The following are key points to remember about this scientific statement from the American Heart Association (AHA) on sleep apnea and cardiac arrhythmias:

1. 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. SDB subtypes relevant to this scientific statement include obstructive sleep apnea (OSA), central sleep apnea (CSA), and Cheyne-Stokes breathing (CSB).
2. Obstructive sleep apnea (OSA) is characterized by repetitive occlusion or narrowing of the upper airway, resulting in apneas and hypopneas, that is, the absence or reduction, respectively, of inspiratory airflow for ≥10 seconds.
3. CSA is characterized by a transient cessation of or decrease in ventilatory effort generated by the pontomedullary respiratory pacemaker during sleep. This results from a reduction in the partial pressure of CO₂ below the apneic threshold, resulting in breathing cessation.
4. CSB is a form of CSA often occurring in heart failure and characterized by heightened ventilatory chemosensitivity resulting in alternating crescendo-decrescendo apneic and hyperpneic ventilatory periods, which can lead to decreased intrathoracic pressure during periods of hyperventilation.
5. Robust 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.
6. 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.
7. 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.
8. High-level evidence from clinical trials that supports a role for SDB intervention on rhythm control is lacking, however.
9. Epidemiological studies integrating detailed cardiac function and measures of visceral adiposity are needed to better discern the interrelationships of SDB, other sleep disorders, and metabolic mechanisms that contribute to cardiac arrhythmia.
10. Key opportunities at this time 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.

Clinical Topics: Arrhythmias and Clinical EP, Diabetes and Cardiometabolic Disease, Heart Failure and Cardiomyopathies, Prevention, Implantable Devices, SCD/Ventricular Arrhythmias, Atrial Fibrillation/Supraventricular Arrhythmias, Acute Heart Failure, Sleep Apnea

Keywords: Adiposity, Arrhythmias, Cardiac, Atrial Fibrillation, Cheyne-Stokes Respiration, Electrocardiography, Electrophysiology, Heart Failure, Hyperventilation, Hypoxia, Brain, Metabolic Syndrome, Primary Prevention, Sleep Apnea, Central, Sleep Apnea Syndromes, Sleep Apnea, Obstructive, Stroke, Telemedicine

< Back to Listings