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 cycles of hypoxia-reoxygenation are associated with oxidative stress that, in turn, triggers the activation of pathways that lead to cardiovascular damage. These pathways include an increased chemoreflex sensitivity that induces the over-activation of the sympathetic nervous system, decreased baroreflex sensitivity, the activation of systemic inflammation pathways mediated primarily by the nuclear transcriptional factor kappaB that favors the development of atherosclerosis through the synthesis of cytokines and the expression of adhesion molecules, endothelial dysfunction with a decreased availability of nitric oxide, dyslipidemia, insulin resistance and stimulation of the renin-angiotensin system. Other mechanisms proposed include arousals that increase sympathetic activity and exaggerated intrathoracic pressure changes that generate high transmural pressure. Most of these mechanisms respond favorably to treatment with CPAP. A better understanding of the mechanisms of cardiovascular damage opens the possibility of instituting new treatments that will contribute to limiting the cardiovascular consequences associated with OSAS.