Night-time bradyarrhythmia in a patient with mild obstructive sleep apnea syndrome is reversed with CPAP treatment

Tags: polysomnography, POEMS syndrome, OSAS, oxygen saturation, Journal of Clinical Sleep Medicine, sleep efficiency, heart rate, sleep stages, heart block, patient, tendon reflexes, obstructive hypopneas, Neurologic examination, skin changes, polyneuropathy, endocrinopathy, Rainer Dziewas, hour, Cardiac arrhythmia, normal distribution, arterial hypertension, monoclonal gammopathy, REM sleep, Sleep-induced apnea, conduction disturbances, sleep apnoea syndrome, J Cardiol, sleep apnea, obstructive sleep apnea, Cardiac arrhythmias, J Electrocardiol, Guilleminault C, atrioventricular block, respiratory events, Becker E, sleep, Wichert P. Reversal, sinus arrest, arrhythmia
Content: case reportS
Night-time Bradyarrhythmia in a Patient with Mild Obstructive sleep apnea Syndrome is Reversed With CPAP Treatment Rainer Dziewas, M.D.; Tanya Imai, M.D.; Ralf Dittrich, M.D.; Marius Humpert, M.D.; Benjamin Hopmann, M.D.; Matthias Bцntert, M.D.; Peter Lьdemann, M.D.; Peter Young, M.D.
Department of Neurology, University Hospital of Mьnster, Mьnster, Germany
Abstract: Nocturnal cardiac arrhythmia is a common clinical feature of obstructive sleep apnea syndrome. Pathologically relevant rhythm disturbances such as atrioventricular block or ventricular tachycardia are known to occur mainly in patients with a high apnea-hypopnea index and marked oxygen desaturation. We report on a patient with mild obstructive sleep apnea syndrome who nevertheless showed intermittent second-degree atrioventricular block during stages of rapid eye movement sleep-associated hypopneas. Cardiac arrhythmia was reversed with the initiation of nasal continuous positive airway pressure treatment. Based
on this case report and taking into account known facts from the literature, the finding of intermittent second-degree atrioventricular block in our patient with mild obstructive sleep apnea syndrome supports careful evaluation of electrocardiogram recording acquired during polysomnography in all patients with suspected obstructive sleep apnea syndrome. Keywords: Arrhythmia, sleep apnea, CPAP Citation: Dziewas R; Imai T; Dittrich R et al. Night-time bradyarrhythmia in a patient with mild obstructive sleep apnea syndrome is reversed with CPAP treatment. J Clin Sleep Med 2006;2(4):454-457.
Nocturnal cardiac arrhythmia, especially apnea-associated bradycardia with or without alternating tachycardia, has been frequently reported in patients with obstructive sleep apnea syndrome (OSAS).1-6 The occurrence of pathologically relevant rhythm disturbances--such as second- or third-degree atrioventricular block (AV block), ventricular tachycardia, or complex ventricular ectopy--is supposed to be a feature of severe OSAS. Thus, a significant correlation between OSAS severity and the severity of rhythm disturbances was documented by Harbison et al.7 Furthermore, Guilleminault reported that bradycardic arrhythmias exclusively occurred during apneas with oxygen saturation below 72%.1 Finally, Becker et al found bradycardic arrhythmias only in patients with an apnea-hypopnea index (AHI) of 60 or more per hour.8 Here we wish to report on a patient with mild OSAS who nevertheless presented with pathologically relevant nocturnal bradyarrhythmia and therefore does not fit in known patterns. CASE REPORT A 63-year-old male retired postal worker was admitted to our sleep laboratory because of a long-standing history of nocturnal snoring and mild daytime sleepiness. History taking was remark- Disclosure Statement Drs. Dziewas, Imai, Dittrich, Humpert, Hopmann, Boentert, and Young have indicated no financial conflicts of interest.
able for POEMS syndrome (polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, and Skin changes) diagnosed 5 years before, arterial hypertension, and hypercholesterolemia. neurologic examination revealed muscle wasting, weakness, and hypoesthesia in the distal legs. The ankle tendon reflexes were absent, and the knee tendon reflexes were diminished on both sides. The remainder of the patient's neurologic status was normal. Electrocardiogram recording was normal. During the first night of standard overnight polysomnography9 the time in bed was 6 hours and 37 minutes, the sleep efficiency was 82%, and the sleep stages were distributed normally (Figure 1a). Polysomnography documented an AHI of 7.0 per hour of sleep and a snoring index of 128 per hour. The CT90 (ie, the percentage of nighttime below 90% saturation) was 2%, and the minimal oxygen saturation was 86%. Obstructive hypopneas and oxygen desaturations mainly occurred during rapid eye movement (REM) sleep. Interestingly, we found intermittent seconddegree AV-block during the stages of REM sleep-associated hypopneas (Figure 2). As is demonstrated in Figure 1, these rhythm disturbances were depicted as frequent drops in heart rate. On the second night, nasal continuous airway pressure (CPAP) was started. Again, the patient slept well (time in bed, 6 hours 35 minutes; sleep efficiency, 80%) with a Normal Distribution of sleep stages (Figure 1a). The AHI was reduced to 0.8 per hour, and the snoring index to 5 per hour. The CT90 was 1%, and the minimal oxygen saturation was 89%. No intermittent second-degree AV block was recorded during this night.
Submitted for publication November 23, 2005 Accepted for publication April 3, 2006 Address correspondence to: Rainer Dziewas, MD, Department of Neurology, University Hospital of Mьnster, Albert-Schweitzer-Strasse 33, 48129 Mьnster, Germany; Tel: 0049 2518347955; Fax: 0049 2518348181; E-mail: [email protected]
DISCUSSION In patients with OSAS, the occurrence of pathologically relevant nocturnal arrhythmias is known to be linked to the severity of the disease.1,7,8 Therefore, the finding of an intermittent second-degree AV-block in our patient who had an AHI of only 7.0
Journal of Clinical Sleep Medicine, Vol. 2, No. 4, 2006
454
Night-time Bradyarrhythmia in Mild OSAS Figure 1--Electrocardiogram recordings during the first night of polysomnography showing second-degree atrioventricular block (A = high time resolution, B = low time resolution).
Figure 2a--Hypnogram, oxygen saturation, respiratory events (obstructive hypopneas), and heart rate during the first night without treatment. Recurring episodes of intermittent second-degree atrioventricular block are marked with *.
Journal of Clinical Sleep Medicine, Vol. 2, No. 4, 2006
455
R Dziewas, T Imai, R Dittrich et al
Figure 2b--Hypnogram, oxygen saturation, respiratory events (obstructive hypopneas), and heart rate after initiation of treatment with nasal continuous positive airway pressure. There were no episodes of second-degree atrioventricular block recorded.
per hour is remarkable. However, one has to take into account that our patient suffered from POEMS syndrome, which is known to be associated with different cardiac complications and may even lead to congestive heart failure.10 Hence, the observed nocturnal arrhythmia may be partly due to an underlying cardiomyopathy, which was aggravated by obstructive apneas. Pathophysiologically, apnea-associated hypoxemia is supposed to cause vagal stimulation, leading to bradycardia, which can be prevented by vagal blockaDe With atropine.11 Furthermore, a substantial increase in the number of bradycardic arrhythmias during REM sleep has been reported.12,13 Although apneas are generally longer and desaturation is therefore more pronounced during this sleep stage, in the study of Becker and coworkers, REM sleep proved to be an independent Factor Contributing to heart block, after adjusting for desaturation and apnea duration. Interestingly, both mechanisms may be also relevant in our patient because second degree AV-block nearly exclusively occurred during clusters of obstructive hypopneas that were found in REM sleep. In line with our observation, few studies have shown that nCPAP effectively treats night-time arrhythmia. Thus, Becker and
coworkers reported that the number of arrhythmias was reduced from 1575 to 165 episodes per night in 17 patients.8 Confirming these findings, 2 other studies have demonstrated reversal of heart block in 13 of 15 patients and in 7 of 8 patients, respectively, after initiation of therapy with nasal CPAP.7,14 Taken together, the finding of intermittent second-degree AVblock in our patient with mild OSAS only supports careful evaluation of electrocardiogram recording acquired during polysomnography in all patients with suspected OSAS. Treatment with nasal CPAP effectively prevents arrhythmias in 80% to 90% of patients. ACKNOWLEDGMENT The authors are grateful to Angelika Okegwo for expert technical assistance with the sleep study. This work was supported by "Innovative Medizinische Forschung" (IMF DZ 120140). REFERENCES 1. Guilleminault C, Connolly SJ, Winckle RA. Cardiac arrhythmia and conduction disturbances during sleep in 400 patients with sleep
Journal of Clinical Sleep Medicine, Vol. 2, No. 4, 2006
456
apnea syndrome. Am J Cardiol 1983;52:490-94. 2. Hoffstein V Mateika S. Cardiac arrhythmias, snoring, and sleep ap- nea. Chest 1994;106:466-71. 3. Randazzo DN, Winters SL, Schweitzer P. Obstructive sleep apnea- induced supraventricular tachycardia. J Electrocardiol 1996;29:657. 4. Bolm-Audorff U, Kцhler U, Becker E, et al. Nдchtliche Herzrhythmusstцrungen bei Schlafapnoe-Syndrom. Dtsch Med Wochenschr 1984;109:853-6. 5. Miller WP. Cardiac arrhythmias and conduction disturbances in the sleep apnea syndrome. Prevalence and significance. Am J Med 1982;73:317-21. 6. Guilleminault C, Connolly SJ, Winkle R, Melvin K, Tilkian AG. Cyclical variation of the heart rate in sleep apnoea syndrome: mechanisms and usefulness of 24 h electrocardiography as a screening technique. Lancet 1984;1:126-31. 7. Harbison JA, O'Reilly P, McNicholas WT. Cardiac rhythm disturbances in the obstructive sleep apnea syndrome: effects of nasal continuous positive airway pressure therapy. Chest 2000;118:5915. 8. Becker HF, Brandenburg U, Peter JH, Wichert P. Reversal of sinus arrest and atrioventricular conduction block in patients with sleep apnea during nasal continuous positive airway pressure. Am J Respir Crit Care Med 1995;151:215-8. 9. Rechtschaffen A and Kales A, A Manual of Standardized Terminology, Techniques and scoring system for Sleep Stages in human subjects. Washington: NIH Publication 204; 1968. 10. Dispenzieri A, Kyle RA, Lacy MO, et al. POEMS syndrome: definitions and long-term outcome. Blood 2003;101:2496-506. 11. Tilkian AG, Guilleminault C, Schroeder JS, Lehrmann KL, Simmons FB, Dement WC. Sleep-induced apnea syndrome. Prevalence of cardiac arrhythmias and their reversal after tracheostomy. Am J Med 1977;63:348-58. 12. Guilleminault C, Pool P, Motta J, Gillis A. Sinus arrest during REM sleep in young adults. N Engl J Med 1984;311:1006-10. 13. Becker HF, Koehler U, Stammnitz A, Peter JH. Heart block in patients with sleep apnea. Thorax 1998;53 (Suppl.1):S29-32. 14. Grimm W, Hoffmann J, Menz V, et al. Electrophysiologic evaluation of sinus node function and atrioventricular conduction in patients with prolonged ventricular asystole during obstructive sleep apnea. Am J Cardiol 1996;77:1310-4.
Night-time Bradyarrhythmia in Mild OSAS
Journal of Clinical Sleep Medicine, Vol. 2, No. 4, 2006
457

File: night-time-bradyarrhythmia-in-a-patient-with-mild-obstructive.pdf
Title: JCSM_October.indd
Published: Mon Oct 16 14:42:09 2006
Pages: 4
File size: 0.79 Mb


Hosea and Gomer Revisited, 6 pages, 0.05 Mb

Professions for women, 4 pages, 0.07 Mb
Copyright © 2018 doc.uments.com