Central sleep apnoea (CSA) and Cheyne-Stokes respiration are prevalent in patients with heart failure and contribute to disease progression, increased risk of death, heart failure hospitalisations and reduced quality of life. The 2025 American Academy of Sleep Medicine Clinical Practice Guideline for the Treatment of Central Sleep Apnea in Adults represents a major advance, recognising transvenous phrenic nerve stimulation as an evidence-based therapy for adults with CSA, including those with heart failure, as well as updating the clinical data on adaptive servo-ventilation. This review summarises key updates in the American Academy of Sleep Medicine 2025 guideline, examines the pathophysiological link between CSA and heart failure, and evaluates the clinical evidence and practical considerations for treatment. Current evidence indicates improvements in apnoea indices, oxygenation and quality of life, while the effect on mortality and hospitalisation needs additional prospective randomised data. Identification of patients with signs and symptoms which are likely due to central sleep apnoea is often missed in clinical practice, and treatment has a significant impact on quality of life.

Idiopathic central sleep apnoea (ICSA) is a form of periodic hyperventilation followed by central apnea that occurs in the absence of a clear etiologic factor. ICSA generally develops beyond the 5th decade of life and may occur in the presence of cardiovascular risk factors. The natural history and prognostic implications of ICSA are not well understood. In this context, the role of long-term suppressive treatment has not been established. For patients presenting with suspected ICSA, we suggest a careful evaluation for underlying metabolic or physiologic disturbances, monitoring of symptoms and consideration of referral to an expert center.

Central sleep apnea (CSA) is a heterogeneous and relatively rare sleep breathing disorder characterized by recurrent reductions in respiratory drive and airflow during sleep. Its complex and not fully understood pathophysiology reflects challenges in respiratory control mechanisms. CSA is associated with cardiovascular, neurologic, systemic, and genetic conditions, and remains a key area for further research, particularly in improving diagnosis and understanding mechanisms. This article outlines the definition, diagnostic approaches, classification, and provides an overview of the underlying pathophysiology of CSA.

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.