Key result
Sleep respiratory disturbances linked to ~17.5-fold higher odds of immediate nocturnal PAF or NSVT.
Why the study?
Sleep-disordered breathing is associated with an increased risk of atrial fibrillation, non-sustained ventricular tachycardia, and nocturnal sudden cardiac death, but prior research had not established whether respiratory disturbances act as immediate triggers for nocturnal arrhythmias.
Do sleep-related respiratory disturbances (apneas and hypopneas) act as acute transient triggers for nocturnal episodes of paroxysmal atrial fibrillation or non-sustained ventricular tachycardia in individuals with sleep-disordered breathing?
Case-Control (n=57)
Single-blind
Yes
Do sleep-related respiratory disturbances (apneas and hypopneas) act as acute transient triggers for nocturnal episodes of paroxysmal atrial fibrillation or non-sustained ventricular tachycardia in individuals with sleep-disordered breathing?
Answers are grounded in this paper and cite their sources.
Provides direct temporal evidence that sleep-disordered breathing events (apneas and hypopneas) acutely trigger nocturnal paroxysmal atrial fibrillation and non-sustained ventricular tachycardia, increasing relative arrhythmia odds nearly 18-fold within 90 seconds even though the absolute event rate per disturbance is low.
Objectives: This study sought to evaluate respiratory disturbances as potential triggers for arrhythmia in those with sleep-disordered breathing (SDB). Background: SDB is associated with increased risk of atrial fibrillation (AF) and non-sustained ventricular tachycardia (NSVT) as well as a predilection for sudden cardiac death during nocturnal sleeping hours. However, prior research has not established whether respiratory disturbances operate as triggers for nocturnal arrhythmias. Methods: Overnight polysomnograms (PSGs) from the Sleep Heart Health Study (n = 2816) were screened for paroxysmal atrial fibrillation (PAF) and NSVT. We used the case-crossover design to determine whether apneas and/or hypopneas are temporally associated with episodes of PAF or NSVT. For each arrhythmia, 3 periods of sinus rhythm were identified as control intervals. PSGs were examined for the presence of respiratory disturbances, oxygen desaturations, and cortical arousals within a 90-second hazard period preceding each arrhythmia or control period. Results: Fifty-seven participants with a wide range of SDB contributed 62 arrhythmias (76% NSVT). The odds of an arrhythmia following a respiratory disturbance were nearly 18-times (OR 17.5; 95% CI 5.3–58.4) the odds of an arrhythmia occurring following normal breathing. The absolute rate of arrhythmia associated with respiratory disturbances was low (1 excess arrhythmia/40000 respiratory disturbances). Neither hypoxia nor EEG-defined arousals alone increased arrhythmia risk. Conclusions: Although the absolute arrhythmia rate is low, the relative risk of PAF and NSVT during sleep is markedly increased shortly after a respiratory disturbance. These results support a direct temporal link between SDB events and the development of these arrhythmias.
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Monahan et al. (2009) conducted a case-control in Sleep-disordered breathing (SDB) with nocturnal paroxysmal atrial fibrillation (PAF) or non-sustained ventricular tachycardia (NSVT) (n=57). Respiratory disturbance (apnea or hypopnea) vs. Normal nocturnal breathing (3 matched 90-second referent periods of sinus rhythm per arrhythmia in the same sleep stage) was evaluated on Occurrence of nocturnal arrhythmia (paroxysmal atrial fibrillation [PAF] or non-sustained ventricular tachycardia [NSVT]) within a 90-second hazard period (OR 17.5, 95% CI 5.3-58.4). Respiratory disturbances during sleep increased the odds of nocturnal PAF or NSVT nearly 18-fold within 90 seconds compared to normal breathing (OR 17.5; 95% CI 5.3-58.4).
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