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Abstract
Obstructive sleep apnea (OSA) is present in at least 2% to 4% of the general population.
Central sleep apnea (CSA), though less common, is highly prevalent in patients with
heart failure. Both forms of sleep apnea exert strong modulatory effects on the autonomic
nervous system at night through a number of mechanisms including central respiratory-cardiac
coupling in the brainstem, chemoreflex stimulation, baroreflexes, and reflexes relating
to lung inflation. Arousals also contribute to the autonomic disturbance. Although
sleep is normally a time when parasympathetic modulation of the heart predominates
and myocardial electrical stability is enhanced, OSA and CSA disturb this quiescence,
creating an autonomic profile in which both profound vagal activity leading to bradyarrhythmias,
and sympatho-excitation favoring ventricular ectopy are observed. The resulting tendency
toward cardiac arrhythmia may directly contribute to sudden cardiac death and premature
mortality in patients with sleep apnea. Therapy consists largely of treatment with
continuous positive airway pressure, which has been shown to improve autonomic profile
and reduce nocturnal arrhythmias.