Obstructive sleep apnea (OSA) is a common disorder characterized by repetitive interruption of ventilation during sleep caused by recurrent upper airway collapse, which leads to intermittent hypoxia. The disorder is commonly undiagnosed despite its relationship with substantial cardiovascular morbidity and mortality. Moreover, the effects of the disorder appear to be particularly dangerous in young subjects. In the last decade, substantial clinical evidence has identified OSA as independent risk factor for both bradyarrhythmias and tachyarrhythmias. To date the mechanisms leading to such arrhythmias have not been completely understood. However, recent data from animal models and new molecular analyses have increased our knowledge of the field, which might lead to future improvement in current therapeutic strategies mainly based on continuous positive airway pressure. This paper aims at providing readers a brief and specific revision of current knowledge about the mechanisms underlying atrial arrhythmias in OSA and their clinical and therapeutic implications. 1. Introduction Obstructive sleep apnea (OSA) is a relevant health problem because of its high prevalence and concomitant severe effects in the general population [1]. Although the disorder is mainly present in obese men, other clinical characteristics such as age 65 years or older, smoking, and alcohol consumption are also common [1]. OSA is characterized by repetitive interruption of ventilation during sleep caused by recurrent upper airway collapse, which is associated with increasing respiratory efforts and intermittent arterial oxygen desaturation. Nocturnal arousals, loud intermittent snoring, and increased daytime sleepiness are the main symptoms [2]. Obstructive apneas and hypopneas are considered significant if they last for more than 10 seconds. Such episodes can be recorded and quantified by a polysomnography study, which remains the standard technique for the diagnosis. Currently, international guidelines consider the diagnosis of OSA in the presence of an apnea-hypopnea index ≥5 and persistent respiratory effort during the episodes [2]. Cardiovascular morbidity and mortality significantly increase in patients with untreated severe OSA [3]. Moreover, the effects of the disorder appear to be particularly dangerous in young subjects [3, 4]. Substantial evidence supports the association between OSA and cardiovascular diseases, among which atrial arrhythmias and conduction disorders are of particular interest [5, 6]. Abnormalities such as hypoxia or sympathovagal imbalance are consistently
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