrated the presence of central sleep apnea due to Cheyne-Stokes respiration. A total of 373 central events were scored and central apnea-hypopnea index was 47.4 events/h. Overnight continuous positive airways pressure was commenced via a nasal mask. Both child and mother reported improved well-being on continuous positive airways pressure, and a repeat cardiorespiratory polygraphy on continuous positive airways pressure noted a fall in central apnea-hypopnea index to 1.2 events/h. We believe this to be the first case describing successful treatment of central sleep apnea due to Cheyne-Stokes respiration in a child using continuous positive airways pressure. The improvement in patient well-being highlights the importance of a sleep history and/or sleep studies in children with cardiac failure.

The Alertapnée study followed 555 adults with obstructive sleep apnea treated with CPAP and found that the occurrence of Cheyne-Stokes respiration (CSR) was linked to a 14-fold increase in the risk of significant cardiac events (SCE) after one year. However, the progression and clinical significance of CSR episodes over time remain unclear. This ancillary study aimed to assess CSR progression and clinical outcomes during a second year of follow-up in 66 patients who had experienced at least one CSR episode in the first year. The study focused on the number of nights with CSR, percentage of CSR, SCEs. Results showed that 62 of 66 patients with CSR in the first year also experienced CSR in the second year, with a significant increase in the median number of CSR nights, particularly when CSR was related to cardiovascular conditions (37 vs. 19 nights, p = 0.006). Patients who experienced a SCE in year 2 had significantly more nights with CSR (median 48/90nights; IQR = 35) and a significantly greater mean percentage of CSR (median 13.8%; interquartile range (IQR) = 13.7) as compared with patients free of SCE (median 9.5/90 nights IQR = 27.8 (p = 0.012); 6.1% IQR = 4.5 (p = 0.008), respectively). In conclusion, CSR occurrence and severity depend on the underlying condition. CSR related to cardiovascular aetiology increases over time and is associated with SCEs, whereas CSR linked to non-cardiovascular conditions does not indicate a poor prognosis. Identifying CSR patterns related to cardiovascular aetiologies could enable early detection of SCEs through telemonitoring in CPAP-treated patients.

Background: Impairment in autonomic activity is a prognostic marker in patients with heart failure (HF), and its involvement has been suggested in cardiovascular complications of obstructive sleep apnea syndrome (OSAS) and Cheyne-Stokes respiration (CSR). This prospective observational study aims to investigate the implications of sleep-disordered breathing (SDB) on hemodynamic regulation and autonomic activity in chronic HF patients. Methods: Chronic HF patients, providing confirmation of reduced ejection fraction (≤35%), underwent polysomnography, real-time hemodynamic, heart rate variability (HRV), and baroreceptor reflex sensitivity (BRS) assessments using the Task Force Monitor. BRS was assessed using the sequencing method during resting conditions and stress testing. Results: Our study population (n = 58) was predominantly male (41 vs. 17), with a median age of 61 (±11) yrs and a median BMI of 30 (±5) kg/m[2]. Patients diagnosed with CSR were 13.8% (8/58) and 50.0% (29/58) with OSAS. No differences in the real-time assessment of hemodynamic regulation, heart rate variability, or baroreceptor reflex function were found between patients with OSAS, CSR, and patients without SDB. A subgroup analysis of BRS and HRV in patients with severe SDB (AHI > 30/h) and without SDB (AHI < 5) revealed numerically reduced BRS and increased LF/HF-RRI values under resting conditions, as well as during mental testing in patients with severe SDB. Patients with moderate-to-severe SDB had a shorter overall survival, which was, however, dependent upon age. Conclusions: Chronic HF patients with severe SDB may exhibit lower baroreceptor function and impaired cardiovascular autonomic function in comparison with HF patients without SDB.