Schwerpunkt Herz 2014 DOI 10.1007/s00059-014-4063-8 © Urban & Vogel 2014
H. Fox · T. Bitter · D. Horstkotte · O. Oldenburg Department of Cardiology, Heart and Diabetes Center North RhineWestphalia, Ruhr University Bochum, Bad Oeynhausen
Termination of adaptive servoventilation after successful long-term therapy Case report of a heart failure patient with nocturnal Cheyne–Stokes respiration
Sleep-disordered breathing (SDB) represents a highly prevalent, but widely under-recognized and under-appreciated comorbidity in heart failure (HF) patients. Especially in HF, obstructive (OSA) as well as central (CSA) sleep apnea with Cheyne–Stokes respiration (CSR) have a negative impact on prognosis [1, 2]. Hospitalization for deterioration of cardiac function impairs quality of life and is a predictor of mortality in these patients [3]. Sleep apnea in general and CSA with CSR has been shown to be associated with increasing severity of HF, and exacerbation of HF is associated with deterioration in SDB [4]. CSA with CSR is usually seen during non-rapid eye movement (REM) sleep in approximately 30% of patients with chronic HF [5, 6, 7] and is characterized by a typical waxing and waning pattern in breathing amplitude, interspersed with central apneas or hypopneas. Some studies have reported complete disappearance of CSA after normalization of heart function, but the available data are not consistent [8, 9, 10, 11]. It is not known whether previously introduced ventilation therapy for the treatment of SDB can be safely withdrawn after improvement of cardiac function and the disappearance of nocturnal respiratory events. Earlier case reports suggest that normalization of heart function after cardiac transplantation resulted in complete disappearance of CSA [8], with residu-
al OSA then documented in some cases [8, 9]. However, the feasibility of withdrawing ventilation therapy after successful long-term ASV therapy for nocturnal CSR has not previously been reported.
Case report Here, we report the case of a 56-year-old male patient who had been diagnosed with dilated non-inflammatory cardiomyopathy and severely impaired left ventricular function 6 years previously, probably secondary to years of uncontrolled arterial hypertension [initial New York Heart Association (NYHA) functional classification IV, left ventricular systolic ejection fraction (LVEF) 35%, brain natriuretic peptide (BNP) level 943 pg/ml]. Guideline-based HF medication was introduced (ACE inhibitors, β-blocker, and aldosterone antagonist). Co-existing coronary artery and inflammatory heart disease had been ruled out by coronary angiography and endomyocardial biopsy. HF was subsequently managed according to current European Society of Cardiology (ESC) guidelines and the patient was closely monitored in our outpatient HF department. The patient was screened for SDB using multichannel cardiorespiratory polygraphy (PG) followed by polysomnography (PSG). Both recordings revealed severe CSA with a CSR breathing pattern (. Tab. 1). The initial apnea/hypopnea index (AHI) was 67/h, with ap-
nea durations up to 41 s, hypopnea durations up to 55 s, mean oxygen saturation of 93% (minimum 83%), and mean desaturation of 5% (. Tab. 1). Based on these findings, and in addition to optimal ESC guideline-recommended medical management for HF, adaptive servoventilation (ASV) therapy was initiated (AutoSet CS2™, ResMed). ASV was given via a full-face Quattro™ mask (ResMed) at settings of 5 cm H2O end-expiratory pressure (EEP), 3 cm H2O minimal pressure, and 10 cm H2O maximal pressure; these were well tolerated by the patient. The principle of ASV is to provide a baseline level of ventilatory support. The subject’s ventilation is servocontrolled with a highgain integral controller to equal a moving target ventilation of 90% of the long-term average ventilation (time constant 3 min). If the subject suddenly ceases all central respiratory effort, machine support (i.e., pressure swing amplitude) increases from the minimum pressure up to whatever is required to maintain ventilation at 90% of the long-term average (reached in approximately 12 s). If the subject then resumes normal spontaneous breathing efforts, support will fall back to the minimum pressure over a similar time period. Smaller or slower changes in a patient’s breathing efforts will result in proportionally smaller, slower changes in the degree of support. In the steady state, ventilation exceeds the 90% target, so support stays at the minimum pressure [12]. Herz 2014
| 1
Schwerpunkt Tab. 1 Patient data before initiation of adaptive servoventilation (ASV) during therapy and after ASV therapy withdrawal
Initial presentation for HF
ASV therapy and optimal medical therapy [2]
ASV therapy and optimal medical therapy [3]
20/02/2008 67 48.4 19 Severe Prevalent 41
ASV therapy and optimal medical therapy [1] 04/03/2008 3.6 0.2 3.4 None None 10
23/04/2009 0.4 0 0.4 None None 0
03/05/2011 1 0 1 None None 0
ASV withdrawal and optimal medical therapy 07/11/2013 10 1 15 Mild None 14
Date, DD/MM/YYYY AHI/h AI/h HI/h CSA CSR Maximum apnea duration, s Maximum hypopnea duration, s Mean oxygen saturation, % Minimum oxygen saturation, % Mean desaturation, % Snoring time, min Snoring time, % NYHA class LVEF, % LAD, mm LVEDD, mm LVESD, mm IVS, mm MV:E/A ratio BNP, pg/ml pCO2, mmHg HCVR, l/min/mmHg VO2 max, ml/kg/min Treadmill test, maximum watts 6MWD, m Medical therapy
55
62
14
41
33
93
94
96
95
93
83
89
94
90
88
5 6 1.4 IV 35 49 66 56 18 1.21 943 41.2 28.84 N/A N/A
4 27.5 8.3 II 50 44 62 35 17 0.79 133 40.6 N/A 25.69 168
4 0 0 II 50 44 50 33 18 0.68 77.8 34.3 N/A 26.72 200
5 0 0 II 50 40 50 31 14 0.93 61.7 39.9 N/A 20.88 158
4 21.3 7.7 II 50 42 49 31 15 0.74 12.7 38 N/A 21.43 200
N/A ACE inhibitor, AA
N/A β-blocker, diuretics, ACE inhibitor, AA Y
520 β-blocker, diuretics, ACE inhibitor, AA
640 β-blocker, diuretics, ACE inhibitor, AA
660 β-blocker, diuretics, ACE inhibitor, AA
ASV therapy
N
Y
Y
N
6MWD 6-minute walk distance, AA aldosterone antagonist, ACE angiotensin converting enzyme, AHI apnea–hypopnea index, AI apnea index, ASV adaptive servoventilation, BNP brain natriuretic peptide, CSA central sleep apnea, CSR Cheyne–Stokes respiration, E/A early (E) to late (A) ventricular filling velocity ratio, HCVR hypercapnic ventilatory response, HF heart failure, HI hypopnea index, LAD left atrial diameter, LVEDD left ventricular end-diastolic diameter, LVEF left ventricular ejection fraction, LVESD left ventricular end-systolic diameter, MV minute ventilation, N no, N/A not applicable NYHA New York Heart Association, pCO2, carbon dioxide pressure, VO2 max maximal oxygen consumption, Y yes
Repeated PSG findings during ASV confirmed effective suppression of CSA and CSR, and good compliance (AHI 1/h, average nightly usage 5 h, 23 min); no withdrawal of ASV therapy during optimal medical HF treatment was contemplated. In addition, improvements in LVEF (from 35 to 50%) and NYHA class (from IV to II) were documented. The patient was able to undertake his daily routine again and had few cardiac complaints.
2 |
Herz 2014
During a later routine visit to our sleep laboratory for ASV therapy validation and adherence by multichannel polygraphy, an attempt to withdraw ASV therapy was made. Persistent CSA was noted, but this was only mild and there was no CSR or relevant oxygen desaturations. AHI was 10/h, with apnea durations up to 14 s, hypopnea durations up to 33 s, mean oxygen saturation of 93% (minimum 88%), and mean desaturation of 4% (. Tab. 1). Since the withdrawal of ASV therapy, the
patient has remained stable (NYHA II, LVEF 50%, BNP 12.7 pg/ml), and there have been no serious adverse events (e.g., hospitalizations). It has been hypothesized that the occurrence and severity of CSA–CSR in HF patients mirror cardiac function. This theory is supported by various studies showing an improvement or disappearance of CSR with effective HF treatments, such as cardiac resynchronization therapy [16, 25], β-blocker and/or ACE inhibitor ther-
Compliance with ethical guidelines
apy [26, 27, 28]. In addition, large-scale randomized controlled trials such as the SERVE-HF (Treatment of Predominant Central Sleep Apnoea by Adaptive Servoventilation in Patients With Heart Failure) trial and its major substudy [13] will provide data on the effect of ASV on cardiac function and outcome in HF patients.
Conflict of interest. H. Fox, T. Bitter, D. Horstkotte, and O. Oldenburg state that there are no conflicts of interest.
Conclusion
References
We, for the first time, present the case of a patient with severe systolic HF and severe CSR, treated by optimal medical therapy and ASV therapy in a longterm setting, in whom improvement of symptoms and cardiac function resulted in termination of ASV therapy. The beneficial effects of ASV in this patient are probably secondary to improved oxygenation, prevention of hypercapnia, decrease in intrathoracic pressure swings, and decreased sympathetic tone [14, 15]. While the patient’s improved clinical condition coincided with the initiation of ASV, we cannot prove that ASV was solely responsible for the benefit seen. Late effects of conventional medical HF therapy might have also contributed, but various recent studies show improvements in symptoms, quality of life, cardiac function, and outcome [3, 16, 17, 18, 19, 20, 21, 22, 23, 24] with the addition of ASV. While data from largescale randomized controlled trials of ASV in HF will not be available until late 2015, sample evidence exists to suggest that physicians should not ignore the diagnosis and treatment of SDB in patients with HF.
1. Oldenburg O, Lamp B, Faber L, Teschler H et al (2007) Sleep-disordered breathing in patients with symptomatic heart failure: a contemporary study of prevalence in and characteristics of 700 patients. Eur J Heart Fail 9:251–257 2. Javaheri S, Shukla R, Zeigler H, Wexler L (2007) Central sleep apnea, right ventricular dysfunction, and low diastolic blood pressure are predictors of mortality in systolic heart failure. J Am Coll Cardiol 49:2028–2034 3. Jilek C, Krenn M, Sebah D et al (2011) Prognostic impact of sleep disordered breathing and its treatment in heart failure: an observational study. Eur J Heart Fail 13:68–75 4. Jelic S, Le Jemtel TH (2009) Sleep-disordered breathing in acute decompensated heart failure. Curr Heart Fail Rep 6:169–175 5. Javaheri S, Parker TJ, Liming JD et al (1998) Sleep apnea in 81 ambulatory male patients with stable heart failure: types and their prevalences, consequences, and presentations. Circulation 97:2154– 2159 6. Solin P, Bergin P, Richardson M et al (1999) Influence of pulmonary capillary wedge pressure on central apnea in heart failure. Circulation 99:1574– 1579 7. Sin DD, Fitzgerald F, Parker JD et al (1999) Risk factors for central and obstructive sleep apnea in 450 men and women with congestive heart failure. Am J Respir Crit Care Med 160:1101–1106 8. Braver HM, Brandes WC, Kubiet MA et al (1995) Effect of cardiac transplantation on Cheyne-Stokes respiration occurring during sleep. Am J Cardiol 76:632–634 9. Collop NA (1993) Cheyne-Stokes ventilation converting to obstructive sleep apnea following heart transplantation. Chest 104:1288–1289 10. Murdock DK, Lawless CE, Loeb HS et al (1986) The effect of heart transplantation on Cheyne-Stokes respiration associated with congestive heart failure. J Heart Transplant 5:336–337 11. Thalhofer SA, Kiwus U, Dorow P (2000) Influence of orthotopic heart transplantation on breathing pattern disorders in patients with dilated cardiomyopathy. Sleep Breath 4:121–126 12. Teschler H, Döhring J, Wang YM, Berthon-Jones M (2001) Adaptive pressure support servo-ventilation: a novel treatment for Cheyne-Stokes respiration in heart failure. Am J Respir Crit Care Med 164:614–619 13. Cowie MR, Woehrle H, Wegscheider K, Angermann C et al (2013) Rationale and design of the SERVEHF study: treatment of sleep-disordered breathing with predominant central sleep apnoea with adaptive servo-ventilation in patients with chronic heart failure. Eur J Heart Fail 15:937–943
Corresponding address O. Oldenburg Department of Cardiology, Heart and Diabetes Center North Rhine-Westphalia, Ruhr University Bochum Georgstr. 11, 32545 Bad Oeynhausen Germany [email protected]
The accompanying manuscript does not include studies on humans or animals.
14. Yoshihisa A, Suzuki S, Yamaki T, Sugimoto K et al (2013) Impact of adaptive servo-ventilation on cardiovascular function and prognosis in heart failure patients with preserved left ventricular ejection fraction and sleep-disordered breathing. Eur J Heart Fail 15:902–909 15. Koyama T, Watanabe H, Tamura Y, Oguma Y et al (2013) Adaptive servo-ventilation therapy improves cardiac sympathetic nerve activity in patients with heart failure. Eur J Heart Fail 15:902– 909 16. Oldenburg O, Bitter T, Lehmann R, Korte S (2011) Adaptive Servoventilation improves cardiac function and respiratory stability. Clin Res Cardiol 100:107–116 17. Bitter T, Gutleben KJ, Nölker G, Westerheide N et al (2013) Treatment of Cheyne-Stokes respiration reduces arrhythmic events in chronic heart failure. J Cardiovasc Electrophysiol (in press). DOI 10.1111/ jce.12197 18. Oldenburg O, Horstkotte D (2008) Quality of life in patients with chronic heart failure and CheyneStokes respiration. Sleep Med 9:601–602 19. Damy T, Margarit L, Noroc A, Bodez D et al (2012) Prognostic impact of sleep-disordered breathing and its treatment with nocturnal ventilation for chronic heart failure. Eur J Heart Fail 14:1009–1019 20. Pepperell JC, Maskell NA, Jones DR, LangfordWiley BA et al (2003) A randomized controlled trial of adaptive ventilation for Cheyne-Stokes breathing in heart failure. Am J Respir Crit Care Med 168:1109–1114 21. Philippe C, Stoïca-Herman M, Drouot X, Raffestin B et al (2006) Compliance with and effectiveness of adaptive servoventilation versus continuous positive airway pressure in the treatment of CheyneStokes respiration in heart failure over a six month period. Heart 92:337–342 22. Bradley TD, Logan AG, Kimoff RJ, Sériès F et al (2005) Continuous positive airway pressure for central sleep apnea and heart failure. N Engl J Med 353:2025–2033 23. Yoshihisa A, Shimizu T, Owada T, Nakamura Y et al (2011) Adaptive servoventilation improves cardiac dysfunction and prognosis in chronic heart failure patients with Cheyne-Stokes respiration. Int Heart J 52:218–223 24. Kasai T, Narui K, Dohi T, Yanagisawa N et al (2008) Prognosis of patients with heart failure and obstructive sleep apnea treated with continuous positive airway pressure. Chest 133:690–696 25. Sinha AM, Skobel EC, Breithardt OA, Norra C et al (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 26. Tamura A, Kawano Y, Kadota J (2009) Carvedilol reduces the severity of central sleep apnea in chronic heart failure. Circ J 73:295–298 27. Tamura A, Kawano Y, Naono S et al (2007) Relationship between beta-blocker treatment and the severity of central sleep apnea in chronic heart failure. Chest 131:130–135 28. Walsh JT, Andrews R, Starling R, Cowley AJ et al (1995) Effects of captopril and oxygen on sleep apnoea in patients with mild to moderate congestive cardiac failure. Br Heart J 73:237–241
Herz 2014
| 3
H. Fox · T. Bitter · D. Horstkotte · O. Oldenburg Department of Cardiology, Heart and Diabetes Center North RhineWestphalia, Ruhr University Bochum, Bad Oeynhausen
Termination of adaptive servoventilation after successful long-term therapy Case report of a heart failure patient with nocturnal Cheyne–Stokes respiration
Sleep-disordered breathing (SDB) represents a highly prevalent, but widely under-recognized and under-appreciated comorbidity in heart failure (HF) patients. Especially in HF, obstructive (OSA) as well as central (CSA) sleep apnea with Cheyne–Stokes respiration (CSR) have a negative impact on prognosis [1, 2]. Hospitalization for deterioration of cardiac function impairs quality of life and is a predictor of mortality in these patients [3]. Sleep apnea in general and CSA with CSR has been shown to be associated with increasing severity of HF, and exacerbation of HF is associated with deterioration in SDB [4]. CSA with CSR is usually seen during non-rapid eye movement (REM) sleep in approximately 30% of patients with chronic HF [5, 6, 7] and is characterized by a typical waxing and waning pattern in breathing amplitude, interspersed with central apneas or hypopneas. Some studies have reported complete disappearance of CSA after normalization of heart function, but the available data are not consistent [8, 9, 10, 11]. It is not known whether previously introduced ventilation therapy for the treatment of SDB can be safely withdrawn after improvement of cardiac function and the disappearance of nocturnal respiratory events. Earlier case reports suggest that normalization of heart function after cardiac transplantation resulted in complete disappearance of CSA [8], with residu-
al OSA then documented in some cases [8, 9]. However, the feasibility of withdrawing ventilation therapy after successful long-term ASV therapy for nocturnal CSR has not previously been reported.
Case report Here, we report the case of a 56-year-old male patient who had been diagnosed with dilated non-inflammatory cardiomyopathy and severely impaired left ventricular function 6 years previously, probably secondary to years of uncontrolled arterial hypertension [initial New York Heart Association (NYHA) functional classification IV, left ventricular systolic ejection fraction (LVEF) 35%, brain natriuretic peptide (BNP) level 943 pg/ml]. Guideline-based HF medication was introduced (ACE inhibitors, β-blocker, and aldosterone antagonist). Co-existing coronary artery and inflammatory heart disease had been ruled out by coronary angiography and endomyocardial biopsy. HF was subsequently managed according to current European Society of Cardiology (ESC) guidelines and the patient was closely monitored in our outpatient HF department. The patient was screened for SDB using multichannel cardiorespiratory polygraphy (PG) followed by polysomnography (PSG). Both recordings revealed severe CSA with a CSR breathing pattern (. Tab. 1). The initial apnea/hypopnea index (AHI) was 67/h, with ap-
nea durations up to 41 s, hypopnea durations up to 55 s, mean oxygen saturation of 93% (minimum 83%), and mean desaturation of 5% (. Tab. 1). Based on these findings, and in addition to optimal ESC guideline-recommended medical management for HF, adaptive servoventilation (ASV) therapy was initiated (AutoSet CS2™, ResMed). ASV was given via a full-face Quattro™ mask (ResMed) at settings of 5 cm H2O end-expiratory pressure (EEP), 3 cm H2O minimal pressure, and 10 cm H2O maximal pressure; these were well tolerated by the patient. The principle of ASV is to provide a baseline level of ventilatory support. The subject’s ventilation is servocontrolled with a highgain integral controller to equal a moving target ventilation of 90% of the long-term average ventilation (time constant 3 min). If the subject suddenly ceases all central respiratory effort, machine support (i.e., pressure swing amplitude) increases from the minimum pressure up to whatever is required to maintain ventilation at 90% of the long-term average (reached in approximately 12 s). If the subject then resumes normal spontaneous breathing efforts, support will fall back to the minimum pressure over a similar time period. Smaller or slower changes in a patient’s breathing efforts will result in proportionally smaller, slower changes in the degree of support. In the steady state, ventilation exceeds the 90% target, so support stays at the minimum pressure [12]. Herz 2014
| 1
Schwerpunkt Tab. 1 Patient data before initiation of adaptive servoventilation (ASV) during therapy and after ASV therapy withdrawal
Initial presentation for HF
ASV therapy and optimal medical therapy [2]
ASV therapy and optimal medical therapy [3]
20/02/2008 67 48.4 19 Severe Prevalent 41
ASV therapy and optimal medical therapy [1] 04/03/2008 3.6 0.2 3.4 None None 10
23/04/2009 0.4 0 0.4 None None 0
03/05/2011 1 0 1 None None 0
ASV withdrawal and optimal medical therapy 07/11/2013 10 1 15 Mild None 14
Date, DD/MM/YYYY AHI/h AI/h HI/h CSA CSR Maximum apnea duration, s Maximum hypopnea duration, s Mean oxygen saturation, % Minimum oxygen saturation, % Mean desaturation, % Snoring time, min Snoring time, % NYHA class LVEF, % LAD, mm LVEDD, mm LVESD, mm IVS, mm MV:E/A ratio BNP, pg/ml pCO2, mmHg HCVR, l/min/mmHg VO2 max, ml/kg/min Treadmill test, maximum watts 6MWD, m Medical therapy
55
62
14
41
33
93
94
96
95
93
83
89
94
90
88
5 6 1.4 IV 35 49 66 56 18 1.21 943 41.2 28.84 N/A N/A
4 27.5 8.3 II 50 44 62 35 17 0.79 133 40.6 N/A 25.69 168
4 0 0 II 50 44 50 33 18 0.68 77.8 34.3 N/A 26.72 200
5 0 0 II 50 40 50 31 14 0.93 61.7 39.9 N/A 20.88 158
4 21.3 7.7 II 50 42 49 31 15 0.74 12.7 38 N/A 21.43 200
N/A ACE inhibitor, AA
N/A β-blocker, diuretics, ACE inhibitor, AA Y
520 β-blocker, diuretics, ACE inhibitor, AA
640 β-blocker, diuretics, ACE inhibitor, AA
660 β-blocker, diuretics, ACE inhibitor, AA
ASV therapy
N
Y
Y
N
6MWD 6-minute walk distance, AA aldosterone antagonist, ACE angiotensin converting enzyme, AHI apnea–hypopnea index, AI apnea index, ASV adaptive servoventilation, BNP brain natriuretic peptide, CSA central sleep apnea, CSR Cheyne–Stokes respiration, E/A early (E) to late (A) ventricular filling velocity ratio, HCVR hypercapnic ventilatory response, HF heart failure, HI hypopnea index, LAD left atrial diameter, LVEDD left ventricular end-diastolic diameter, LVEF left ventricular ejection fraction, LVESD left ventricular end-systolic diameter, MV minute ventilation, N no, N/A not applicable NYHA New York Heart Association, pCO2, carbon dioxide pressure, VO2 max maximal oxygen consumption, Y yes
Repeated PSG findings during ASV confirmed effective suppression of CSA and CSR, and good compliance (AHI 1/h, average nightly usage 5 h, 23 min); no withdrawal of ASV therapy during optimal medical HF treatment was contemplated. In addition, improvements in LVEF (from 35 to 50%) and NYHA class (from IV to II) were documented. The patient was able to undertake his daily routine again and had few cardiac complaints.
2 |
Herz 2014
During a later routine visit to our sleep laboratory for ASV therapy validation and adherence by multichannel polygraphy, an attempt to withdraw ASV therapy was made. Persistent CSA was noted, but this was only mild and there was no CSR or relevant oxygen desaturations. AHI was 10/h, with apnea durations up to 14 s, hypopnea durations up to 33 s, mean oxygen saturation of 93% (minimum 88%), and mean desaturation of 4% (. Tab. 1). Since the withdrawal of ASV therapy, the
patient has remained stable (NYHA II, LVEF 50%, BNP 12.7 pg/ml), and there have been no serious adverse events (e.g., hospitalizations). It has been hypothesized that the occurrence and severity of CSA–CSR in HF patients mirror cardiac function. This theory is supported by various studies showing an improvement or disappearance of CSR with effective HF treatments, such as cardiac resynchronization therapy [16, 25], β-blocker and/or ACE inhibitor ther-
Compliance with ethical guidelines
apy [26, 27, 28]. In addition, large-scale randomized controlled trials such as the SERVE-HF (Treatment of Predominant Central Sleep Apnoea by Adaptive Servoventilation in Patients With Heart Failure) trial and its major substudy [13] will provide data on the effect of ASV on cardiac function and outcome in HF patients.
Conflict of interest. H. Fox, T. Bitter, D. Horstkotte, and O. Oldenburg state that there are no conflicts of interest.
Conclusion
References
We, for the first time, present the case of a patient with severe systolic HF and severe CSR, treated by optimal medical therapy and ASV therapy in a longterm setting, in whom improvement of symptoms and cardiac function resulted in termination of ASV therapy. The beneficial effects of ASV in this patient are probably secondary to improved oxygenation, prevention of hypercapnia, decrease in intrathoracic pressure swings, and decreased sympathetic tone [14, 15]. While the patient’s improved clinical condition coincided with the initiation of ASV, we cannot prove that ASV was solely responsible for the benefit seen. Late effects of conventional medical HF therapy might have also contributed, but various recent studies show improvements in symptoms, quality of life, cardiac function, and outcome [3, 16, 17, 18, 19, 20, 21, 22, 23, 24] with the addition of ASV. While data from largescale randomized controlled trials of ASV in HF will not be available until late 2015, sample evidence exists to suggest that physicians should not ignore the diagnosis and treatment of SDB in patients with HF.
1. Oldenburg O, Lamp B, Faber L, Teschler H et al (2007) Sleep-disordered breathing in patients with symptomatic heart failure: a contemporary study of prevalence in and characteristics of 700 patients. Eur J Heart Fail 9:251–257 2. Javaheri S, Shukla R, Zeigler H, Wexler L (2007) Central sleep apnea, right ventricular dysfunction, and low diastolic blood pressure are predictors of mortality in systolic heart failure. J Am Coll Cardiol 49:2028–2034 3. Jilek C, Krenn M, Sebah D et al (2011) Prognostic impact of sleep disordered breathing and its treatment in heart failure: an observational study. Eur J Heart Fail 13:68–75 4. Jelic S, Le Jemtel TH (2009) Sleep-disordered breathing in acute decompensated heart failure. Curr Heart Fail Rep 6:169–175 5. Javaheri S, Parker TJ, Liming JD et al (1998) Sleep apnea in 81 ambulatory male patients with stable heart failure: types and their prevalences, consequences, and presentations. Circulation 97:2154– 2159 6. Solin P, Bergin P, Richardson M et al (1999) Influence of pulmonary capillary wedge pressure on central apnea in heart failure. Circulation 99:1574– 1579 7. Sin DD, Fitzgerald F, Parker JD et al (1999) Risk factors for central and obstructive sleep apnea in 450 men and women with congestive heart failure. Am J Respir Crit Care Med 160:1101–1106 8. Braver HM, Brandes WC, Kubiet MA et al (1995) Effect of cardiac transplantation on Cheyne-Stokes respiration occurring during sleep. Am J Cardiol 76:632–634 9. Collop NA (1993) Cheyne-Stokes ventilation converting to obstructive sleep apnea following heart transplantation. Chest 104:1288–1289 10. Murdock DK, Lawless CE, Loeb HS et al (1986) The effect of heart transplantation on Cheyne-Stokes respiration associated with congestive heart failure. J Heart Transplant 5:336–337 11. Thalhofer SA, Kiwus U, Dorow P (2000) Influence of orthotopic heart transplantation on breathing pattern disorders in patients with dilated cardiomyopathy. Sleep Breath 4:121–126 12. Teschler H, Döhring J, Wang YM, Berthon-Jones M (2001) Adaptive pressure support servo-ventilation: a novel treatment for Cheyne-Stokes respiration in heart failure. Am J Respir Crit Care Med 164:614–619 13. Cowie MR, Woehrle H, Wegscheider K, Angermann C et al (2013) Rationale and design of the SERVEHF study: treatment of sleep-disordered breathing with predominant central sleep apnoea with adaptive servo-ventilation in patients with chronic heart failure. Eur J Heart Fail 15:937–943
Corresponding address O. Oldenburg Department of Cardiology, Heart and Diabetes Center North Rhine-Westphalia, Ruhr University Bochum Georgstr. 11, 32545 Bad Oeynhausen Germany [email protected]
The accompanying manuscript does not include studies on humans or animals.
14. Yoshihisa A, Suzuki S, Yamaki T, Sugimoto K et al (2013) Impact of adaptive servo-ventilation on cardiovascular function and prognosis in heart failure patients with preserved left ventricular ejection fraction and sleep-disordered breathing. Eur J Heart Fail 15:902–909 15. Koyama T, Watanabe H, Tamura Y, Oguma Y et al (2013) Adaptive servo-ventilation therapy improves cardiac sympathetic nerve activity in patients with heart failure. Eur J Heart Fail 15:902– 909 16. Oldenburg O, Bitter T, Lehmann R, Korte S (2011) Adaptive Servoventilation improves cardiac function and respiratory stability. Clin Res Cardiol 100:107–116 17. Bitter T, Gutleben KJ, Nölker G, Westerheide N et al (2013) Treatment of Cheyne-Stokes respiration reduces arrhythmic events in chronic heart failure. J Cardiovasc Electrophysiol (in press). DOI 10.1111/ jce.12197 18. Oldenburg O, Horstkotte D (2008) Quality of life in patients with chronic heart failure and CheyneStokes respiration. Sleep Med 9:601–602 19. Damy T, Margarit L, Noroc A, Bodez D et al (2012) Prognostic impact of sleep-disordered breathing and its treatment with nocturnal ventilation for chronic heart failure. Eur J Heart Fail 14:1009–1019 20. Pepperell JC, Maskell NA, Jones DR, LangfordWiley BA et al (2003) A randomized controlled trial of adaptive ventilation for Cheyne-Stokes breathing in heart failure. Am J Respir Crit Care Med 168:1109–1114 21. Philippe C, Stoïca-Herman M, Drouot X, Raffestin B et al (2006) Compliance with and effectiveness of adaptive servoventilation versus continuous positive airway pressure in the treatment of CheyneStokes respiration in heart failure over a six month period. Heart 92:337–342 22. Bradley TD, Logan AG, Kimoff RJ, Sériès F et al (2005) Continuous positive airway pressure for central sleep apnea and heart failure. N Engl J Med 353:2025–2033 23. Yoshihisa A, Shimizu T, Owada T, Nakamura Y et al (2011) Adaptive servoventilation improves cardiac dysfunction and prognosis in chronic heart failure patients with Cheyne-Stokes respiration. Int Heart J 52:218–223 24. Kasai T, Narui K, Dohi T, Yanagisawa N et al (2008) Prognosis of patients with heart failure and obstructive sleep apnea treated with continuous positive airway pressure. Chest 133:690–696 25. Sinha AM, Skobel EC, Breithardt OA, Norra C et al (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 26. Tamura A, Kawano Y, Kadota J (2009) Carvedilol reduces the severity of central sleep apnea in chronic heart failure. Circ J 73:295–298 27. Tamura A, Kawano Y, Naono S et al (2007) Relationship between beta-blocker treatment and the severity of central sleep apnea in chronic heart failure. Chest 131:130–135 28. Walsh JT, Andrews R, Starling R, Cowley AJ et al (1995) Effects of captopril and oxygen on sleep apnoea in patients with mild to moderate congestive cardiac failure. Br Heart J 73:237–241
Herz 2014
| 3
