Sleep Apnea Syndrome in Patients with Atrial Fibrillation 2 Cases Whose Atrial Fibrillation Was Controlled by Treatment for Sleep Apnea Syndrome

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1 Case Report Sleep Apnea Syndrome in Patients with Atrial Fibrillation 2 Cases Whose Atrial Fibrillation Was Controlled by Treatment for Sleep Apnea Syndrome Manabu Fujimoto MD, Yamamoto Masakazu MD Kouseiren Takaoka Hospital A high rate of sleep apnea syndrome (SAS) complicated by atrial fibrillation (AF) has been reported. We reviewed the frequency of SAS complications in AF patients, and reported on the patients for whom SAS was considered to be a cause of the AF. We studied 28 patients with AF who were able to receive a sleep apnea examination. All patients had oxygen saturation measured by an ambulatory percutaneus monitor (PULSOX) during sleep. A sleep apnea examination was performed by polysomnograph (Morpheus) in 19 of the patients. There were 18 patients (64%) with moderate to severe SAS whose apnea hypoxia index (AHI) or 3% oxygen disaturation index was more than 20. In this study, AF was stopped by treating SAS with continuous positive airway pressure (CPAP) or noninvasive positive pressure ventilation (NPPV) in 2 cases. Our study shows a high rate of SAS complications with AF, which is in accord with previous studies. We experienced cases in which AF was stopped by treating SAS with CPAP or NPPV, suggesting it is a cause of AF. (J Arrhythmia 2007; 23: ) Key words: Sleep apnea examination, Apnea hypoxia index, Oxygen disaturation index, Continuous positive airway pressure, Noninvasive positive pressure ventilation Introduction Many cardiovascular diseases are complicated by sleep apnea syndrome (SAS), which is considered to be an aggravating factor. About 60 percent of heart failure patients have SAS, 1 3) and subjective and objective symptoms of heart failure have been improved by treating SAS with oxygen inhalation therapies. 4 7) In addition, SAS has attracted attention as a causative disease in hypertensive patients. 8 13) It has been reported that the rate of SAS complications with atrial fibrillation(af) is high. 14) We reviewed the frequency of SAS complications in AF patients at our hospital, and report cases in whom SAS is considered to be a cause of AF. Case Report We studied 28 patients with chronic atrial fibrillation (Caf) or paroxysmal atrial fibrillation (Paf) who were able to receive a sleep apnea examination in Kouseiren Takaoka Hospital from October, 2004 to January, Caf is a condition in which AF continues for more than 1 year, and in Paf AF lasts for 24 hours or less. When their medical therapy started, the AF was Caf in 12 patients and Paf in 16 Received 2, November, 2006: accepted in final form 4, June, Address for Correspondance: Manabu Fujimoto MD, Kouseiren Takaoka Hospital, 5-10 Eiraku-cho, Takaoka, Toyama, Japan FAX: TEL: 152

2 Fujimoto M Sleep apnea syndrome and atrial fibrillation patients. Four Paf patients had their defibrillation treated successfully with antiarrhythmic drugs (Table 1). The mean age was There were 23 men and 5 women. All patients had their oxygen saturation measured by an ambulatory percutaneus monitor (PULSOX, TEIJIN PHARMA Ltd.) during sleep. When episodes indicating a 3% oxygen disaturation index (3%ODI) more than 10 times every hour were obtained under close observation during hospitalization, which corresponds to an oxygen saturation dose degradation of more than 3%, a sleep apnea examination was performed using Morpheus (TEI- JIN PHAMA Ltd.). This device is able to measure 6 parameters: nasal air flow, chest and abdominal movements, pulse rate, percutaneus oxygen saturation, and physical position. Using Morpheus, we can distinguish the type of SAS, and measured the apnea hypoxia index (AHI), which is the number of apnea and hypoxia events per hour. Apnea is defined as nasal air-flow arrest for more than 10 seconds, and hypoxia as a reduced nasal air flow with an oxygen disaturation of more than 3%. Nineteen patients were evaluated using Morpheus and 9 patients using only PULSOX. Table 1 shows patient characteristics and outcome for all cases. Among the 9 patients we evaluated only using PLUSOX, there were 7 patients whose 3%ODI was 10 or less, 2 patients above 20, and no patients between 11 and 19. Among the 19 patients evaluated using Morpheus, there were 3 patients whose AHI was below 10, 16 patients more than 20, and no Table 1 Clinical characteristics and results for all cases. No initial age sex AHI ODI EF disease Paf or Af Af duration antiarrhythmic drugs SAS treatment 1 O.T. 75 F HT Caf 16y none 2 O.M. 58 M 2 65 MSR Paf bepridil 3 K.J. 74 F 5 76 PE Paf bepridil 4 T.K. 77 M HT Caf 1y< bepridil NPPV 5 T.O. 79 M SSS, HT, HL Paf none CPAP 6 I.K. 60 M MR Caf 5y< none HOT 7 M.Y. 61 M HT Paf bepridil NPPV 8 S.A. 61 M HT, MR Caf->SR 3y< bepridil 9 T.H. 61 F 3 63 SSS Caf bepridil 10 S.H. 53 M none Paf flecainide 11 K.T. 80 M HT, HL Paf pilsicainide 12 M.M. 80 F SSS Paf bepridil+pirmenol HOT 13 H.K. 62 M DCM, HL Paf bepridil 14 M.E. 82 M HT, HL, CRF Paf bepridil 15 S.S. 75 M DM Paf bepridil 16 M.H. 85 M HT, DM, CRF Caf 3y< none 17 H.M. 70 M none Paf bepridil+pilsicainide 18 R.T. 67 F DM, HT Paf none CPAP 19 T.S. 83 M HL Caf 2y< none 20 Y.Y 70 M 9 72 HT Caf->SR 1y bepridil+flecainide 21 Y.T 57 M 1 64 HT, HL Caf->SR 3y< bepridil+flecainide 22 Y.K. 73 M 8 50 SSS, DM Paf bepridil+pilsicainide 23 M.S. 58 M 7 74 HT Caf->SR 1y bepridil 24 N.K. 52 M none Paf bepridil 25 T.M. 59 M SSS, HT Paf bepridil+flecainide 26 M.K. 59 M none Caf 6y none 27 K.M. 46 M 1 74 DM Paf bepridil+pilsicainide 28 Y.S. 58 M 8 70 HT Caf 1y bepridil+flecainide AHI, apnea hypoxia index; ODI, oxygen disaturation index; EF, ejection fraction; HT, hypertension; MSR, mitral stenosis and regurgitation; PE, pulmonary embolism; SSS, sick sinus syndrome; HL, hyperlipidemia; MR, mitral regurgitation; DCM, dilated cardiomyopathy; CRF, chronic renal failure; DM, diabetes mellitus; SR, sinus rhythm; NPPV, noninvasive positive pressure ventilation; CPAP, continuous positive airway pressure; HOT, home oxygen therapy 153

3 patients between 10 and 19. There were 18 patients (64%) with moderate to severe SAS, in whom AHI or 3%ODI was more than 20. In this study, we treated SAS in 6 patients, and 2 had atrial fibrillation treated successfully with SAS. Case 1 was No. 18, a 67 year-old woman with Paf, who was observed to have seizures only during sleep, even when napping. Her episodes of Paf air flow chest abdomen snoring SatO2 HR position Figure 1 Polysomnography in case 1. O, obstructive apnea; H, hypoxia; S, snore; D, disaturation. Although nasal air flow stops, chest and abdominal movements are observed. This is obstructive apnea. (A) (B) (min) Figure 2 (A) Heart rate trend graph for case 1 during sleep. PACs often occur just before heart rate increase. This phase corresponds to the time hyperpnea began. (B) Heart rate trend recorded by 24-hour ambulatory Holter monitor for case 1. During sleep PACs occurred frequently and induced AF. 154

4 Fujimoto M Sleep apnea syndrome and atrial fibrillation air flow chest abdomen snoring SatO2 HR position Figure 3 Polysomnography for case 2. C, central type apnea; M, mixed type apnea. Nasal air flow and chest and abdominal movements stop synchronously. This is central apnea. A I II III V1 V2 V3 avr V4 avl avf V5 V6 B I II III V1 V2 V3 avr V4 avl avf V5 V6 Figure 4 Electrocardiograms for case 2. A, Before treatment of SAS; B, After treatment of SAS. occurred daily. Her AHI was 47, and the type of SAS was obstructive (Figure 1). In this case, premature atrial contractions (PACs) were observed in hyperventilation, which followed apnea (Figure 2A), when we reviewed the onset of Paf at the time of sleep apnea, and shifted to Paf (Figure 2B). AHI was 155

5 improved to single figures by continuous positive airway pressure (CPAP) treatment, and she had no Paf after 1 year of follow-up treatment. Case 2 was No. 4, a 77 year-old man with Caf. Figure 4A shows his ECG. His SAS was central and mixed type, and his AHI was 40 (Figure 3). His AF stopped after starting therapy for SAS with noninvasive positive pressure ventilation (NPPV) on the second day (Figure 4). He had maintained sinus rhythm for more than a half year. Hence, when he could not undergo NPPV because of a cold, Af recurred. After resuming NPPV, sinus rhythm returned. Discussion In our study, the rate of SAS complication to AF was 64%, which is considerably higher than that in a previous report. 14) We experienced 2 cases whose AF was controlled by treating SAS. In case 1, SAS was regarded as a true cause of AF. In this case, premature atrial contractions (PACs) were observed in hyperventilation, which followed apnea. In a previous study of premature ventricular contraction (PVC) in heart failure patients with Cheyne-Stokes breathing, 15,16) there were significantly large numbers of PVCs in hyperpnea phases compared to apnea phases. It has been confirmed that sympathetic activity rises in hyperpnea phases following apnea, 17) and elicitation of rising PACs due to sympathetic activity is thought to be one of the causes of Paf in case 1. In addition, we cannot continuously measure blood carbon dioxide pressure and ph, but alternating these parameters under SAS might contribute to Paf. When treating AF with SAS, we experienced successful prevention or termination of AF with CPAP or NPPV, which sufficiently relieved cardiac load, but did not experience a case terminated only by oxygenation. Conclusions Our study showed as high a rate of SAS complication with AF as in previous studies. We experienced cases in which AF was stopped by SAS treatment, such as CPAP or NPPV, suggesting it could be considered as being the cause of AF. References 1) Javaheri S: Central sleep apnea-hypopnea syndrome in heart failure: prevalence, impact, and treatment. Sleep 1996; 19 (Suppl): S229 S231 2) Javaheri S, Parker TJ, Liming JD, et al: Sleep apnea in 81 ambulatory male patients with stable heart failure. Types and their prevalences, consequences, and presentations. Circulation 1998; 97: ) Lanfranchi PA, Braghiroli A, Bosimini E, et al: Prognostic value of nocturnal Cheyne-Stokes respiration in chronic failure. Circulation; 99: ) Andreas S, Clemens C, Sandholzer H, et al: Improvement of exercise capacity with treatment of Cheyne- Stokes respiration in patients with congestive heart failure. J Am Coll Cardiol 1996; 27: ) Franklin KA, Sandstrom E, Johansson G, et al: Reversal of central sleep apnea with oxygen. Chest 1997; 111: ) Andreas S, von zur Muhlen F, Stevens J, et al: Nocturnal oxygen and hypercapnic ventilatory response in patients with congestive heart failure. Respir Med 1998; 92: ) Staniforth AD, Kinnear WJ, Starling R, et al: Effect of oxygen on sleep quality, cognitive function and sympathetic activity in patients with chronic heart failure and Cheyne-Stokes respiration. Er Heart J 1998; 19: ) Lavie P, Herer P, Hoffstein V: Obstructive sleep apnea syndrome as a risk factor for hypertension: population study. BMJ 2000; 320: ) Nieto FJ, Young TB, Lind BK, et al: Association of sleep-disordered breathing, sleep apnea, and hypertension in a large community-based study. Sleep Heart Health Study. JAMA 2000; 283: ) Bixler EO, Vgontzas AN, Lin HM, et al: Association of hypertension and sleep-disordered breathing. Arch Intern Med 2000; 160: ) Sharabi Y, Scope A, Chorney N, et al: Diastolic blood pressure is the first to rise in association with early subclinical obstructive sleep apnea: lessons from periodic examination screening. Am J Hypertens 2003; 16: ) Moller DS, Lind P, Strunge B, et al: Abnormal vasoactive hormones and 24-hour blood pressure in obstructive sleep apnea. Am J Hypertens 2003; 16: ) Haas DC, Foster GL, Nieto FJ, et al: Age-dependent associations between sleep-disordered breathing and hypertension: importance of discriminating between systolic/diastolic hypertension and isolated systolic hypertension in the Sleep Heart Health Study. Circulation 2005; 111: ) Blackshear JL, Kaplan J, Thompson RC, et al: Nocturnal dyspnea and atrial fibrillation predict Cheyne-Stokes respirations in patients with congestive heart failure. Arch Intern Med 1995; 155: ) Gami AS, Pressman G, Caples SM, et al: Association of atrial fibrillation and obstructive sleep apnea. Circulation 2004; 27: ) Leung RS, Diep TM, Bowman ME, et al: Povocation of ventricular ectopy by Cheyne-Stokes respiration in patients with heart failure. Sleep 2004; 27: ) van de Borne P, Oren R, Abouassaly C, et al: Effect of Cheyne-Stokes respiration on muscle sympathetic nerve activity in severe congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy. Am J Cardiol 1998; 81: