ABSTRACT
It is well known that sleep is associated with unstable breathing in large numbers of otherwise healthy people. Approximately 2% to 3% of children, 2% to 9% of middle aged adults, and up to 15% of adults over age 65 have moderate-to-severe obstructive sleep apnea (OSA) [apnea-hypopnea index (AHI) ≥ 15 events per hour] (1). The definition of clinically-significant sleep apnea is somewhat arbitrary and there is no consensus as to how much sleep apnea should be considered pathological. It is important to note that a clinically-significant AHI in someone with a chronic disease might not be significant in an otherwise healthy individual. That is, there may be an interactive effect of certain chronic diseases with the AHI that can affect mortality (2). While sleep apnea has been associated with significant morbidity, especially cardiovascular disease, cognitive, behavioral and neural deficits, and metabolic disorders (3-5), these data are largely correlative. However, data are accumulating from direct, interventional studies that induce or relieve OSA (6-8) suggesting a link between OSA and hypertension. In addition, animal studies have used intermittent hypoxic exposures to mimic the hypoxemia experienced during OSA and have demonstrated cognitive deficits (9), persistent ventilatory changes (10), and regional changes in brain tyrosine hydroxylase activity (11). Thus, there is growing support for persistent, long-term pathological sequelae of sleep apnea. Given the large number of people that may be affected by sleep apnea, understanding the pathogenesis of sleep apnea/hypopnea is clearly of considerable importance.
