Syncope and obstructive sleep apnea: Mechanisms and clinical scenarios

Obstructive sleep apnea (OSA) is a highly prevalent sleep disorder affecting a considerable proportion of the adult population. It is characterized by chronic intermittent hypoxia (CIH), resulting from recurrent partial (hypopnea) or complete obstruction (apnea) of the upper airway during sleep. Clinically, OSA produces fragmented sleep, loud snoring, excessive daytime somnolence, cognitive dysfunction, and nocturnal diaphoresis. Importantly, OSA is recognized as an independent risk factor for systemic hypertension and is associated with cardiac arrhythmias and stroke. The CIH contributes to these adverse outcomes by enhancing carotid body chemoreceptor sensitivity and promoting sympathetic overactivation, systemic inflammation, and oxidative stress. Syncope is a transient, fully reversible loss of consciousness caused by cerebral hypoperfusion. Although cardiac causes such as atrial fibrillation and brady-arrhythmias are well recognized, the vasovagal syncope (VVS) remains the most common etiology, triggered by exaggerated vagal activation. Emerging evidence suggests that OSA may contribute to VVS, as patients with unexplained syncope show a high prevalence of OSA and often improve with CPAP therapy. This minireview summarizes the potential mechanisms linking OSA to syncope, provides a brief overview of OSA pathophysiology, and discusses autonomic pathways that may underline syncope in this population, highlighting their relevance for clinical management.