Clinical perspective of obstructive sleep apnea-induced cardiovascular complications

Obstructive sleep apnea (OSA) syndrome is a highly prevalent disorder characterized by recurrent upper airway collapse during sleep, and associated with repetitive episodes of transient oxygen desaturation during sleep. It disrupts normal ventilation and sleep architecture, and is typically associated with excessive daytime sleepiness, snoring, and witnessed apneas. Besides being associated with neurocognitive impairment, mood and behavioral effects, and increased risk for work-related and traffic accidents, OSA has also been implicated in the pathogenesis of various cardiovascular diseases, including systemic hypertension, coronary artery disease, congestive heart failure, pulmonary hypertension, stroke, and cardiac arrhythmias. The mechanisms by which OSA affects the cardiovascular system may involve mechanical effects on intrathoracic pressure, increased sympathetic activation, intermittent hypoxia, and endothelial dysfunction. Therapy with continuous positive airway pressure (CPAP) has been demonstrated to improve cardiopulmonary hemodynamics in patients with OSA and may reverse the endothelial cell dysfunction.