Stephane Garrigue, M.D., Philippe Bordier, M.D., Pierre Jaïs, M.D., Dipen C. Shah, M.D., Meleze Hocini, M.D., Chantal Raherison, M.D., Manuel Tunon De Lara, M.D., Michel Haïssaguerre, M.D., and Jacques Clementy, M.D.
Background Many patients with sleep apnea syndrome have nocturnalbradycardia, paroxysmal tachyarrhythmias, or both, which canbe prevented by permanent atrial pacing. We evaluated the effectof using cardiac pacing to increase the heart rate during sleepin patients with sleep apnea syndrome.
Methods We studied 15 patients (11 men and 4 women; mean [±SD]age, 69±9 years) with central or obstructive sleep apneawho had received permanent atrial-synchronous ventricular pacemakersfor symptomatic sinus bradycardia. All patients underwent threepolysomnographic evaluations on consecutive nights, the firstnight for base-line evaluation and then, in random order, onenight in spontaneous rhythm and one in dual-chamber pacing modewith atrial overdrive (basic rate, 15 beats per minute fasterthan the mean nocturnal sinus rate). The total duration andnumber of episodes of central or obstructive sleep apnea orhypopnea were analyzed and compared.
Results The mean 24-hour sinus rate during spontaneous rhythmwas 57±5 beats per minute at base line, as compared with72±3 beats per minute with atrial overdrive pacing (P<0.001).The total duration of sleep was 321±49 minutes in spontaneousrhythm, as compared with 331±46 minutes with atrial overdrivepacing (P=0.48). The hypopnea index (the total number of episodesof hypopnea divided by the number of hours of sleep) was reducedfrom 9±4 in spontaneous rhythm to 3±3 with atrialoverdrive pacing (P<0.001). For both apnea and hypopnea,the value for the index was 28±22 in spontaneous rhythm,as compared with 11±14 with atrial overdrive pacing (P<0.001).
Conclusions In patients with sleep apnea syndrome, atrial overdrivepacing significantly reduces the number of episodes of centralor obstructive sleep apnea without reducing the total sleeptime.
Sleep apnea syndrome is a common and often undiagnosed disorderassociated with substantial cardiovascular morbidity and mortality.1,2,3,4,5,6,7,8Other consequences include an increased incidence of trafficaccidents,9,10,11 social and family disruption,9,10,12 and bradyarrhythmiasor tachyarrhythmias.13,14,15 Treatments such as nasal continuouspositive airway pressure16,17,18 and oral administration oftheophylline19 reduce the number of episodes of apnea but produceside effects such as palpitations. Surgical therapy involvingthe ablation of tissue, such as uvulopalatopharyngoplasty,20,21has also been proposed for patients with apnea that is predominantlyobstructive.
We observed that some patients who had received a pacemakerwith atrial overdrive pacing in order to reduce the incidenceof atrial tachyarrhythmias22,23 reported a reduction in breathingdisorders after the implantation of the pacemaker. We thereforeundertook a study to investigate the efficacy of atrial overdrivepacing in the treatment of sleep apnea syndrome in consecutivepatients who required a pacemaker for conventional indications.
Methods
Study Population
A total of 152 patients with dual-chamber pacemakers that hadbeen implanted at least one year previously were screened. Atotal of 47 patients with problems related to sleep-disorderedbreathing, snoring, daytime sleepiness, frequent arousals atnight, sleep apnea, or some combination of these symptoms wereasked to undergo polysomnography in a sleep laboratory. Of these47 patients, 26 provided written informed consent, and in 15of them, polysomnographic recordings revealed sleep apnea syndrome,as defined by an apnea index (the total number of episodes ofapnea divided by the number of hours of sleep) of 5 or higherand an apnea–hypopnea index (the total number of episodesof either apnea or hypopnea divided by the number of hours ofsleep) of 15 or higher.24,25,26 These 15 patients, who did notengage in regular physical exercise, presented with snoring,daytime sleepiness, fatigue during the morning, and frequentarousals at night; they became the study group. They had noclinical evidence of heart failure, perhaps because they weresedentary, but 11 patients (73 percent) had a left ventricularejection fraction on echocardiography ranging from 40 to 56percent within the six months before the study. None of thepatients were dependent on the pacemaker.
Polysomnography
Polysomnography was performed in the sleep laboratory with monitoringthat included electroencephalography, electromyography of thechin and legs, electro-oculography, oronasal air-flow tracing,recording of the movement of the chest wall and abdomen, fingeroximetry, and electrocardiography with a Holter monitor.27 Airflow was monitored qualitatively with an oronasal thermocouple.An episode of apnea was defined as a complete cessation of airflow for at least 10 seconds.19,27 An episode of hypopnea wasdefined as a decrease of 50 percent or more in the oronasalair flow associated with a 4 percent decrease in arterial oxyhemoglobinsaturation. An obstructive event was recorded if there wererib-cage excursions, abdominal excursions, or both during anepisode of apnea. The simultaneous absence of air-flow thermistortracing and respiratory movements was considered to indicatethe presence of central apnea.19,27 The number of episodes ofarousal due to disordered breathing per hour of sleep was referredto as the arousal index. All polysomnographic recordings werescored by a pneumologist who was unaware of the pacing configurationand not otherwise involved in the study.
Study Protocol
The 15 patients spent three consecutive nights in the sleeplaboratory. Their medications were not changed during the study.All polysomnographic recordings were performed with use of thesame procedures. The polysomnographic recording of the firstnight represents the base line (basic pacing rate, 55 to 60beats per minute), which established the diagnosis of sleepapnea syndrome. The patients were randomly assigned to undergoone of two sets of procedures on the next night and the otherset on the night after that. During one of the two nights, thebasic ventricular rate of the pacemaker (not synchronized withthe atrial activity) was programmed to 40 beats per minute withthe aim of recording spontaneous rhythm for a high percentageof the sleep time in order to assess measures of breathing inthe absence of pacing (the no-pacing phase). During the othernight, atrial overdrive stimulation was provided at a rate thatwas 15 beats per minute faster than the mean nocturnal heartrate (recorded by the memory function of the pacemaker duringthe base-line nocturnal assessment) in order to assess the effectof pacing on breathing (the pacing phase). This level of pacingwas chosen on the basis of its therapeutic effect on vagallyinduced atrial arrhythmias, as reported in recent studies.22,23
Statistical Analysis
Data obtained during the base-line recordings were comparedwith those obtained during the no-pacing and pacing phases.Values are reported as means ±SD. Because of the smallsample size, the Mann–Whitney nonparametric test for paireddata was used to compare intrapatient differences between theoutcome variables during the no-pacing phase and the outcomevariables during the pacing phase. In order to assess the effectsof the order of the two phases of the study (assessment of periodeffects), the patients were divided into two groups —one with no pacing on night 2 and pacing on night 3 and theother with pacing on night 2 and no pacing on night 3. Period-effectsanalysis was performed by means of the Mann–Whitney nonparametrictest for independent samples. This test consisted of comparingthe two groups in terms of the mean differences in the databetween the pacing phase and the no-pacing phase for each variablestudied. A two-tailed P value of less than 0.05 was consideredto indicate statistical significance. Calculations were performedwith the use of Statistica software (StatSoft, Tulsa, Okla.).
Results
Base-Line Polysomnographic Assessment
The base-line characteristics of the patients are summarizedin Table 1. Nine patients had sinus node disease (60 percent),and six (40 percent) had bradycardia–tachycardia syndrome.Six patients were randomly assigned to receive no pacing onnight 2 and nine to receive no pacing on night 3. The 24-hourmean spontaneous heart rate during the base-line phase was similarfor all the patients (57±5 beats per minute). All patientspresented with episodes of both obstructive and central apnea;the study group had a higher central-apnea index (12±14)than obstructive-apnea index (7±4), but the differencewas not statistically significant (P=0.09) (Table 1). Sevenpatients (Patients 1 through 7) had apnea that was predominantlyobstructive (central-apnea index, 5±4; obstructive-apneaindex, 8±4). The other eight patients (Patients 8 through15) had apnea that was predominantly central (central-apneaindex, 18±16; obstructive-apnea index, 6±3) (Table 1).The left ventricular ejection fraction was 56 percent orlower in 11 patients (73 percent) and 65 percent or higher in4 patients (27 percent). The percentage of total sleep timeduring which oxyhemoglobin saturation was below 90 percent was12±8 percent, and the mean arousal index was 21±12.
Table 1. Clinical Characteristics and Sleep-Disordered Breathing Events at Base Line in 15 Patients with a Pacemaker.
No-Pacing Phase
Data collected during the no-pacing phase and the pacing phaseare shown in Table 2. Pacemaker stimulation was used during1.0±0.5 percent of the no-pacing phase because five patientshad short episodes of bradycardia with a heart rate of lessthan 40 beats per minute. The mean total sleep time during theno-pacing phase was 321±49 minutes, the mean apnea–hypopneaindex was 28±22, and the mean arousal index was 18±9.
Table 2. Sleep-Disordered Breathing Events and Arterial Oxygen Saturation Values during the No-Pacing Phase and the Pacing Phase.
Pacing Phase with Atrial Overdrive Pacing
Atrial pacing at a rate 15 beats per minute faster than themean nocturnal heart rate resulted in a significant reductionin the number of episodes of all types of apnea (Table 2). In13 patients (87 percent), the apnea–hypopnea index wasreduced by more than 50 percent. The two remaining patientshad smaller reductions in the apnea–hypopnea index: onepatient had an index of 21 with no pacing and an index of 12with pacing (a 43 percent reduction), and the index of the otherpatient was reduced from 79 to 47 (a 41 percent reduction).
An example of a polysomnographic recording during the no-pacingphase from a patient (Patient 9) who presented with sleep apneathat was predominantly central is shown in Figure 1A. The heart-raterecording shows large variations, with a heart rate below 50beats per minute during episodes of apnea and an increased heartrate (up to 100 beats per minute) during arousals. In contrast,the recording in Figure 1B shows a substantial reduction inthe number of episodes of central apnea and hypopnea associatedwith much less variation in the heart rate when the basic pacingrate was set at 72 beats per minute. An example of polysomnographicrecordings from a patient (Patient 3) with a large number ofepisodes of obstructive apnea is shown in Figure 2A; the numberof episodes was markedly reduced when the heart rate was stabilizedat 75 beats per minute (Figure 2B).
Figure 1. Polysomnographic Recordings in a Patient with Predominantly Central Apnea Obtained with the Pacemaker Programmed to a Fixed Basic Rate of 40 Beats per Minute (No-Pacing Phase) (Panel A) and with Atrial Overdrive Pacing at 72 Beats per Minute (Pacing Phase) (Panel B).
Patient 9 presented with very frequent episodes of central sleep apnea. Each episode of apnea or hypopnea is represented by a vertical line; the height of the line indicates the duration of the episode in seconds.
Figure 2. Polysomnographic Recordings in a Patient with Predominantly Obstructive Apnea Obtained with the Pacemaker Programmed to a Fixed Basic Rate of 40 Beats per Minute (No-Pacing Phase) (Panel A) and with Atrial Overdrive Pacing at 75 Beats per Minute (Pacing Phase) (Panel B).
At presentation, the majority of the episodes of sleep apnea in this patient (Patient 3) were obstructive. Each episode of apnea or hypopnea is represented by a vertical line; the height of the line indicates the duration of the episode in seconds.
The effect of atrial overdrive pacing on the obstructive-apneaindex and the central-apnea index of each of the 15 patientsis shown in Figure 3. Regardless of the severity of the sleepapnea syndrome, there was a reduction in both indexes in everypatient. The reduction in the number of episodes of apnea andhypopnea was associated with a significant increase in the arterialoxyhemoglobin saturation during sleep, reflected by a reductionof the total sleep time during which the oxygen saturation wasless than 90 percent (from 10±6 percent to 6±4percent, P=0.04) (Table 2), in addition to a significant increasein the lowest oxygen saturation value from 83±8 percentto 87±5 percent (P=0.02). There was also a significantdecrease in the number of arousals due to periodic breathingthat were recorded on electroencephalography, but the typicalCheyne–Stokes pattern was found only in Patient 10 andwas present at all three evaluations.
Figure 3. Effect in the 15 Patients of Atrial Overdrive Pacing on Episodes of Central Sleep Apnea (Panel A) and Episodes of Obstructive Sleep Apnea (Panel B).
The central- and obstructive-apnea indexes were calculated as the number of episodes divided by the number of hours of sleep.
The statistical analysis revealed only two significant periodeffects (Table 2): there was a significantly greater reductionin the obstructive-apnea index among patients assigned to pacingon night 3 (P=0.04) and a significantly greater increase inthe lowest oxyhemoglobin saturation value among patients assignedto pacing on night 2 (P=0.04).
Cardiac Rhythm
All the patients tolerated the protocol well: the total sleeptime was similar at base line and during the pacing and no-pacingphases. The Holter monitor tracing and the recordings of thememory function of the pacemaker revealed a significant increasein the mean nocturnal heart rate during the atrial overdrive(pacing) phase (Table 2). The numbers of episodes of atrialarrhythmia that occurred during the pacing and no-pacing phaseswere similar. Three patients had an episode of atrial arrhythmia(one lasting 21 minutes, one lasting 35 minutes, and one lasting6 minutes) during the no-pacing phase, and two patients hadsuch an episode (one lasting 18 minutes and the other lasting27 minutes) during the pacing phase. There were no differencesin the number of isolated premature ventricular contractionsper hour of sleep (13±24 at base line, 16±31 duringthe no-pacing phase, and 12±25 during the pacing phase).Neither ventricular couplets nor episodes of ventricular tachycardiawere observed during the base-line assessment or during thepacing or no-pacing phase of the study.
Discussion
Our observations show that in patients with sleep apnea syndromewho have an atrial pacemaker, atrial overdrive pacing significantlyreduces the number of episodes of obstructive and central sleepapnea and increases arterial oxyhemoglobin saturation withoutaltering total sleep time. A reduction of more than 50 percentin the number of episodes of apnea and hypopnea was achievedwith atrial overdrive pacing in most patients (13 of 15), irrespectiveof whether they had obstructive or central sleep apnea, andwas associated with a reduction in the number of arousals andan increase in arterial oxyhemoglobin saturation. These variablesreturned to the base-line values defining sleep apnea syndromewhen the pacemaker was turned off.
Episodes of apnea are associated with hypoxemia, the retentionof carbon dioxide, bradycardia, and a decrease in blood pressurethat is, in turn, associated with an increase in vagal toneleading to periodic variations in heart rate.24,25,26,27 Ourdata show that reducing the variations in heart rate markedlyreduced the number of episodes of sleep apnea in our study population.These periodic variations in heart rate may result in part fromchanges in autonomic tone and may influence the incidence ofcentral sleep apnea. Consequently, atrial pacing at a high raterelative to that of spontaneous sinus bradycardia may counteractsustained increases in vagal tone by maintaining sympatheticactivity.
This hypothesis is compatible with the results of recent studies28,29,30showing the efficacy of atrial overdrive pacing in the treatmentof vasovagal syncope. In addition, clinical studies have demonstratedthat atrial overdrive pacing can suppress vagally induced episodesof atrial fibrillation.22,23,31 The hypothesis is further supportedby a previous study suggesting that the therapeutic effectsof theophylline in patients with central sleep apnea may bemediated by adenosine antagonism.32 The beneficial effect oftheophylline on sleep apnea syndrome might be at least partiallyexplained by its ability to reduce vagal tone.
In contrast to the effect on central sleep apnea, the mechanismof the amelioration of obstructive sleep apnea by atrial overdrivepacing is not clear. Obstructive apnea is caused mainly by thepresence of excessive soft tissue (i.e., the soft palate, thetonsils, and the base of the tongue) or by hypotonia of thepharyngeal muscles during sleep.33,34,35,36 We did not expectthat atrial overdrive pacing would reduce the obstructive-apneaindex, since this type of apnea results primarily from anatomicalobstruction. The mechanisms involved remain to be explained.
We observed a reduction of more than 50 percent in the apnea–hypopneaindex with atrial overdrive. Thus, in our population of patientswith symptomatic bradycardia, cardiac pacing could be consideredas an alternative to treatment with continuous positive airwaypressure or oral theophylline.16,17,18,19,37 The ablation oftissue has been proposed as a surgical method for the treatmentof snoring and obstructive apnea. Improvement has been achievedin 38 to 50 percent of the patients who have undergone sucha surgical procedure.38,39,40,41
In our study, cardiac pacing was effective in patients withsymptomatic bradyarrhythmias and frequent variations in heartrate. Whether similar beneficial effects could be achieved withatrial pacing in patients who had no indications for pacemakerimplantation (typically, sinus node disease or bradycardia–tachycardiasyndrome) remains to be determined. In addition, all but fourof our patients presented with a reduced left ventricular ejectionfraction. Therefore, our results cannot yet be extrapolatedto patients with normal cardiac function who have sleep apneasyndrome, even though our four patients with normal cardiacfunction had more than a 50 percent reduction in the sleep-apneaindex.
Atrial overdrive pacing substantially reduced the number ofepisodes of central and obstructive apnea in patients with pacemakersthat had previously been implanted for the treatment of thesick sinus syndrome or the bradycardia–tachycardia syndrome.Further studies are needed to elucidate the mechanisms involvedin achieving these reductions and to assess the precise roleof cardiac pacing in preventing symptoms, disability, and deathin the general population of patients with sleep apnea syndrome.
Source Information
From the Hôpital Cardiologique du Haut-Lévêque (S.G., P.B., P.J., D.C.S., M. Hocini, M. Haïssaguerre, J.C.) and the Department of Lungs and Respiratory Disease, Hôpital du Haut-Lévêque (C.R., M.T.D.), University of Bordeaux, Bordeaux, France.
Address reprint requests to Dr. Garrigue at the Cardiac Pacing and Clinical Electrophysiology Department, Hôpital Cardiologique du Haut-Lévêque, 19, ave. de Magellan, Pessac, CEDEX 33604, France, or at stgarrigue{at}aol.com.
References
Mooe T, Rabben T, Wiklund U, Franklin KA, Eriksson P. Sleep-disordered breathing in men with coronary artery disease. Chest 1996;109:659-663. [CrossRef][ISI][Medline]
Franklin KA, Nilsson JB, Sahlin C, Naslund U. Sleep apnoea and nocturnal angina. Lancet 1995;345:1085-1087. [CrossRef][ISI][Medline]
Krieger J, Grucker D, Sforza E, Chambron J, Kurtz D. Left ventricular ejection fraction in obstructive sleep apnea: effects of long-term treatment with nasal continuous positive airway pressure. Chest 1991;100:917-921. [ISI][Medline]
Partinen M, Jamieson A, Guilleminault C. Long-term outcome for obstructive sleep apnea syndrome patients: mortality. Chest 1988;94:1200-1204. [CrossRef][ISI][Medline]
Roux F, D'Ambrosio C, Mohsenin V. Sleep-related breathing disorders and cardiovascular disease. Am J Med 2000;108:396-402. [CrossRef][ISI][Medline]
Veale D, Chailleux E, Hoorelbeke-Ramon A, et al. Mortality of sleep apnoea patients treated by nasal continuous positive airway pressure registered in the ANTADIR observatory. Eur Respir J 2000;15:326-331. [Abstract]
Newman AB, Spiekerman CF, Enright P, et al. Daytime sleepiness predicts mortality and cardiovascular disease in older adults. J Am Geriatr Soc 2000;48:115-123. [ISI][Medline]
Javaheri S. Central sleep apnea-hypopnea syndrome in heart failure: prevalence, impact, and treatment. Sleep 1996;19:Suppl:S229-S231. [ISI][Medline]
Cassel W, Ploch T, Becker C, Dugnus D, Peter JH, von Wichert P. Risk of traffic accidents in patients with sleep-disordered breathing: reduction with nasal CPAP. Eur Respir J 1996;9:2606-2611. [Abstract]
Yamamoto H, Akashiba T, Kosaka N, Ito D, Horie T. Long-term effects nasal continuous positive airway pressure on daytime sleepiness, mood and traffic accidents in patients with obstructive sleep apnoea. Respir Med 2000;94:87-90. [CrossRef][ISI][Medline]
Terán-Santos J, Jiménez-Gómez A, Cordero-Guevara J, Cooperative Group Burgos-Santander. The association between sleep apnea and the risk of traffic accidents. N Engl J Med 1999;340:847-851. [Free Full Text]
Findley L, Smith C, Hooper J, Dineen M, Suratt PM. Treatment with nasal CPAP decreases automobile accidents in patients with sleep apnea. Am J Respir Crit Care Med 2000;161:857-859. [Free Full Text]
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;77:1310-1314. [CrossRef][ISI][Medline]
Stegman SS, Burroughs JM, Henthorn RW. Asymptomatic bradyarrhythmias as a marker for sleep apnea: appropriate recognition and treatment may reduce the need for pacemaker therapy. Pacing Clin Electrophysiol 1996;19:899-904. [CrossRef][Medline]
Becker HF, Koehler U, Stammnitz A, Peter JH. Heart block in patients with sleep apnoea. Thorax 1998;53:Suppl 3:S29-S32. [Free Full Text]
Davies RJ, Harrington KJ, Ormerod OJ, Stradling JR. Nasal continuous positive airway pressure in chronic heart failure with sleep-disordered breathing. Am Rev Respir Dis 1993;147:630-634. [ISI][Medline]
Issa FG, Sullivan CE. Reversal of central sleep apnea using nasal CPAP. Chest 1986;90:165-171. [CrossRef][Medline]
Sullivan CE, Issa FG, Berthon-Jones M, Eves L. Reversal of obstructive sleep apnoea by continuous positive airway pressure applied through the nares. Lancet 1981;1:862-865. [ISI][Medline]
Javaheri S, Parker TJ, Wexler L, Liming JD, Lindower P, Roselle GA. Effect of theophylline on sleep-disordered breathing in heart failure. N Engl J Med 1996;335:562-567. [Free Full Text]
Fujita S, Conway W, Zorick F, Roth T. Surgical correction of anatomic abnormalities in obstructive sleep apnea syndrome: uvulopalatopharyngoplasty. Otolaryngol Head Neck Surg 1981;89:923-934. [ISI][Medline]
Woodson BT, Wooten MR. Manometric and endoscopic localization of airway obstruction after uvulopalatopharyngoplasty. Otolaryngol Head Neck Surg 1994;111:38-43. [Medline]
Garrigue S, Barold SS, Cazeau S, et al. Is there a synergic effect of propafenone associated with atrial overdrive pacing for atrial arrhythmia prevention? A randomised crossover study. Heart 2000;83:172-177. [Free Full Text]
Garrigue S, Barold SS, Cazeau S, et al. Prevention of atrial arrhythmias during DDD pacing by atrial overdrive. Pacing Clin Electrophysiol 1998;21:1751-1759. [CrossRef][Medline]
Guilleminault C, Tilkian AG, Dement WC. The sleep apnea syndromes. Annu Rev Med 1976;27:465-484. [CrossRef][ISI][Medline]
Coccagna G, Mantovani M, Brignani F, Parchi C, Lugaresi E. Continuous recording of the pulmonary and systemic arterial pressure during sleep in syndromes of hypersomnia with periodic breathing. Bull Physiopathol Respir (Nancy) 1972;8:1159-1172.
Guilleminault C, Connolly S, Winkle R, Melvin K, Tilkian A. Cyclical variation of the heart rate in sleep apnoea syndrome: mechanisms, and usefulness of 24 h electrocardiography as a screening technique. Lancet 1984;1:126-131. [CrossRef][ISI][Medline]
Narkiewicz K, Montano N, Cogliati C, van de Borne PJ, Dyken ME, Somers VK. Altered cardiovascular variability in obstructive sleep apnea. Circulation 1998;98:1071-1077. [Free Full Text]
Deharo JC, Peyre JP, Ritter PH, Chalvidan T, Le Tallec L, Djiane P. Treatment of malignant primary vasodepressive neurocardiogenic syncope with a rate responsive pacemaker driven by heart contractility. Pacing Clin Electrophysiol 1998;21:2688-2690. [CrossRef][Medline]
Abe H, Iwami Y, Nagatomo T, Miura Y, Nakashima Y. Treatment of malignant neurocardiogenic vasovagal syncope with a rate drop algorithm in dual chamber cardiac pacing. Pacing Clin Electrophysiol 1998;21:1473-1475. [Medline]
Sheldon R. Role of pacing in the treatment of vasovagal syncope. Am J Cardiol 1999;84:Suppl:26Q-32Q. [Medline]
Coumel P, Friocourt P, Mugica J, Attuel P, Leclercq JF. Long-term prevention of vagal atrial arrhythmias by atrial pacing at 90/minute: experience with 6 cases. Pacing Clin Electrophysiol 1983;6:552-560. [CrossRef][Medline]
Sin DD, Man GC, Jones RL. Central sleep apnea and heart failure. N Engl J Med 2000;342:293-293. [Free Full Text]
Hudgel DW. Variable site of airway narrowing among obstructive sleep apnea patients. J Appl Physiol 1986;61:1403-1409. [Free Full Text]
Hillarp B, Nylander G, Rosen I, Wickstrom O. Videoradiography of patients with habitual snoring and/or sleep apnea: technical description and presentation of videoradiographic results during sleep concerning occurrence of apnea, type of apnea and site of obstruction. Acta Radiol 1996;37:307-314. [ISI][Medline]
Kuna ST. Respiratory-related activation and mechanical effects of the pharyngeal constrictor muscles. Respir Physiol 2000;119:155-161. [CrossRef][ISI][Medline]
Isono S, Tanaka A, Nishino T. Effects of tongue electrical stimulation on pharyngeal mechanics in anaesthetized patients with obstructive sleep apnoea. Eur Respir J 1999;14:1258-1265. [Abstract]
Javaheri S. Effects of continuous positive airway pressure on sleep apnea and ventricular irritability in patients with heart failure. Circulation 2000;101:392-397. [Free Full Text]
Finkelstein Y, Shapiro-Feinberg M, Stein G, Ophir D. Uvulopalatopharyngoplasty vs laser-assisted uvulopalatoplasty. Arch Otolaryngol Head Neck Surg 1997;123:265-276. [CrossRef][ISI][Medline]
Sher AE, Schechtman KB, Piccirillo JF. The efficacy of surgical modifications of the upper airway in adults with obstructive sleep apnea syndrome. Sleep 1996;19:156-177. [ISI][Medline]
Langin T, Pepin JL, Pendlebury S, et al. Upper airway changes in snorers and mild sleep apnea sufferers after uvulopalatopharyngoplasty (UPPP). Chest 1998;113:1595-1603. [CrossRef][ISI][Medline]
Powell NB, Riley RW, Troell RJ, Li K, Blumen MB, Guilleminault C. Radiofrequency volumetric tissue reduction of the palate in subjects with sleep-disordered breathing. Chest 1998;113:1163-1174. [Medline]
Atrial Pacing in Sleep Apnea Syndrome
Wellman A., Malhotra A., White D. P., Schotland H. M., Stein P., Duntley S., Garrigue S., Bordier P., Haïssaguerre M.
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347:445-446, Aug 8, 2002.
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51: e1-e62
[Full Text]
Epstein, A. E., DiMarco, J. P., Ellenbogen, K. A., Estes, N.A. M. III, Freedman, R. A., Gettes, L. S., Gillinov, A. M., Gregoratos, G., Hammill, S. C., Hayes, D. L., Hlatky, M. A., Newby, L. K., Page, R. L., Schoenfeld, M. H., Silka, M. J., Stevenson, L. W., Sweeney, M. O.
(2008). ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices): Developed in Collaboration With the American Association for Thoracic Surgery and Society of Thoracic Surgeons. Circulation
117: e350-e408
[Full Text]
Buyse, B., the participants of working group 2,
(2007). Treatment effects of sleep apnoea: where are we now?. ERR
16: 146-168
[Abstract][Full Text]
Authors/Task Force Members, , Vardas, P. E., Auricchio, A., Blanc, J.-J., Daubert, J.-C., Drexler, H., Ector, H., Gasparini, M., Linde, C., Morgado, F. B., Oto, A., Sutton, R., Trusz-Gluza, M., ESC Committee for Practice Guidelines (CPG), , Vahanian, A., Camm, J., De Caterina, R., Dean, V., Dickstein, K., Funck-Brentano, C., Filippatos, G., Hellemans, I., Kristensen, S. D., McGregor, K., Sechtem, U., Silber, S., Tendera, M., Widimsky, P., Zamorano, J. L., Document Reviewers, , Priori, S. G., Blomstrom-Lundqvist, C., Brignole, M., Terradellas, J. B., Camm, J., Castellano, P., Cleland, J., Farre, J., Fromer, M., Le Heuzey, J.-Y., Lip, G. Y., Merino, J. L., Montenero, A. S., Ritter, P., Schalij, M. J., Stellbrink, C.
(2007). Guidelines for cardiac pacing and cardiac resynchronization therapy: The Task Force for Cardiac Pacing and Cardiac Resynchronization Therapy of the European Society of Cardiology. Developed in Collaboration with the European Heart Rhythm Association. Europace
9: 959-998
[Full Text]
Authors/Task Force Members, , Vardas, P. E., Auricchio, A., Blanc, J.-J., Daubert, J.-C., Drexler, H., Ector, H., Gasparini, M., Linde, C., Morgado, F. B., Oto, A., Sutton, R., Trusz-Gluza, M., ESC Committee for Practice Guidelines (CPG), , Vahanian, A., Camm, J., De Caterina, R., Dean, V., Dickstein, K., Funck-Brentano, C., Filippatos, G., Hellemans, I., Kristensen, S. D., McGregor, K., Sechtem, U., Silber, S., Tendera, M., Widimsky, P., Zamorano, J. L., Document Reviewers, , Priori, S. G., Blomstrom-Lundqvist, C., Brignole, M., Terradellas, J. B., Camm, J., Castellano, P., Cleland, J., Farre, J., Fromer, M., Le Heuzey, J.-Y., Lip, G. Y., Merino, J. L., Montenero, A. S., Ritter, P., Schalij, M. J., Stellbrink, C.
(2007). Guidelines for cardiac pacing and cardiac resynchronization therapy: The Task Force for Cardiac Pacing and Cardiac Resynchronization Therapy of the European Society of Cardiology. Developed in Collaboration with the European Heart Rhythm Association. Eur Heart J
28: 2256-2295
[Full Text]
Stanchina, M. L., Ellison, K., Malhotra, A., Anderson, M., Kirk, M., Benser, M. E., Tosi, C., Carlisle, C., Millman, R. P., Buxton, A.
(2007). The Impact of Cardiac Resynchronization Therapy on Obstructive Sleep Apnea in Heart Failure Patients: A Pilot Study. Chest
132: 433-439
[Abstract][Full Text]
Griffioen, K. J., Gorini, C., Jameson, H., Mendelowitz, D.
(2007). Purinergic P2X Receptors Mediate Excitatory Transmission to Cardiac Vagal Neurons in the Nucleus Ambiguus After Hypoxia. Hypertension
50: 75-81
[Abstract][Full Text]
Lang, C. C, Mancini, D. M
(2007). Non-cardiac comorbidities in chronic heart failure. Heart
93: 665-671
[Abstract][Full Text]
Garrigue, S., Pepin, J.-L., Defaye, P., Murgatroyd, F., Poezevara, Y., Clementy, J., Levy, P.
(2007). High Prevalence of Sleep Apnea Syndrome in Patients With Long-Term Pacing: The European Multicenter Polysomnographic Study. Circulation
115: 1703-1709
[Abstract][Full Text]
Tzeng, Y. C., Larsen, P. D., Galletly, D. C.
(2007). Mechanism of cardioventilatory coupling: insights from cardiac pacing, vagotomy, and sinoaortic denervation in the anesthetized rat. Am. J. Physiol. Heart Circ. Physiol.
292: H1967-H1977
[Abstract][Full Text]
Griffioen, K. J. S., Kamendi, H. W., Gorini, C. J., Bouairi, E., Mendelowitz, D.
(2007). Reactive Oxygen Species Mediate Central Cardiorespiratory Network Responses to Acute Intermittent Hypoxia. J. Neurophysiol.
97: 2059-2066
[Abstract][Full Text]
Eckert, D. J., Jordan, A. S., Merchia, P., Malhotra, A.
(2007). Central Sleep Apnea: Pathophysiology and Treatment. Chest
131: 595-607
[Abstract][Full Text]
McNicholas, W. T., Bonsignore, M. R., the Management Committee of EU COST ACTION B26,
(2007). Sleep apnoea as an independent risk factor for cardiovascular disease: current evidence, basic mechanisms and research priorities. Eur Respir J
29: 156-178
[Abstract][Full Text]
Simantirakis, E. N., Vardas, P. E.
(2006). Cardiac pacing in sleep apnoea: diagnostic and therapeutic implications.. Europace
8: 984-987
[Abstract][Full Text]
Teramoto, S., Kume, H., Yamaguchi, Y., Yamamoto, H., Ishii, M., Ishii, T., Ouchi, Y.
(2006). Heart rate variation analysis may not effectively detect sleep apnoeas in heart failure.. Eur Respir J
28: 457-458
[Full Text]
Arzt, M., Bradley, T. D.
(2006). Treatment of Sleep Apnea in Heart Failure. Am. J. Respir. Crit. Care Med.
173: 1300-1308
[Abstract][Full Text]
Sinha, A.-M., Skobel, E. C., Breithardt, O.-A., Zheng, H., Zhan, H., Wilcox, I., Booth, V., Lattimore, J., Chhajed, P. N., Tamm, M., Strobel, W., Neuberger, H.-R., Bohm, M., Mewis, C., Bradley, T. D., Floras, J. S., Logan, A. G., Yaggi, H. K., Concato, J., Mohsenin, V.
(2006). Sleep apnea and heart disease.. NEJM
354: 1086-1089
[Full Text]
Krahn, A. D., Yee, R., Erickson, M. K., Markowitz, T., Gula, L. J., Klein, G. J., Skanes, A. C., George, C. F.P., Ferguson, K. A.
(2006). Physiologic Pacing in Patients With Obstructive Sleep Apnea: A Prospective, Randomized Crossover Trial. J Am Coll Cardiol
47: 379-383
[Abstract][Full Text]
Simantirakis, E. N., Schiza, S. E., Chrysostomakis, S. I., Chlouverakis, G. I., Klapsinos, N. C., Siafakas, N. M., Vardas, P. E.
(2005). Atrial Overdrive Pacing for the Obstructive Sleep Apnea-Hypopnea Syndrome. NEJM
353: 2568-2577
[Abstract][Full Text]
Gottlieb, D. J.
(2005). Can Sleep Apnea Be Treated without Modifying Anatomy?. NEJM
353: 2604-2606
[Full Text]
Caples, S. M., Wolk, R., Somers, V. K.
(2005). Influence of cardiac function and failure on sleep-disordered breathing: evidence for a causative role. J. Appl. Physiol.
99: 2433-2439
[Abstract][Full Text]
Unterberg, C., Luthje, L., Szych, J., Vollmann, D., Hasenfuss, G., Andreas, S.
(2005). Atrial overdrive pacing compared to CPAP in patients with obstructive sleep apnoea syndrome. Eur Heart J
26: 2568-2575
[Abstract][Full Text]
Ferrier, K., Campbell, A., Yee, B., Richards, M., O'Meeghan, T., Weatherall, M., Neill, A.
(2005). Sleep-Disordered Breathing Occurs Frequently in Stable Outpatients With Congestive Heart Failure. Chest
128: 2116-2122
[Abstract][Full Text]
Cormican, L J, Williams, A
(2005). Sleep disordered breathing and its treatment in congestive heart failure. Heart
91: 1265-1270
[Abstract][Full Text]
Ryan, C F
(2005). Sleep {middle dot} 9: An approach to treatment of obstructive sleep apnoea/hypopnoea syndrome including upper airway surgery. Thorax
60: 595-604
[Abstract][Full Text]
Luthje, L., Unterberg-Buchwald, C., Dajani, D., Vollmann, D., Hasenfuss, G., Andreas, S.
(2005). Atrial Overdrive Pacing in Patients with Sleep Apnea with Implanted Pacemaker. Am. J. Respir. Crit. Care Med.
172: 118-122
[Abstract][Full Text]
Sinha, A.-M., Stellbrink, C., Skobel, E. C., Scharf, C., Bloch, K. E., Brunckhorst, C., Duru, F., Candinas, R., Cho, Y. K., Balaban, K., Foldvary, N., Liu, L., Burgess, R. C., Wilkoff, B. L.
(2005). Letter Regarding Article by Scharf et al, "Diagnosis of Sleep-Related Breathing Disorders by Visual Analysis of Transthoracic Impedance Signals in Pacemakers" * Response. Circulation
111: e301-e302
[Full Text]
Pepin, J-L., Defaye, P., Garrigue, S., Poezevara, Y., Levy, P.
(2005). Overdrive atrial pacing does not improve obstructive sleep apnoea syndrome. Eur Respir J
25: 343-347
[Abstract][Full Text]
Scharf, C., Cho, Y. K., Bloch, K. E., Brunckhorst, C., Duru, F., Balaban, K., Foldvary, N., Liu, L., Burgess, R. C., Candinas, R., Wilkoff, B. L.
(2004). Diagnosis of Sleep-Related Breathing Disorders by Visual Analysis of Transthoracic Impedance Signals in Pacemakers. Circulation
110: 2562-2567
[Abstract][Full Text]
Gami, A. S., Pressman, G., Caples, S. M., Kanagala, R., Gard, J. J., Davison, D. E., Malouf, J. F., Ammash, N. M., Friedman, P. A., Somers, V. K.
(2004). Association of Atrial Fibrillation and Obstructive Sleep Apnea. Circulation
110: 364-367
[Abstract][Full Text]
Sinha, A.-M., Skobel, E. C., Breithardt, O.-A., Norra, C., Markus, K. U., Breuer, C., Hanrath, P., Stellbrink, C.
(2004). Cardiac resynchronization therapy improves central sleep apnea and Cheyne-Stokes respiration in patients with chronic heart failure. J Am Coll Cardiol
44: 68-71
[Abstract][Full Text]
Porthan, K. M., Melin, J. H., Kupila, J. T., Venho, K. K. K., Partinen, M. M.
(2004). Prevalence of Sleep Apnea Syndrome in Lone Atrial Fibrillation: A Case-Control Study. Chest
125: 879-885
[Abstract][Full Text]
Gula, L J, Krahn, A D, Skanes, A C, Yee, R, Klein, G J
(2004). Clinical relevance of arrhythmias during sleep: guidance for clinicians. Heart
90: 347-352
[Full Text]
Hedner, J., Kraiczi, H., Peker, Y., Murphy, P.
(2003). Reduction of Sleep-disordered Breathing after Physostigmine. Am. J. Respir. Crit. Care Med.
168: 1246-1251
[Abstract][Full Text]
Shamsuzzaman, A. S. M., Gersh, B. J., Somers, V. K.
(2003). Obstructive Sleep Apnea: Implications for Cardiac and Vascular Disease. JAMA
290: 1906-1914
[Abstract][Full Text]
Lattimore, J. o-D. L., Celermajer, D. S., Wilcox, I.
(2003). Obstructive sleep apnea and cardiovascular disease. J Am Coll Cardiol
41: 1429-1437
[Abstract][Full Text]
Arzt, M., Harth, M., Luchner, A., Muders, F., Holmer, S. R., Blumberg, F. C., Riegger, G. A.J., Pfeifer, M.
(2003). Enhanced Ventilatory Response to Exercise in Patients With Chronic Heart Failure and Central Sleep Apnea. Circulation
107: 1998-2003
[Abstract][Full Text]
Harper, R. M., Macey, P. M., Henderson, L. A., Woo, M. A., Macey, K. E., Frysinger, R. C., Alger, J. R., Nguyen, K. P., Yan-Go, F. L.
(2003). fMRI responses to cold pressor challenges in control and obstructive sleep apnea subjects. J. Appl. Physiol.
94: 1583-1595
[Abstract][Full Text]
Resnick, H. E., Redline, S., Shahar, E., Gilpin, A., Newman, A., Walter, R., Ewy, G. A., Howard, B. V., Punjabi, N. M.
(2003). Diabetes and Sleep Disturbances: Findings from the Sleep Heart Health Study. Diabetes Care
26: 702-709
[Abstract][Full Text]
Henderson, L. A., Woo, M. A., Macey, P. M., Macey, K. E., Frysinger, R. C., Alger, J. R., Yan-Go, F., Harper, R. M.
(2003). Neural responses during Valsalva maneuvers in obstructive sleep apnea syndrome. J. Appl. Physiol.
94: 1063-1074
[Abstract][Full Text]
Gozal, D.
(2002). The Brain in Sleep-disordered Breathing: Is It the Chicken or Is It the Egg?. Am. J. Respir. Crit. Care Med.
166: 1305-1306
[Full Text]
Wellman, A., Malhotra, A., White, D. P., Schotland, H. M., Stein, P., Duntley, S., Garrigue, S., Bordier, P., Haissaguerre, M.
(2002). Atrial Pacing in Sleep Apnea Syndrome. NEJM
347: 445-446
[Full Text]
A correction has been published: N Engl J Med 2002;346(11):872.
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