Sleep-disordered breathing (SDB), characterized by specific underlying physiological mechanisms, comprises obstructive and central pathophysiology, affects nearly 1 billion individuals worldwide, and is associated with excessive cardiopulmonary morbidity. Strong evidence implicates SDB in cardiac arrhythmogenesis. Immediate consequences of SDB include autonomic nervous system fluctuations, recurrent hypoxia, alterations in carbon dioxide/acid-base status, disrupted sleep architecture, and accompanying increases in negative intrathoracic pressures directly affecting cardiac function. Day-night patterning and circadian biology of SDB-induced pathophysiological sequelae collectively influence the structural and electrophysiological cardiac substrate, thereby creating an ideal milieu for arrhythmogenic propensity. Cohort studies support strong associations of SDB and cardiac arrhythmia, with evidence that discrete respiratory events trigger atrial and ventricular arrhythmic events. Observational studies suggest that SDB treatment reduces atrial fibrillation recurrence after rhythm control interventions. However, high-level evidence from clinical trials that supports a role for SDB intervention on rhythm control is not available. The goals of this scientific statement are to increase knowledge and awareness of the existing science relating SDB to cardiac arrhythmias (atrial fibrillation, ventricular tachyarrhythmias, sudden cardiac death, and bradyarrhythmias), synthesizing data relevant for clinical practice and identifying current knowledge gaps, presenting best practice consensus statements, and prioritizing future scientific directions. Key opportunities identified that are specific to cardiac arrhythmia include optimizing SDB screening, characterizing SDB predictive metrics and underlying pathophysiology, elucidating sex-specific and background-related influences in SDB, assessing the role of mobile health innovations, and prioritizing the conduct of rigorous and adequately powered clinical trials.

中文翻译：

---

成人睡眠呼吸障碍和心律失常：机制见解和临床意义：美国心脏协会的科学声明

睡眠呼吸障碍 (SDB) 具有特定的潜在生理机制，包括阻塞性和中枢性病理生理学，影响全球近 10 亿人，并与过度的心肺发病率相关。强有力的证据表明 SDB 与心律失常发生有关。SDB 的直接后果包括自主神经系统波动、反复缺氧、二氧化碳/酸碱状态改变、睡眠结构紊乱以及伴随的胸内负压增加，直接影响心脏功能。SDB 引起的病理生理后遗症的昼夜模式和昼夜节律生物学共同影响结构和电生理心脏基质，从而为心律失常倾向创造理想的环境。队列研究支持 SDB 与心律失常之间的密切关联，有证据表明离散呼吸事件会引发房性和室性心律失常事件。观察性研究表明，SDB 治疗可减少节律控制干预后心房颤动的复发。然而，尚无来自临床试验的高级证据支持 SDB 干预对节律控制的作用。本科学声明的目标是提高对 SDB 与心律失常（房颤、室性快速性心律失常、心源性猝死和缓慢性心律失常）相关的现有科学的知识和认识，综合与临床实践相关的数据并确定当前的知识差距，提出最佳的解决方案。实践共识声明，并优先考虑未来的科学方向。确定的针对心律失常的关键机会包括优化 SDB 筛查、表征 SDB 预测指标和潜在病理生理学、阐明 SDB 中性别特异性和背景相关的影响、评估移动健康创新的作用以及优先考虑进行严格和充分的研究动力临床试验。