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Full list of author information is available at the end of the articleBackground Obstructive sleep apnea syndrome (OSAS) is a respiratory disorder of sleep characterized by recurrent episodes of complete or partial airway obstruction, associated with intermittent arterial oxygen desaturation. The repetitive nocturnal hypoxemia experienced by patients with OSAS is associated with activation of a number of neural, hu-moral, thrombotic, metabolic, and inflammatory disease mechanisms, all of which play a role in the pathophysi-ology of cardiac and vascular diseases [1-3]. Moreover, several etiological factors in OSAS overlap with those of cardiovascular diseases making it difficult to distinguish the direct cardiovascular consequences of OSAS from its role in exacerbating concomitant cardiovascular disease [4,5]. OSAS is also associated with obesity, hypertension and metabolic dysregulation which themselves contribute to endothelial dysfunction [6,7]. In recent studies [8,9] the association of OSAS and coronary artery disease (CAD) has been documented