Sleep—Sometimes a Test of Survival

Abstract & Commentary

By Charles P. Pollak, MD, Professor, Clinical Neurology, Weill College of Medicine. Dr. Pollak is a stockholder for Merck, and is on the speaker's bureau for Merck.

Synopsis: Sleep-disordered breathing is a significant risk factor for cardiac arrhythmias and sudden death.

Source: Mehra R, et al. Association of Nocturnal Arrhythmias with Sleep-disordered Breathing. The Sleep Heart Health Study. Am J Respir Crit Care Med. 2006;173:910-916.

Of all sleep disorders, the ones of greatest concern are those grouped under the rubric sleep-disordered breathing (SDB). They include obstructive sleep apnea, central sleep apnea, sleep hypoventilation, and related disorders. We have long known that SDB, especially obstructive sleep apnea, is associated with cardiac arrhythmias, including some that are dangerous. However, the extent to which SDB raises the arrhythmia risk has not been known, nor has it been clear whether it is SDB itself or associated characteristics such as age, obesity, and gender that are responsible. Some answers can now be given thanks to a multicenter, longitudinal study of 6441 participants organized in the mid-1990s.

Subjects were divided into those with severe SDB (30 apneas or hypopneas per hour of sleep) and those free of SDB (< 5 apneas or hypopneas). It was postulated that the 228 participants with severe SDB had a higher prevalence of nocturnal cardiac arrhythmias than the 338 who were unaffected. SDB was considered the main risk in this study; correlates included age, BMI, sex, and coronary heart disease.

Arrhythmias were analyzed using ECG interpretation software and were scored as ventricular, ventricular ectopic, or normal beats. Ventricular arrhythmias included premature ventricular contraction, bigeminy, trigeminy, quadrigeminy, nonsustained ventricular tachycardia, or complex ventricular ectopy (nonsustained ventricular tachycardia, bigeminy, trigeminy, or quadrigeminy). Atrial arrhythmias included premature atrial contraction, supraventricular tachycardia, and atrial fibrillation. Conduction delay arrhythmias were coded as first-, second-, and third-degree avioventricular block, intraventricular conduction delay, and sinus pauses lasting at lease 3 seconds.

Arrhythmias that were more common in the SDB group included atrial fibrillation (odds ratio 4.02), nonsustained ventricular tachycardia (OR 3.40), and complex ventricular ectopy (OR 3.40). SDB status was a significant predictor of the number of ventricular ectopic beats per hour (75% higher in those with SDB than those without).


Recent studies have shown that the risk of nocturnal sudden death from cardiac causes (as well as stroke) is more than doubled in people with SDB. This study offers a possible explanation. It has also recently been found that increased airway pressure (CPAP) decreases ventricular ectopy in SDB patients, suggesting that the risks associated with nocturnal arrhythmias may be reducible with CPAP. Future systematic investigations of CPAP in such well-defined populations as the one described here are, therefore, anxiously awaited. Meanwhile, the present findings mandate the use of at least one ECG lead in all diagnostic sleep recordings. It also seems desirable that sleep disorders centers secure the ongoing participation of cardiologists, either as team members or consultants. Referring physicians ought to expect polysomnographic reports always to include a section assessing the cardiac rhythm during sleep.