Obstructive sleep apnea syndrome (OSAS) is the most common sleep breathing disorder with a prevalence of 2–4% in middle-aged population. According to the International Classification of Sleep Disorders, patients with OSAS complain about daytime sleepiness, non-restorative sleep, fatigue, or insomnia symptoms, including irritability and altered cognitive performance, and wake up with breath holding, gasping, or choking. In order to diagnose OSAS, the VPSG or the OCST should demonstrate at least five predominantly obstructive events (obstructive and mixed apneas, hypopneas, or respiratory effort-related arousal) per hour of sleep during a VPSG or per hour of monitoring.

The clinical relevance of OSAS is related to its strong association with obesity, hypertension, and increased cardiovascular risk [5, 6]. Recurrent apneas have three main effects: hypoxia and hypercapnia due to alterations in gas exchange, sleep fragmentation with repetitive arousal, and finally modification of sympathetic activity, with increased BP and HR. Although the pathophysiological factors linking OSAS and cardiovascular risk are not completely understood, several evidences support the hypothesis that sleep fragmentation and intermittent hypoxia during each apnoeic event cause a chronic hyperactivation of the sympathetic nervous system during both sleep and wakefulness. A further increase in sympathetic activity could be related to the depression of spontaneous baroreflex sensitivity (BRS) as a consequence of the arousal response. Furthermore, patients with OSAS may show a sinus brady-tachyarrhythmia during obstructive events, mediated by cyclical changes in parasympathetic and sympathetic neural activity. Compared to controls, OSAS patients are characterized by a lower total HRV and a possible shift of the sympatho-vagal balance toward a sympathetic predominance and a vagal withdrawal during wakefulness and sleep.