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European Journal of Heart Failure 2008 10(6):581-586; doi:10.1016/j.ejheart.2008.04.007
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© 2008 European Society of Cardiology

Adaptive servoventilation improves cardiac function in patients with chronic heart failure and Cheyne–Stokes respiration

Olaf Oldenburga,*, Anke Schmidtb, Barbara Lampa, Thomas Bittera, Bogdan G. Munteana, Christoph Langera and Dieter Horstkottea

a Department of Cardiology, Heart and Diabetes Centre North Rhine-Westphalia, Ruhr University Bochum Bad Oeynhausen, Germany
b Cardiac Research Unit Bad Oeynhausen, Germany

* Corresponding author. Department of Cardiology, Heart and Diabetes Centre North Rhine-Westphalia, Ruhr, University Bochum, Georgstrasse 11, D-32545 Bad Oeynhausen, Germany. Tel.: +49 5731 97 1258; fax: +49 5731 97 2194. E-mail address: akohlstaedt{at}hdz-nrw.de


   Abstract
Top
 Abstract
1. Background
 2. Methods
 3. Results
 4. Discussion
 5. Limitations
 6. Conclusions
 Conflict of interest
 References
 
Background and aims: Sleep disordered breathing (SDB), especially Cheyne–Stokes respiration (CSR) is common in patients with chronic heart failure (CHF). Adaptive servoventilation (ASV) was recently introduced to treat CSR in CHF. The aim of this study was to investigate the effects of ASV on CSR and CHF parameters.

Methods: In 29 male patients (63.9±9 years, NYHA≥II, left ventricular ejection fraction [LV-EF]≤40%), cardiorespiratory polygraphy, cardiopulmonary exercise (CPX) testing, and echocardiography were performed and concentrations of NT-proBNP determined before and after 5.8±3.5 months (median 5.7 months) of ASV (AutoSet CSTM2, ResMed) treatment. All patients also received guideline-driven CHF therapy.

Results: Apnoea–hypopnoea-index was reduced from 37.4±9.4/h to 3.9±4.1/h (p<0.001). Workload during CPX testing increased from 81±26 to 100±31 W (p=0.005), oxygen uptake (VO2) at the anaerobic threshold from 12.6±3 to 15.3±4 ml/kg/min (p=0.01) and predicted peak VO2 from 58±12% to 69±17% (p=0.007). LV-EF increased from 28.2±7% to 35.2±11% (p=0.001), and NT-proBNP levels decreased significantly (2285±2192 pg/ml to 1061±1293 pg/ml, p=0.01).

Conclusions: In selected patients with CHF and CSR, addition of ASV to standard heart failure therapy is able to improve SDB, CPX test results, LV-EF and NT-proBNP concentrations.

Key Words: Adaptive servoventilation • Chronic heart failure • Cheyne–Stokes respiration • Sleep disordered breathing

Received November 26, 2007; Revised March 20, 2008; Accepted April 11, 2008


   1. Background
Top
 Abstract
 1. Background
2. Methods
 3. Results
 4. Discussion
 5. Limitations
 6. Conclusions
 Conflict of interest
 References
 
The prevalence of sleep disordered breathing (SDB) in patients with chronic heart failure (CHF) is remarkably high. Even if treated according to current guidelines, central sleep apnoea (CSA) with Cheyne-Stokes-respiration (CSR) is found in up to 40% of patients with symptomatic heart failure (NYHA class≥II) and impaired left ventricular function (left ventricular ejection fraction, LV-EF≤40%) [1]. CSA and CSR cause repetitive episodes of hypoxia and arousals from sleep leading to activation of the sympathetic nervous system. This predisposes to arrhythmias and might be an independent risk factor for major cardiac events and death [2-5].

Sustained and effective heart failure therapy has been shown to reduce the severity of CSA [6-8], but whether treatment of CSA contributes to improvement of cardiac function or prognosis in CHF patients is still uncertain [3,9,10].

Adaptive servoventilation (ASV) has been introduced to treat CSR in CHF patients. ASV uses low levels of background expiratory positive airway pressures (EPAP) to which a variable amount of inspiratory pressure support is added. If breathing effort decreases, ventilatory support is increased and when effort increases, ventilatory support is reduced. CSR in patients with CHF is characterized by chronic hyperventilation with reduced pCO2 during sleep [11,12]. ASV is designed to reduce hyperventilation by targeting a minute ventilation that is 90% of the average over the previous few minutes [12].

The aim of this study was to evaluate the use of ASV therapy in CHF patients with sustained CSR, who were receiving optimal heart failure therapy. The study uses data from our ASV registry, which was initiated in August 2005. Clinical, humoral, echocardiographic, and cardiopulmonary exercise data were systematically recorded in all patients receiving the AutoSetTM CS2-ASV device (ResMed, Germany). The registry was initiated to test the hypothesis that ASV improves cardiac function in CHF patients with CSR during sleep.


   2. Methods
Top
 Abstract
 1. Background
 2. Methods
3. Results
 4. Discussion
 5. Limitations
 6. Conclusions
 Conflict of interest
 References
 
2.1. Patients
Screening heart failure patients for the presence of SDB is routine clinical practice in our institution [13,14]. CSA is remarkably common and may improve in parallel with improvements in cardiac performance, for example in patients receiving cardiac resynchronisation therapy [7]. In this study, ASV therapy was only used in patients in whom there were no further conventional therapeutic options. ASV therapy was performed using an AutoSetTM CS2 device (ResMed, Germany). Patients with CSR and symptomatic, systolic CHF (NYHA class≥II; LV-EF≤40%) with moderate to severe CSA (Apnoea Hypopnoea Index (AHI) of at least 15/h) and on optimal heart failure therapy for at least 3 months were eligible to be included in the study. Patients with pacemakers, defibrillators or resynchronisation devices were only enrolled more than 6 months after implantation. A history and physical examination were performed at baseline and during follow-up.

The whole study was performed in accordance with local ethical guidelines and German law. All patients gave informed consent.

2.2. Cardiorespiratory polygraphy
Sleep studies were performed by in-hospital unattended cardiorespiratory polygraphy (EmblettaTM, Embla, The Netherlands) as previously described [1,13]. In summary, nasal air flow, chest and abdominal effort, pulse oximetry, and body position were recorded continuously. Automated analysis was performed using Somnologica for EmblettaTM software (Medcare, Embla, The Netherlands). The analysis was subsequently reviewed and corrected by two independent SDB specialists who were not involved in the treatment of these patients. Hypopnoea was defined as a ≥30% reduction in airflow in combination with a drop in oxygen saturation of at least 3%. Apnoea was defined as a cessation of airflow for ≥10 s, and was classified as either obstructive (if accompanied by typical thoraco-abdominal breathing effort) or central (if there was no effort). To be classified as CSR, more than 80% of all respiratory events had to be central with either typical CSR (crescendo-decrescendo ventilation with interposed central apnoea) or periodic breathing (crescendo-decrescendo ventilation with interposed hypopnoea). An AHI≥15/h was considered to indicate moderate to severe SDB. In addition, cardiorespiratory polygraphy on therapy was performed at each follow-up visit to document therapeutic efficacy.

2.3. ASV therapy
Cardiorespiratory polygraphy results and the rationale for ASV therapy were discussed with each patient individually. Therapy was initiated using the AutoSetTM CS2 device and full face masks (Ultra MirageTM; both ResMed, Germany). The aim was to reduce the AHI to ≤10/h before discharge from hospital using a minimum of positive airway pressure support. The normal settings used on the first night of treatment were: EPAP 4-5 cmH2O, inspiratory positive airway pressure (IPAP): minimum 3 cmH2O, maximum 8-10 cmH2O. Over the first 20 min of therapy, heart rate and blood pressure were monitored every minute.

2.4. Compliance and efficacy data
The AutoSetTM CS2 device stores compliance and efficacy data, which were downloaded and analysed using ResScanTM software (ResMed Germany) at follow-up visits. The data recorded include days, hours, and minutes the device was used, respiratory rate, tidal volume, leak, minute ventilation, AHI, and apnoea-index (AI).

2.5. NT-proBNP
N-terminal pro-brain natriuretic peptide (NT-proBNP) was used as a marker of heart failure severity (Elecsys 2010; Roche, Switzerland). Blood samples were taken before the initiation of ASV therapy and then at each follow-up visit. Patients were rested before blood samples were taken.

2.6. Echocardiography
Two-dimensional echocardiography (Vingmed/GE, Germany) was performed to evaluate left ventricular function in all patients. LV-EF was determined from the apical 4-chamber view using Simpson's method. The echocardiographers were blinded to the cardiorespiratory polygraphy results and were not involved in the treatment of these patients.

2.7. Spiroergometry
Symptom-limited bicycle exercise testing with spirometry (CPX) was used to evaluate exercise tolerance, peak oxygen consumption, and oxygen consumption at the individual aerobic-anaerobic threshold (ZAN Ferraris, Germany). Exercise testing started at 10 W workload with a continuous increase of 10 W/min. Maximum workload and total exercise time were recorded; predicted VO2 peak was calculated automatically taking sex and age into account.

2.8. Statistics
Continuous data are expressed as mean value±SD. Statistical analyses were performed with SigmaStatTM software (SPSS Inc., Chicago, Illinois, USA). For continuous and normally distributed data, paired t-tests and ANOVA for repeated measures, in case of non-normally distributed data Wilcoxon signed rank tests were used to test differences before and during ASV therapy. A value of p<0.05 was considered significant for all comparisons.


   3. Results
Top
 Abstract
 1. Background
 2. Methods
 3. Results
4. Discussion
 5. Limitations
 6. Conclusions
 Conflict of interest
 References
 
3.1. Patients
Between August 2005 and November 2006 ASV therapy was offered to 51 patients who met the inclusion criteria. Eight patients declined therapy before ASV titration for the following reasons: mask intolerance (n=3), subjective intolerance to positive airway pressure (n=3), and no specific reason (n=2). A total of 43 patients were successfully titrated on ASV (AHI≤10/h). These patients agreed to continue ASV therapy and a follow-up visit was organised within the next 6 months. Before the first follow-up visit, 2 patients (4.7%) died in other hospitals due to low cardiac-output syndrome, and 3 patients (7%) requested follow-up in hospitals closer to their homes. These patients were contacted by phone, but detailed follow-up was not performed. Nine patients (21%) stopped ASV therapy before the first follow-up: 3 due to mask problems, 1 developed severe depression and was not able to continue using the device, and 5 stopped therapy without indicating a specific reason. The remaining 29 patients (67%) continued ASV therapy and underwent at least one follow-up assessment. Follow-up investigations were performed between 3 and 14 months, mean follow-up was 5.8±3.5 months with a median at 5.7 months. When several follow-up investigations were available, the most recent was used for analysis. Demographic and clinical data for the 29 patients who underwent at least one follow-up assessment are summarised in Table 1. Medication did not change during the follow-up, apart from short-term adjustments in diuretics.


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  		Table 1 Demographic and clinical data for the 29 patients using ASV therapy

 
3.2. ASV device settings, compliance, and efficacy data
Average device settings were: EPAP 5.3±0.9 cmH2O (4-7 cmH2O), minimal IPAP remained at 3 cmH2O, and maximal IPAP 9.9±1.2 cmH2O (8-12 cmH2O). Compliance and efficacy data downloaded from the device are summarised in Table 2. Patients who continued treatment were generally compliant and had efficacious treatment.


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  		Table 2 Apnoea-hypopnoea-index (AHI) and apnoea-index (AI) during ASV therapy, and compliance data

 
3.3. Cardiopulmonary polygraphy
Results of cardiorespiratory polygraphy recordings before ASV initiation and at the time of the most recent follow-up are shown in Table 3. AHI and AI normalised during therapy. Obstructive events were rare and central events were significantly reduced with ASV therapy. Maximum apnoea duration as well as mean and minimum nocturnal oxygen saturation, and mean desaturation improved significantly during ASV therapy. There was a trend towards a reduction in hypopnoea duration, but this did not reach statistical significance.


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  		Table 3 Cardiorespiratory polygraphy results before ASV initiation (baseline) and at follow-up

 
3.4. History and physical examination
Mean NYHA class decreased from 2.43±0.50 to 1.93±0.75 (p<0.001). There were no documented changes in blood pressure or resting heart rate.

3.5. NT-proBNP and blood gas analysis
There was a significant fall in NT-proBNP concentration from 2285±2192 pg/ml to 1061±1293 pg/ml (p=0.012). Daytime pCO2 was 36.4±4.6 mmHg at baseline and increased significantly to 37.5±5.3 mmHg at follow-up (p=0.027). Values for pH, pO2, SaO2 and base excess were within normal limits before ASV therapy and remained unchanged at follow-up.

3.6. Spiroergometry
There were significant improvements in CPX testing parameters (Table 4): maximum workload, oxygen consumption at the individual anaerobic threshold (VO2-AT) as well as peak oxygen consumption (VO2 peak) and predicted VO2 peak increased substantially. There was a trend towards an increase in exercise time and towards a fall in the VE/VCO2 slope, but these did not reach statistical significance.


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  		Table 4 Results of standardised cardiopulmonary exercise testing (spiroergometry) before and after 5.8±3.5 months of ASV therapy. n. s.: not significant; C.I.: 95% confidence interval

 
3.7. Echocardiography
There was a significant increase in LV-EF from 28.2±6.9% at baseline to 35.2±10.6% at follow-up (p=0.001; median=+10%; confidence interval: 3.8-14.8%). No significant changes were documented for left atrial diameters during systole (52.3±7.9 mm vs 51.1±7.8 mm), or for left ventricular diameters during diastole (66.0±9.0 mm vs 67.5±13.5 mm) and systole (55.3±9.6 mm vs 55.0±13.7 mm).


   4. Discussion
Top
 Abstract
 1. Background
 2. Methods
 3. Results
 4. Discussion
5. Limitations
 6. Conclusions
 Conflict of interest
 References
 
This study demonstrates that in CHF patients with nocturnal CSR, treated according to current guidelines, ASV therapy is able to further improve heart failure symptoms and objective cardiopulmonary parameters. With additional ASV therapy there was an improvement in NYHA class, decrease in NT-proBNP, increase in LV-EF, and increased peak oxygen consumption.

The use of ASV therapy in heart failure patients was first described by Teschler and co-workers [12]. In a cross-over single night study in 14 patients with stable heart failure, control of SDB and sleep quality during ASV therapy was superior to oxygen, CPAP- or BIPAP-therapy. Specifically, the AHI decreased from 44.5±3.4/h to 6.3±0.9 (p<0.001) and central arousal index decreased from 35.8±2.9/h to 3.3±0.5/h (p<0.001) within a single night. In another study, Zhang and co-workers reported a reduction in AHI from 34.5±6.1/h to 6.5±0.8/h (p<0.01) after 2 weeks of ASV therapy [15]. In contrast to our study, Zhang et al. did not titrate pressure levels individually, instead they used the default settings of the AutoSetTM CS2 system (EPAP 5 cmH2O, IPAP 3-10 cmH2O). Kasai et al. were able to effectively treat SDB in 4 CHF patients, in whom CPAP therapy failed to suppress respiratory events [16]. In these 4 patients, AHI decreased from 62.7±10.1/h to 5.9±2.2/h (p=0.0006) and central AHI improved from 54.5±6.7/h to 5.6±2.3/h (p=0.0007). However, the authors were forced to use relatively high pressure levels in their patients (EPAP 6-7 cmH2O, IPAP min. 6-14 cmH2O to max. 16-20 cmH2O) because of a high baseline number of obstructive events in the cohort (obstructive AHI=8.2±4.6/h).

Pepperell compared the effects of ASV therapy with effective pressure levels to a sham device delivering sub-therapeutic pressure levels [17]. ASV therapy decreased AHI from 24.7±11.3/h at baseline to 5.0±1.9/h during a follow-up of 5.0±1.4 months. In this study, AHI at baseline was measured by polysomnography, but at follow-up AHI was determined using AutoSetTM CS2 algorithms. In our study, AHI determined by the device over the entire follow-up period was 3.6±3.3/h and AHI measured by cardiorespiratory polygraphy at follow-up was 2.48±3.03/h, thus showing close agreement between the data recorded by the device and cardiopulmonary polygraphy. Philippe and co-workers compared ASV to CPAP and found that in contrast to CPAP, ASV was able to reduce AHI to below 10/h at up to 6 months [10]. A reduction in AHI after 12 months of ASV therapy was documented by Schädlich et al., who reported that AHI decreased from 44.3±13.4/h to 3.4±8.0/h (p<0.001) [18]. Our findings are in keeping with these previously published data in showing that ASV therapy effectively suppresses SDB in CHF patients over extended periods of time.

The 10 patients in the study by Philippe et al. used the ASV device for approximately 4 h/night after 3 months and 5 h/night after 6 months [10]. In contrast, in a similar group of patients using CPAP compliance declined over 6 months. In the largest study of positive airway pressure therapy (CPAP) in heart failure patients, the CANPAP trial, the drop out rate in the CPAP arm was 15.5% [9]. In addition, CPAP use decreased from 4.3 h/night after the first 3 months to 3.6 h/night after 12 months. The average usage of ASV therapy in our study was 6±1.5 h/night after approximately 6 months. These results confirm our clinical experience and the results of Teschler's initial study, in which ASV therapy was preferred compared to CPAP therapy with similar mean pressures [12]. Once patients are established on ASV therapy they generally use the device regularly.

In our study, 51 patients had an indication for ASV therapy, but 8 refused initiation of therapy and 9 stopped ASV therapy before the first follow-up. Most of these patients claimed mask problems or intolerance to positive airway pressure as the reason for discontinuation of ASV treatment. Improved mask design, and more advanced ventilator technologies may help to improve compliance, but in the end, ASV therapy may be suitable for the majority, but not all patients.

We measured a number of parameters of heart failure severity in our patients and demonstrated considerable improvements. While the lack of a control group is a weakness of the study design the magnitude of the changes observed is larger than would be expected in a group of stable CHF patients. Besides a significant improvement in NYHA class, NT-proBNP levels, which are used for diagnosis and follow-up in heart failure patients [19], were significantly reduced by ASV therapy. In patients with advanced cardiac failure, Gardner et al. propose superiority of NT-proBNP as a prognostic marker, when compared to LV-EF or peak oxygen consumption during spiroergometry [21]. Cardiac resynchronisation therapy (CRT) has been shown to improve left ventricular and cardiopulmonary function, and reduce BNP and NT-proBNP levels [23,24]. However, there is still some controversy about whether BNP concentrations have prognostic value in CHF [19,20,22]. Our results are comparable with those of Peperell et al., who demonstrated a significant decrease in BNP concentrations from 363 pg/ml to 278 pg/ml (p<0.001) after initiation of ASV therapy [17].

Zhang and co-workers describe an improvement in LV-EF from 30.2±4.6% to 37.2±4.1% (p<0.05) 2 weeks after initiation of ASV therapy [15]. This represents a 7% increase and a relative increase of about 23%. Schädlich et al. documented an increase in LV-EF from 37.1% to 43.3% (p<0.05) 3 months after initiation of ASV treatment, an increase of 6.2% and a relative improvement of 16.7%, respectively [18]. In the study by Philippe et al., LV-EF was determined after 6 months of ASV treatment in 7 patients only [10]. The authors describe an increase in LV-EF of approximately 7%, although it is unclear whether this represents an absolute or relative increase. In our study LV-EF improved from 28.2±6.7% to 35.2±10.8% (absolute 7%, relative 24.8%; p=0.001). Thus, our results are in close agreement with those of Zhang and Schädlich [15,18].

The effects of ASV therapy on LV-EF are comparable to those achieved by modern drug or resynchronisation therapy [7]. In a double blind randomised trial investigating the effects of 3 months of carvedilol therapy on left ventricular function and symptoms in patients with symptomatic heart failure (NYHA≥II and LV-EF≤35%), a significant increase in LV-EF from 20±1% to 31±2% was documented (p<0.0001), representing a relative improvement of 52% [25]. A similar effect was reported using metoprolol. After a mean treatment duration of 10 months, LV-EF improved from 26% to 31% (p=0.009) [26]. With CRT, beneficial effects on LV-EF are seen after 6 months. For example, in the MIRACLE trial LV-EF improved by 5.8±8.5% and in the MIRACLE-ICD trial by 4.1±8.4% [27]. In our study ASV was added to maximal conventional heart failure therapy, therefore the beneficial effects are additive to guideline therapy.

An inverse relationship between LV-EF and mortality has been documented in patients with systolic heart failure [28]. Below a LV-EF of 45%, there is a 45% increase in the risk of total events with any further 10% impairment in LV-EF. Conversely, if LV-EF is <45% any increase in LV-EF leads to a significant reduction in mortality [29]. The significant improvement in LV-EF seen in our patients may therefore result in improved prognosis, but further studies, including randomised and placebo controlled trails are required to investigate potential effects on morbidity and mortality.

To our knowledge, the present study is the first to use CPX testing to objectively measure cardiopulmonary function during ASV treatment. Significant improvements in CPX parameters were seen. The beneficial effects on oxygen uptake are equivalent to those observed during CRT [29,30]. In the MIRACLE trial, a significant increase in median peak VO2 of 1.1 ml/kg/min [C. I.: 0.6-1.7 ml/kg/min)] was observed after 6 months of therapy. The median improvement in peak VO2 of 0.8 ml/kg/min [C. I.: 0.7-3.5 ml/kg/min] in this study is of similar magnitude [30]. In the PATH-II trial, peak VO2 increased by 1.8 ml/kg/min and VO2-AT increased by 1.1 ml/kg/min after 12 months of CRT [23]. The changes observed in this study were similar, with peak VO2 increasing by 2.1±3.7 ml/kg/min and VO2-AT by 2.6±4.2 ml/kg/min.


   5. Limitations
Top
 Abstract
 1. Background
 2. Methods
 3. Results
 4. Discussion
 5. Limitations
6. Conclusions
 Conflict of interest
 References
 
This study involved small number of patients, was uncontrolled and used surrogate markers of heart failure severity, therefore the results should be interpreted with caution. However, the study showed clinically and statistically significant improvements in patients with no other therapeutic options, and further studies of ASV therapy are warranted. The first multicenter randomised placebo controlled trial to investigate the effects of ASV on mortality in CHF patients with sleep disordered breathing (SERVE-HF) commenced in February 2008. However, results are not expected before 2012.


   6. Conclusions
Top
 Abstract
 1. Background
 2. Methods
 3. Results
 4. Discussion
 5. Limitations
 6. Conclusions
Conflict of interest
 References
 
In selected patients with CHF and moderate to severe CSR, ASV may be a therapeutic option in addition to guideline based therapy. ASV therapy may lead to an improvement in subjective (NYHA class) and objective (workload and oxygen consumption during CPX testing) parameters, an increase in LV-EF and a decrease in natriuretic peptide concentrations (NT-proBNP) in symptomatic patients already receiving maximal therapy.


   Conflict of interest
Top
 Abstract
 1. Background
 2. Methods
 3. Results
 4. Discussion
 5. Limitations
 6. Conclusions
 Conflict of interest
References
 
O.O. and B.L. have occasionally received reimbursement for attending and/or a fee for speaking at symposia from ResMed GmbH, Germany, manufacturer and distributor of the AutoSet CS2 device mentioned in this paper.


   References
Top
 Abstract
 1. Background
 2. Methods
 3. Results
 4. Discussion
 5. Limitations
 6. Conclusions
 Conflict of interest
 References
 

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