Endothelial mechanisms of endothelial dysfunction in patients with obstructive sleep apnea

Obstructive sleep apnea (OSA) occurs in 2% of middle-aged women and 4% of middle-aged men in the general population and the prevalence is much higher in specific patient groups. Intermittent hypoxia (IH, oxygen desaturation and re-oxygenation) cycle, a major pathophysiologic character of OSA, and the physiological responses this evokes are thought to be responsible for its association with increased cardiovascular morbidity and mortality. Endothelial dysfunction, resulting from IH and as a key early event in atherosclerosis, was demonstrated repeatedly in patients with OSA and in animal models of IH, providing an important mechanistic link between the acute cyclical IH during sleep and the increased prevalence of chronic vascular diseases.

From this work, we conclude that IH from OSA may result in endothelial dysfunction, as a potential promoter of atherosclerosis, through nitric oxide unavailability, oxidative stress and inflammation, cell apoptosis, the crosstalk between endothelial cells and circulating inflammatory cells, microparticles, and damage repairing process. Though effective continuous positive airway pressure (CPAP) may specifically improve endothelial function, more controlled larger interventional trials that will include multiple centers and randomized allocation of CPAP therapy are needed to see if such changes are reversible before cause and effect can be implied finally, while further studies on cellular and animal level are also needed to elucidate molecular biologic/pathologic pathways.