Elsevier

Sleep Medicine

Volume 13, Issue 6, June 2012, Pages 759-762
Sleep Medicine

Brief Communication
Rem sleep brady-arrhythmias: An indication to pacemaker implantation?

https://doi.org/10.1016/j.sleep.2012.03.001Get rights and content

Abstract

Objectives

Important adjustments in the autonomic nervous system occur during sleep. Bradycardia, due to increased vagal tone, and hypotension, caused by reduction of sympathetic activity, may occur during non rapid eye movement (REM) sleep (NREM). Increased sympathetic activity, causing increased heart rate, is conversely a feature of phasic REM sleep. During REM sleep, sinus arrests and atrioventricular (AV) blocks unrelated to apnea or hypopnea have been described. These arrhythmias are very rare and only a few cases have been reported in the literature.

Patients/methods

Following an ECG performed for other reasons, two patients with no history of sleep complaints nor symptoms of heart failure or heart attack were referred to our center for nocturnal brady-arrhythmias.

Results

24 h ECG Holter recorded several episodes of brady-arrhythmia with sinus arrest in the first patients and brady-arrhythmias with complete AV block in the second patient. In both patients, episodes of brady-arrhythmia were prevalent in the second part of the night. Nocturnal polysomnography (PSG) demonstrated that episodes occurred only during REM sleep, particularly during phasic events. Treatment with pacemaker was considered only for the patient with complete AV blocks.

Conclusions

These types of brady-arrhythmias are usually detected accidentally due to their lack of symptoms. It has been suggested that in some patients they may lead to sudden unexpected death. Thus, the identification of predisposing factors is mandatory in order to prevent potentially dangerous arrhythmic events.

Introduction

In 1984 Guilleminault et al. described a syndrome characterized by sinus arrest during rapid eye movement (REM) sleep in four patients with apparently no heart disease or sleep apnoeas [1].

A few other similar cases have been reported in the literature [2], [3], [4], [5], [6], [7]. An autonomic dysfunction during phasic REM sleep has been hypothesized as the pathophysiological mechanism of REM sleep arrhythmias [8].

In most cases, REM sleep arrhythmias involve healthy individuals who underwent electrocardiogram (ECG) monitoring for other reasons. A few patients reported aspecific complaints (faintness, light headedness, atypical thoracic pain) during diurnal activities, apparently unrelated to REM sleep arrhythmias. In all patients ECG-Holter and polysomnogram (PSG) monitoring have never shown arrhythmias during wakefulness. Nor have they shown sinus arrests or AV blocks related to respiratory disturbances during sleep (RDS). RDS must be ruled out in these patients because, independent of REM sleep, obstructive sleep apnea syndrome (OSAS) may be associated with nocturnal arrhythmias responsive to continuous positive airway pressure (CPAP) [9], [10]. Differently, REM sleep arrhythmias unrelated to RDS have been generally treated with PM implantation [8].

We report a case of sinus arrest and a case of complete AV block appearing only during REM sleep in two otherwise healthy individuals.

Patient 1: A 43 year-old man was referred to our center by his cardiologist for nocturnal brady-arrhythmia. No sleep complaints or symptoms of heart failure or heart attack were reported. Physical examination was normal (body mass index [BMI] 23.7). He did not take any drugs and did not smoke. An occasional brady-arrhythmia was found in a routine ECG, performed for his sporting activity. Consequently, a 24 h Holter ECG was recorded, showing several episodes of brady-arrhythmia with sinus arrest (maximum RR interval [invterval between ventricular depolarizations] 13.8 s at 4.37 h a.m.). The occurrence of these episodes was more frequent in the second part of the night and the maximum index of ventricular events per hour occurred between 4 and 5 a.m. The average heart rate was 47 bpm, with a minimum of 29 bpm and a maximum of 147 bpm. The 24 h blood pressure monitoring was normal.

In order to better investigate the relationship between his sleep patterns and the episodes of brady-arrhythmia, the patient underwent two consecutive PSGs. Electroencephalogram (EEG), electrooculogram (EOG), submental electromyogram (EMG), tibialis EMG, ECG, nasal and oral airflow, movements of the chest and abdomen, snoring, transcutaneous oxygen saturation, and pulse rate were recorded. Sleep was scored according to the standard rules [11], Hypnogram was normal. The analysis showed just one hypopnea, 35 s long, during the REM stage of sleep. Mean oxygen saturation was 96.6% and lowest SaO2 was 86.0%. The mean heart rate in REM sleep was 35.5 ± 4.5 (min. 26.0, max. 69.0); in NREM sleep it was 34.4 ± 2.1 (min. 27.0, max. 84.0).

Several episodes of brady-arrhythmia with sinus arrest were recorded during REM sleep, particularly related to phasic events, with the longest one lasting 5.08 s (at 6:23 a.m.). There was no relationship between sinus arrests and respiratory events. The patient was evaluated by a cardiologist in another Hospital who decided not to implant a pacemaker. At a follow up visit after four years the patient is still asymptomatic.

Patient 2: A 20 year-old man was admitted to the emergency unit because of a car accident. During the ECG monitoring, several ECG pauses (up to four seconds) due to complete atrioventricular (AV) block were detected during sleep.

All these episodes were asymptomatic. The car accident was not caused by a syncope and there was no evidence of myocardial contusion. The echocardiogram was normal and troponine test was negative. No sleep complaints or symptoms of heart failure or heart attack were reported. The patient denied tachycardia, extrasystolic beats, syncope and presyncope, blurred vision, dizziness, precordial pain, dyspnoea, and weakness without reasonable causes. Physical examination was normal (BMI 23.88). He did not take any drugs and did not smoke. He did not practice any sport activities. His family history was unremarkable. He underwent a 24 h Holter ECG recording that detected several episodes of brady-arrhythmia with complete AV block (maximum pause of 10 s at 7:24 a.m.) between 5 a.m. and 7:30 a.m. The average heart rate was 76 bpm with a minimum of 25 bpm and a maximum of 159 bpm.

In order to better investigate the relationship between his sleep patterns and the episodes of brady-arrhythmia, he underwent a nocturnal PSG. The hypnogram was normal. No sleep related respiratory disorders were detected. Mean oxygen saturation was 97.7% and the lowest SaO2 was 94.0%. The mean heart rate during REM sleep was 49.7 ± 6.8 (min. 27.0, max. 82.0). ECG showed five episodes of brady-arrhythmia, all occurring during REM sleep and particularly related to phasic events, with the longest episode lasting 10.7 s (at 3:02 a.m.). The occurrence of these episodes was usually in the second part of the night and the maximum index of ventricular events per hour occurred between 4 and 5 a.m. (Fig. 1). No brady-arrhythmias were recorded during NREM sleep. The 24 h blood pressure monitoring did not show anything abnormal. A cardiologist decided to implant a pacemaker (atrio-ventricular “DDD”). In order to exclude a familiar disorder, all first degree family members were then studied with Holter ECG. All exams came back negative. At the follow up (14 months) the analysis of the PM activity data demonstrated a 1.7% of activation in DDD.

Section snippets

Discussion

Both our patients were asymptomatic and presented REM sleep arrhythmias recorded fortuitously during phasic events of REM sleep, a sleep stage usually associated with vagal nerve suppression and a surge of sympathetic activity. Therefore, these arrhythmias may be regarded as the consequence of an altered autonomic activity appearing only at night and, specifically, during phasic REM sleep. Cases previously reported present very similar features: lack of symptoms, occasional detection of

Conflict of Interest

The ICMJE Uniform Disclosure Form for Potential Conflicts of Interest associated with this article can be viewed by clicking on the following link: doi:http://dx.doi.org/10.1016/j.sleep.2012.03.001.

. ICMJE Form for Disclosure of Potential Conflicts of Interest form.

Acknowledgements

We are grateful to Prof. Giorgio Coccagna (Bologna) and Prof. Gianfranco Parati (Milan) for kindly agreeing to review this manuscript before submission.

References (18)

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