Obstructive sleep apnea syndrome (OSAS) is an independent and modifiable risk factor for cardiovascular diseases; however, the pathophysiological mechanisms underlying this association are not yet fully understood. Intermittent hypoxemia, one of the physiological markers of OSAS, is characterized by transient periods of oxygen desaturation followed by reoxygenation. The hypoxia-reoxygenation cycles are associated with oxidative stress that, in turn, triggers the activation of pathways that lead to cardiovascular damage. The results of several studies show that OSAS causes oxidative stress and that nasal continuous positive airway pressure therapy normalizes these biological abnormalities. In conclusion, treatment of OSAS with continuous positive airway pressure may lower cardiovascular risk by reducing sympathetic nerve activity, ambulatory blood pressure and arterial stiffness, and by increasing sensitivity of the arterial baroreflex. Newer modalities such as C-Flex and A-Flex also show promise as treatment options in the future. However, the evidence supporting the use of these alternative modalities remains scant, in particular with regards to long-term cardiovascular outcomes.