Central sleep apnoea: not just one phenotype

Central sleep apnoea: not just one phenotype

2024 | Winfried Randerath, Sébastien Baillieul, Renaud Tamisier
Central sleep apnoea (CSA) is a group of sleep-related breathing disorders characterized by reductions or complete cessation of ventilation during sleep. Recent scientific advancements have highlighted the heterogeneity of CSA in terms of underlying causes, pathophysiological concepts, treatment responses, and outcomes. This review aims to describe the current understanding of the pathophysiology of different clinical entities of CSA and provide an update on the role of adaptive servo-ventilation (ASV) in its treatment. The pathophysiological characteristics of CSA include loop gain, apnoeic threshold, breathing regulation, and neuromuscular mechanics. Chronic heart failure (CHF) is the most common underlying cause, leading to nonhypercapnic CSA due to increased loop and controller gain. Other factors such as stroke, medication use, and high altitude can also contribute to CSA. The diagnosis of CSA is primarily based on polysomnography, which measures the apnoea-hypopnoea index (AHI). However, there are limitations in differentiating central from obstructive hypopnoeas, and the precise number of central events required for diagnosis is not well-defined. The severity and type of CSA can vary significantly between patients, and night-to-night variability in CSA severity has been poorly explored. The treatment of CSA includes positive pressure therapies, oxygen supplementation, noninvasive ventilation (NIV), and pharmaceutical options. Continuous positive airway pressure (CPAP) is the first-line therapy, but its effectiveness in improving cardiovascular outcomes or mortality in CSA is uncertain. NIV is recommended for hypercapnic CSA associated with central hypoventilation syndromes. ASV is the most effective option for treating periodic breathing (PB) in CSA, improving AHI, left ventricular ejection fraction (LVEF), and 6-minute walking distance. Pharmacological treatments for CSA are limited by small sample sizes and short follow-up periods. Hypnotic agents and carbonic anhydrase inhibitors like acetazolamide have shown some promise, but more high-quality trials are needed. The FACE trial and the ADVENT-HF study have provided valuable insights into the impact of ASV on survival and cardiovascular outcomes in patients with CHF and CSA. The results of these studies will help refine treatment algorithms and guide clinicians in their therapeutic decisions. In conclusion, the phenotyping of CSA based on underlying aetiology, pathophysiological characteristics, and treatment response is crucial for individualized therapy. Further research is needed to improve the understanding and management of CSA, particularly in patients with CHF.Central sleep apnoea (CSA) is a group of sleep-related breathing disorders characterized by reductions or complete cessation of ventilation during sleep. Recent scientific advancements have highlighted the heterogeneity of CSA in terms of underlying causes, pathophysiological concepts, treatment responses, and outcomes. This review aims to describe the current understanding of the pathophysiology of different clinical entities of CSA and provide an update on the role of adaptive servo-ventilation (ASV) in its treatment. The pathophysiological characteristics of CSA include loop gain, apnoeic threshold, breathing regulation, and neuromuscular mechanics. Chronic heart failure (CHF) is the most common underlying cause, leading to nonhypercapnic CSA due to increased loop and controller gain. Other factors such as stroke, medication use, and high altitude can also contribute to CSA. The diagnosis of CSA is primarily based on polysomnography, which measures the apnoea-hypopnoea index (AHI). However, there are limitations in differentiating central from obstructive hypopnoeas, and the precise number of central events required for diagnosis is not well-defined. The severity and type of CSA can vary significantly between patients, and night-to-night variability in CSA severity has been poorly explored. The treatment of CSA includes positive pressure therapies, oxygen supplementation, noninvasive ventilation (NIV), and pharmaceutical options. Continuous positive airway pressure (CPAP) is the first-line therapy, but its effectiveness in improving cardiovascular outcomes or mortality in CSA is uncertain. NIV is recommended for hypercapnic CSA associated with central hypoventilation syndromes. ASV is the most effective option for treating periodic breathing (PB) in CSA, improving AHI, left ventricular ejection fraction (LVEF), and 6-minute walking distance. Pharmacological treatments for CSA are limited by small sample sizes and short follow-up periods. Hypnotic agents and carbonic anhydrase inhibitors like acetazolamide have shown some promise, but more high-quality trials are needed. The FACE trial and the ADVENT-HF study have provided valuable insights into the impact of ASV on survival and cardiovascular outcomes in patients with CHF and CSA. The results of these studies will help refine treatment algorithms and guide clinicians in their therapeutic decisions. In conclusion, the phenotyping of CSA based on underlying aetiology, pathophysiological characteristics, and treatment response is crucial for individualized therapy. Further research is needed to improve the understanding and management of CSA, particularly in patients with CHF.
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