Association of Nocturnal Arrhythmias with Sleep-disordered Breathing

Abstract

Rationale: Sleep-disordered breathing recurrent intermittent hypoxia and sympathetic nervous system activity surges provide the milieu for cardiac arrhythmia development. Objective: We postulate that the prevalence of nocturnal cardiac arrhythmias is higher among subjects with than without sleepdisordered breathing. Methods: The prevalence of arrhythmias was compared in two samples of participants from the Sleep Heart Health Study frequencymatched on age, sex, race/ethnicity, and body mass index: (1 ) 228 subjects with sleep-disordered breathing (respiratory disturbance index у 30) and (2 ) 338 subjects without sleep-disordered breathing (respiratory disturbance index Ͻ 5). Supported by National Heart, Lung and Blood Institute cooperative agreements U01HL53940 (University of Washington), U01HL53941 (Boston University), U01HL53938 (University of Arizona), U01HL53916 (University of California, Davis), U01HL53934 (University of Minnesota), U01HL53931 (New York University), U01HL53937 and U01HL64360 (Johns Hopkins University), U01HL63463 (Case Western Reserve University), and U01HL63429 (Missouri Breaks Research).The opinions expressed in this paper are those of the authors and do not necessarily reflect the views of the Indian Health Service.Correspondence and requests for reprints should be addressed to Reena Mehra, M.D., M.S., Case Western Reserve University, University Hospitals of Cleveland, 11100 Euclid Avenue, Cleveland, OH 44106. E-mail: mehrar@ameritech.net This article has an online supplement, which is accessible from this issue's table of contents at www.atsjournals.org Patients with sleep-disordered breathing (SDB) may be predisposed to arrhythmias because of alterations in sympathetic and parasympathetic nervous system activity occurring with SDBassociated hypoxemia, acidosis, apneas, and arousal (1-3). Mechanisms of arrhythmogenesis involve abnormal automaticity, triggered automaticity, and reentry mechanisms. Abnormal automaticity involves spontaneous cardiac impulse formation and may occur in SDB due to hypoxemia and respiratory acidosis accompanying apneic events (4). Triggered automaticity, pacemaker activity due to a stimulated action potential, may arise in SDB due to enhanced sympathetic nervous system activity associated with respiratory event-related hypoxemia and arousal (5). Reentry mechanisms may occur through the vagal stimulation that results from respiration against a partially occluded airway, which may lead to bradycardia-dependent increased dispersion of atrial repolarization predisposing to intraatrial entry (5-7). Also, SDB-related mechanical effects of negative intrathoracic pressure on the atrial and ventricular free walls promote cardiac stretch, which may predispose to arrhythmias via mechanicalelectrical feedback mechanisms (8).Despite the biological plausibility for SDB-associated hypoxemia, arousals, and autonomic nervous system dysregulation causing generation of abnormal cardiac electrophysiologic impulses, only limited research has rigorously characterized the association...

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