An estimated 15 to 20 million American adults have obstructive sleep apnea (OSA), a prevalence comparable to diabetes.1 OSA occurs when inspiratory airflow is either partly (hypopnea) or completely (apnea) occluded during sleep. The combination of sleep-disordered breathing with daytime sleepiness is referred to as the OSA syndrome.
Although loud snoring and severely disturbed sleep have made OSA a social curiosity, several factors have contributed to its emergence as an important medical condition. First, sleep deprivation with consequent daytime somnolence has been linked to motor vehicle and workplace-related accidents. Second, the epidemic of obesity has led to a high and rising prevalence of OSA. Third, and especially important, has been the evolving recognition of OSA as a mediator of cardiovascular disease. In this review, we will examine the characteristics, pathophysiology, and epidemiology of OSA, the cardiovascular disease mechanisms activated by OSA, and the evidence implicating OSA in cardiac, vascular, and related disease conditions. Particular emphasis will be placed on recent data linking OSA to inflammatory and metabolic dysregulation, and on newer information implicating OSA in atrial fibrillation (AF), stroke, myocardial infarction, and sudden cardiac death.