Different pathophysiological mechanisms underlie the morbid associations observed between sleep apnea syndrome (SAS) and cardiovascular disease. Cardiovascular responses to apnea can be divided into acute cardiovascular modifications following each nocturnal respiratory event and chronic adaptations of the cardiovascular system. The same stimuli always trigger acute cardiovascular response: hypoxemia, hypercapnea, changes in the intra-thoracic pressure, micro-arousals. Each obstructive or central respiratory event is associated with a peak in blood pressure, changes in the heart rate, generally bradycardia at onset of apnea and tachycardia when respiration is renewed. Oxygen desaturation is the strongest stimulus explaining the observed acute cardiovascular responses. When these stimuli are repeated every night, the cardiovascular system adapts with a higher sympathetic tone and lower parasympathetic tone during the diurnal period. Baroreceptors also become less sensitive in apneic patients. Finally, endothelial function is altered in SAS patients with a desensitization of the alpha and beta-2 adrengeric receptors, altered NO-dependent vasodilatation, and hypersensitivity to vasoconstriction induced, for example, by angiotensin 2. The cardiovascular morbidity associated with SAS is currently thought to concern the development of diurnal hypertension (dose-effect response), left ventricular failure, higher risk of coronary or cerebral events. Very recently, epidemiological studies suggested that continuous positive pressure ventilation in SAS patients can reduce the cardiovascular risk.