PACING/ICD/CRT
Cardiac pacing in sleep apnoea: diagnostic and therapeutic implications
Cardiology Department, Heraklion University Hospital, PO Box 1352, Stavrakia, Heraklion, Crete, Greece
Manuscript submitted 19 March 2006. Accepted after revision 8 July 2006.
* Corresponding author. Tel: +30 2810 392877; fax: +30 2810 542055. E-mail address: cardio{at}med.uoc.gr
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Abstract |
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The sleep apnoea syndrome is a particularly common health problem associated with increased cardiovascular morbidity and mortality, as well as harmful socioeconomical and familial complications. In this article, the diagnostic and therapeutic role of cardiac pacing in this syndrome is discussed.
Key Words: Cardiac pacing, Sleep apnoea
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Introduction |
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TopAbstractIntroductionCardiac pacing and the...Cardiac pacing and the...ConclusionsReferences |
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The sleep apnoea syndrome is the most common respiratory disturbance during sleep. It is known to afflict 4% of middle-aged men and 2% of women, although a high percentage of patients in the general population remain undiagnosed.1
The syndrome is defined as a total or partial interruption of inspiratory airflow during sleep, leading to a reduction in oxyhaemoglobin saturation and to sleep fragmentation. Sleep apnoea syndrome is classified as either central or obstructive. In the former type, the apnoea or hypopnoea is due to the interruption of diaphragm activity because of dysfunction of the central regulation mechanisms for respiration control, whereas in the latter, the muscle tone in the upper airways is insufficient to maintain their patency.
The syndrome causes serious social and economic problems, not only because of its high prevalence but also because it is associated with increased cardiovascular morbidity and mortality.2,3 Patients with sleep apnoea often have arterial and pulmonary hypertension, a high risk of coronary artery disease, and heart failure, whereas a high percentage of patients show heart rhythm disturbances.4 In addition, these patients are at increased risk of being involved in traffic accidents, as well as suffering a decline in their family, social, and professional lives.5,6 Therefore, the prompt diagnosis and effective treatment of these patients could be of great importance. The gold standard for the diagnosis of sleep apnoea syndrome is overnight polysomnography, and the treatment of choice is the application of continuous positive airway pressure (CPAP). However, the shortage of sleep laboratories and the high cost of polysomnography render this method inadequate for widespread screening and monitoring. Furthermore, CPAP therapy, although particularly effective, is uncomfortable and is not well tolerated by patients and their bed partners.7,8 For these reasons, in recent years, there have been attempts to develop alternative diagnostic and therapeutic methods with a view to simplifying the diagnosis and making treatment less disagreeable for the patient.
Towards this end, cardiac pacing would seem to have a place in the diagnostic and perhaps the therapeutic part of the problem. In the first case, it appears that, in patients paced with rate-responsive pacemakers that use minute ventilation sensors in the control of heart rate, these are able to detect periods of apnoea or hypopnoea during sleep by evaluating transthoracic impedance. In the second case, the increase in mean heart rate during sleep appears to reduce the number of episodes of apnoea or hypopnoea in certain subgroups of patients, and this has attracted a good deal of recent research interest.
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Cardiac pacing and the diagnosis of sleep apnoea syndrome |
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On the basis of international guidelines, the diagnosis of the syndrome is made using overnight polysomnography. This involves continuous monitoring of the electroencephalogram, electro-oculogram, electromyograms of the chin and anterior tibialis, oronasal airflow, chest and abdominal respiratory movements, arterial oxyhaemoglobin saturation, electrocardiogram, body position, and snoring noise. Another alternative diagnostic method is impedance pneumography. This is based on changes in the electrical impedance of a conductor, depending on the relative fluid and air capacities of the chest cavity. Thus, this method is able to evaluate changes in ventilation and, therefore, to detect periods of apnoea or hypopnoea. At this point, it should be noted that apnoea is defined as the complete cessation of airflow for at least 10 s, whereas hypopnoea is a decrease of 50% or more in the oronasal airflow, associated with a 4% decrease in arterial oxyhaemoglobin saturation.
Rate-responsive pacemakers with minute ventilation sensors are based on precisely the same principle used in impedance pneumography. A subthreshold current pulse is injected between the pacemaker can and one of the pacing electrodes and the voltage is measured between the can and another electrode, located on the same or another lead. Transthoracic impedance, which is directly proportional to this voltage, rises with inspiration and falls with expiration. The sensor can estimate minute ventilation and can discriminate between wakefulness and sleep on the basis of a significant reduction in minute ventilation, respiratory rate, and amplitude,9 although it is also capable of detecting sustained cessation or reduction of respiration during sleep, i.e. episodes of apnoea or hypopnoea.10 The Talent 3DR pacemaker device (ELA Medical/Sorin Group, Paris, France) provides such a sleep respiratory disturbance monitoring function. After pacemaker interrogation, an index corresponding to the mean number of events detected per hour of estimated sleep is automatically downloaded and displayed on the programmer.
A recent study by Defaye et al.10 used these pacemakers and compared the information provided by this function with the apnoea/hypopnoea index (AHI) given by a concurrent overnight polysomnographic recording. The study included 42 patients who presented with a conventional indication for DDDR pacing or cardiac resynchronization and determined that those with severe sleep apnoea syndrome (AHI
30) could be identified with high sensitivity and specificity (75% sensitivity and 94% specificity). In another study by Scharf et al.11 in 22 patients, analogue waveforms of the transthoracic impedance signal measured by the pacemaker's minute ventilation sensor (Kappa 400, Medtronic, Minneapolis, MN, USA) over the course of the night were visualized, scored for apnoea/hypopnoea events, and compared with simultaneous polysomnography. The authors found that the apnoea/hypopnoea events identified by analysis of the pacemaker signal led to the identification of 94% of patients with an AHI >5 and to the correct diagnosis of moderate-to-severe sleep apnoea (AHI >20) with 100% sensitivity and specificity.
In clinical practice, given that the prevalence of sleep apnoea in paced patients is high, this diagnostic capability could be used for screening and monitoring of sleep-related breathing disorders in patients who have a rate-responsive pacemaker with a minute ventilation sensor, and indeed with no added cost. Furthermore, it might be possible to assess the correlation between the episodes of apnoea or hypopnoea and the arrhythmia that patients with sleep apnoea often exhibit or even to evaluate the efficacy of various therapeutic interventions. Thus, although this diagnostic capability of rate-responsive pacemakers with minute ventilation sensors can never replace polysomnography (for example, it cannot distinguish between apnoea episodes of central or obstructive type, nor to recognize the different stages of sleep), it could still be useful in the evaluation of sleep apnoea in patients who already have a permanent pacemaker.
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Cardiac pacing and the treatment of sleep apnoea syndrome |
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The prompt commencement of treatment for sleep apnoea syndrome is beneficial for the patient. It has been found that in the obstructive form of the syndrome, a reduction in episodes of apnoea or hypopnoea, in arousals, and in oxyhaemoglobin desaturation is associated with a reduction in motor vehicle accidents, a normalization of blood pressure, baroreceptor sensitivity, and production of nitric oxide derivatives, as well as with a reduction in sympathetic nervous system activity and the number of arrhythmias observed in these patients.12
–22 In addition, there is evidence to suggest that CPAP therapy reduces cardiovascular risk and has a positive effect on mortality.23,24
In the case of the central type of the syndrome, which is usually seen in patients with heart failure, treatment with CPAP, although not affecting survival, attenuates central sleep apnoea, improves nocturnal oxygenation, increases ejection fraction, lowers noradrenaline levels, and improves functional capacity.25 Although interventions have been used to treat the syndrome, such as upper airway surgery and oral appliances, in recent years it has become clear that CPAP is the most effective. However, acceptance of CPAP by patients is low (65–80%), mainly because of problems with the nasal–mask interface and inadequate educational programmes before the CPAP titration. Thus, the search for alternative therapeutic techniques continues.
The evaluation, several years ago, of cardiac pacing as an alternative therapeutic method was based on the observation that some patients with sleep apnoea reported an improvement in their sleep-related symptoms after having a permanent pacemaker implanted for the treatment of symptomatic bradyarrhythmias. Although there were already findings from a smaller study26 suggesting a benefit for patients with sleep apnoea as a result of pacing, the results of a study by Garrigue et al.27 were particularly impressive. Those authors, in a well-organized study with crossover design, included 15 patients who were already being paced for symptomatic bradycardia and suffered from sleep apnoea. After a full night of pacing at a rate 15 bpm higher than the mean nocturnal heart rate, there was a mean 57% decrease in AHI. In this study, the mean AHI was 27 (moderate severity) and 60% of the patients had left ventricular systolic dysfunction. In addition, most of the patients had predominantly central sleep apnoea, whereas in those with predominantly obstructive sleep apnoea, the percentage of episodes of central type was high. Even though haemodynamic measurements were not made, it is likely that the increased heart rate during pacing improved cardiac function and reduced the episodes of central type apnoea, followed by a reduction in obstructive episodes, as an improvement in cardiac function by any means, pharmaceutical or not, has been found to improve central sleep apnoea, which is related to the appearance or aggravation of existing obstructive sleep apnoea.28–30
In any case, however, even if these patients' improvement was due to the effects of atrial overdrive pacing, the same has not been seen in patients with predominantly obstructive sleep apnoea. In a recent study at our centre,31 we investigated 16 patients with purely obstructive type sleep apnoea (mean AHI 49 per hour), excluding patients with central type apnoea, left ventricular systolic dysfunction, or heart failure. The study evaluated the effect of atrial overdrive pacing during the first 24 h and after 1 month, comparing its efficacy with that of CPAP, in a randomized, crossover design. We found that CPAP therapy was extremely effective, both acutely and after 1 month, whereas atrial overdrive pacing appeared to have no effect on the various sleep parameters that were evaluated. What is more, the findings of another four published studies involving similar patient populations were in agreement with our own.32–35 It seems that in these studies, which examined predominantly obstructive sleep apnoea, the upper airway obstruction, which is due mainly to anatomical reasons, is unaffected by the functional changes caused by atrial overdrive pacing, whereas in patients like those studied by Garrigue et al.,27 the changes in the function of the heart, and probably the autonomic nervous system, affect the pathophysiology of respiration disturbances during sleep that are unlikely to be due to any great degree to anatomical causes36. Finally, it should be mentioned that biventricular pacing in patients with heart failure, ventricular desynchronization, and sleep-related breathing disorders has been found to reduce significantly the episodes of central type sleep apnoea and to improve the quality of sleep. In a recent study by Sinha et al.,37 cardiac resynchronization therapy led to a significant decrease in AHI (19.2±10.3 to 4.0±4.4, P<0.001) and Pittsburgh sleep quality index (10.4±1.6 to 3.9±2.4, P<0.001) without Cheyne–Stokes respiration and to a significant increase in oxygen saturation SaO2min (84±5 to 89±2%, P<0.001). Also, Skobel et al.38 found that in such patients, cardiac resynchronization therapy reduced Cheyne–Stokes respiration with an improvement in sleep quality and symptomatic depression.
Apart from cardiac resynchronization, it is possible that atrial overdrive pacing could play a beneficial role in central sleep apnoea in patients with heart failure, who also have bradycardia because of sinus node disease or medication. A low cardiac output, a long circulation time, and pulmonary congestion are factors that have been related to the development of central sleep apnoea. In such cases, atrial overdrive pacing might help eliminate the syndrome by improving these factors, but further research is needed in this area.
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Conclusions |
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TopAbstractIntroductionCardiac pacing and the...Cardiac pacing and the...ConclusionsReferences |
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It is clear from the above that cardiac pacing is rather ineffective in obstructive sleep apnoea, but may be helpful in other subgroups of patients with sleep-related breathing disorders, and mainly in those with the central type of the syndrome, or mixed sleep apnoea without a significant anatomical contribution to the upper airway obstruction. However, further studies will be needed to determine precisely in which patient populations such a therapeutic approach might be most beneficial.
As regards the monitoring of sleep apnoea by rate-responsive pacemakers with minute ventilation sensors, the progress in technology is likely to permit the better screening and monitoring of treatment effects in already paced patients, with a consequent benefit to their health status.
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References |
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[1] Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med 1993; 328: 1230–5.
[2] Shahar E, Whitney CW, Redline S, et al. Sleep-disordered breathing and cardiovascular disease: cross-sectional results of the Sleep Heart Health Study. Am J Respir Crit Care Med 2001; 163: 19–25.
[3] Peker Y, Hedner J, Kraiczi H, Loth S. Respiratory disturbance index: an independent predictor of mortality in coronary artery disease. Am J Respir Crit Care Med 2000; 162: 81–6.
[4] Leung RS and Bradley TD. Sleep apnea and cardiovascular disease. Am J Respir Crit Care Med 2001; 164: 2147–65.
[5] Teran-Santos J, Jimenez-Gomez A, Cordero-Guevara J. The association between sleep apnea and the risk of traffic accidents. Cooperative Group Burgos Santander. N Engl J Med 1999; 18: 847–51.
[6] Yamamoto H, Akashiba T, Kosaka N, et al. Long term effects of 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][Web of Science][Medline]
[7] Rolfe I, Olson LG, Saunders NA. Longterm acceptance of continuous positive airway pressure in obstructive sleep apnea. Am Rev Respir Dis 1991; 144: 1130–3.[Web of Science][Medline]
[8] Pepin JL, Krieger J, Rodenstein D, et al. Effective compliance during the first 3 months of continuous positive airway pressure: a European prospective study of 121 patients. Am J Respir Crit Care Med 1999; 160: 1124–9.
[9] Bonnet JL, Vai F, Pioger G, Garrigue S, Clémenty J, Cazeau S. Circadian variations in minute ventilation can be reproduced by a pacemaker sensor. Pacing Clin Electrophysiol 1998; 21: 701–5.[CrossRef][Medline]
[10] Defaye P, Pepin JL, Poezevara Y, et al. Automatic recognition of abnormal respiratory events during sleep by a pacemaker transthoracic impedance sensor. J Cardiovasc Electrophsiol 2004; 15: 1034–40.
[11] Scharf C, Cho YK, Bloch KE, et al. Diagnosis of sleep-related breathing disorders by visual analysis of transthoracic impedance signals in pacemakers. Circulation 2004; 110: 2562–7.
[12] George CF. Reduction in motor vehicle collisions following treatment of sleep apnoea with nasal CPAP. Thorax 2001; 56: 508–12.
[13] Wilcox I, Grunstein RR, Hedner JA, et al. Effect of nasal continuous positive airway pressure during sleep on 24-hour blood pressure in obstructive sleep apnea. Sleep 1993; 16: 539–44.[Web of Science][Medline]
[14] Dimsdale JE, Loredo JS, Profant J. Effect of continuous positive airway pressure on blood pressure: a placebo trial. Hypertension 2000; 35: 144–7.
[15] Tkacova R, Dajani HR, Rankin F, et al. Continuous positive airway pressure improves nocturnal baroreflex sensitivity of patients with heart failure and obstructive sleep apnea. J Hypertens 2000; 18: 1257–62.[CrossRef][Web of Science][Medline]
[16] Schulz R, Schmidt D, Blum A, et al. Decreased plasma levels of nitric oxide derivatives in obstructive sleep apnoea: response to CPAP therapy. Thorax 2000; 55: 1046–51.
[17] Somers VK, Dyken ME, Clary MP, Abboud FM. Sympathetic neural mechanisms in obstructive sleep apnea. J Clin Invest 1995; 96: 1897–904.[Web of Science][Medline]
[18] Narkiewicz K, Kato M, Phillips BG, Pesek CA, Davison DE, Somers VK. Nocturnal continuous positive airway pressure decreases daytime sympathetic traffic in obstructive sleep apnea. Circulation 1999; 100: 2332–5.
[19] Ziegler MG, Mills PJ, Loredo JS, Ancoli-Israel S, Dimsdale JE. Effect of continuous positive airway pressure and placebo treatment on sympathetic nervous activity in patients with obstructive sleep apnea. Chest 2001; 120: 887–93.
[20] Simantirakis EN, Schiza SI, Marketou ME, et al. Severe bradyarrhythmias in patients with sleep apnoea: the effect of continuous positive airway pressure treatment: a long-term evaluation using an insertable loop recorder. Eur Heart J 2004; 25: 1070–6.
[21] Javaheri S. Effects of continuous positive airway pressure on sleep apnea and ventricular irritability in patients with heart failure. Circulation 2000; 101: 392–7.
[22] Harbison J, O'Reilly P, McNicholas WT. Cardiac rhythm disturbances in the obstructive sleep apnoea syndrome: effects of nasal continuous positive airway pressure therapy. Chest 2000; 118: 591–955.
[23] Marin JM, Carrizo SJ, Vicente E, Agusti AG. Long-term cardiovascular outcomes in men with obstructive sleep apnoea–hypopnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet 2005; 365: 1046–53.[Web of Science][Medline]
[24] Campos-Rodriguez F, Pena-Grinan N, Reyes-Nunez N, De la Cruz-Moron I, Perez-Ronchel J, De la Vega-Gallardo F, et al. Mortality in obstructive sleep apnea–hypopnea patients treated with positive airway pressure. Chest 2005; 128: 624–33.
[25] Bradley TD, Logan AG, Kimoff RJ, et al. Continuous positive airway pressure for central sleep apnea and heart failure. N Engl J Med 2005; 353: 2070–3.
[26] Kato I, Shiomi T, Sasanabe R, et al. Effects of physiological cardiac pacing on sleep-disordered breathing in patients with chronic brady-dysrhythmias. Psychiatry Clin Neurosci 2001; 55: 257–8.[Medline]
[27] Garrigue S, Bordier P, Jaïs P, et al. Benefit of atrial pacing in sleep apnea syndrome. N Engl J Med 2002; 346: 404–12.
[28] Ryan CM and Bradley TD. Periodicity of obstructive sleep apnea in patients with and without heart failure. Chest 2005; 127: 536–42.
[29] Hudgel DW, Chapman KR, Faulks C, Hendricks C. Changes in inspiratory muscle electrical activity and upper airway resistance during periodic breathing induced by hypoxia during sleep. Am Rev Respir Dis 1987; 135: 899–906.[Web of Science][Medline]
[30] Warner G, Skatrud JB, Dempsey JA. Effect of hypoxia-induced periodic breathing on upper airway obstruction during sleep. J Appl Physiol 1987; 62: 2201–11.
[31] Simantirakis EN, Schiza SE, Chrysostomakis SI, et al. Atrial overdrive pacing for the obstructive sleep apnea–hypopnea syndrome. N Engl J Med 2005; 353: 2568–77.
[32] Pepin J-L, Defaye P, Garrigue S, Poezevara Y, Levy P. Overdrive atrial pacing does not improve obstructive sleep apnoea syndrome. Eur Respir J 2005; 25: 343–7.
[33] Luthje L, Unterberg-Buchwald C, Dajani D, Vollmann D, Hasenfuss G, Andreas S. Atrial overdrive pacing in patients with sleep apnea with implanted pacemaker. Am J Respir Crit Care Med 2005; 172: 118–22.
[34] Unterberg C, Luthje L, Szych J, Vollmann D, Hasenfuss G. Atrial overdrive pacing compared to CPAP in patients with obstructive sleep apnoea syndrome. Eur Heart J 2005; 26: 2658–75.
[35] Krahn AD, Yee R, Erickson MK, Markowitz T, Gula LJ, Klein GJ, et al. Physiologic pacing in patients with obstructive sleep apnea: a prospective, randomized crossover trial. J Am Coll Cardiol 2006; 47: 379–83.
[36] Gottlieb DJ. Can sleep apnea be treated without modifying anatomy? N Engl J Med 2005; 353: 2604–6.
[37] Sinha AM, Skobel EC, Breithardt OA, et al. Cardiac resynchronization therapy improves central sleep apnea and Cheyne–Stokes respiration in patients with chronic heart failure. J Am Coll Cardiol 2004; 44: 68–71.
[38] Skobel EC, Sinha AM, Norra C, et al. Effect of cardiac resynchronization therapy on sleep quality, quality of life, and symptomatic depression in patients with chronic heart failure and Cheyne–Stokes respiration. Sleep Breath 2005; 9: 159–66.[CrossRef][Medline]
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