Obstructive sleep apnea drug therapy: apnea–hypopnea index leaves us high and dry

[摘要] The past four decades of sleep apnea research have yielded tremendous insight into the pathophysiology of obstructive sleep apnea (OSA). Elegant research has substantiated that sleep state–dependent upper airway collapse obstructs ventilation, inducing intermittent reductions in oxygen, coincidental with increases in carbon dioxide, autonomic instability, and, typically, a brief arousal.1 We understand that upper airway collapse occurs, at least in part, because of reduced activity of upper airway dilator muscles in sleep, and we now understand more fully some of the sleep state–dependent alterations in neurotransmitters and modulators at the relevant motoneurons.2 Based on these advances, one would have anticipated 10–20 years ago that by now we would have one or more successful pharmacotherapies for OSA. The need for a pharmacotherapy is readily appreciable by most physicians and patients. OSA is an independent risk factor for myocardial infarction, stroke, hypertension, motor vehicle accidents, depression, and altered glucose metabolism.3–5 The mainstay therapy, positive airway pressure (PAP), while highly effective in palliating OSA, is a difficult therapy for many individuals; consequently, many patients have given up on PAP or use it for only a fraction of their sleep.6

[学科分类] 生理学