CPAP Effect on Vascular Function in Obstructive Sleep Apnea

Obstructive sleep apnea (OSA) syndrome is responsible of vascular damage. Intermittent hypoxia causes oxidative stress and low-grade inflammation. By the way of increased sympathetic outflow, it's resulting endothelial dysfunction, atherosclerosis and an increase of arterial stiffness. Finally these mechanisms are responsible of cardiovascular comorbidities: hypertension, cardiac arrhythmias or Left ventricular dysfunction. This patients presented coronary diseases or Strokes. OSA characterized by intermittent hypoxia, is associated with atherosclerosis and vascular inflammation. Polymorphonuclear leukocytes (PMNs) are implicated in vascular inflammation by producing oxidizing radicals and proteolytic enzymes during PMN-endothelium interactions. Reactive oxygen species (ROS) production is increased in activated cells and after attachment, PMNs release additional ROS inducing endothelial cell injury. Continuous positive airway pressure (CPAP) is the current "gold standard" treatment for OSA, Use of CPAP restored the respiratory flow, prevents nocturnal respiratory events and daytime symptoms. Arterial stiffness and endothelial dysfunction are linked to obstructive sleep apnea severity with a dose-effect relationship. And meta-analyse showed significant improvements in all indices of arterial stiffness after CPAP treatment in patients with OSA. Assessment of pulse wave velocity and peripheral arterial tone are study measurements of arterial stiffness. And are strong predictors of late cardiovascular events The investigators will compare long term evolution in arterial stiffness (PWV) and endothelial dysfunction (Peripheral arterial tone) for patients with OSA treated by Positive Airway Pressure Therapies.