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European Journal of Heart Failure 2007 9(8):820-826; doi:10.1016/j.ejheart.2007.03.009
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© 2007 European Society of Cardiology

Influence of cardiac resynchronisation therapy on different types of sleep disordered breathing

Olaf Oldenburga,*, Lothar Fabera, Jürgen Vogta, Anja Dorszewskia, Florian Szabadosb, Dieter Horstkottea and Barbara Lampa

a Department of Cardiology, Heart and Diabetes Center North Rhine-Westphalia, Ruhr University Bochum Georgstrasse 11, D-32545 Bad Oeynhausen, Germany
b Institute of Laboratory and Transfusion Medicine, Heart and Diabetes Center North Rhine-Westphalia, Ruhr University Bochum Georgstrasse 11, D-32545 Bad Oeynhausen, Germany

* Corresponding author. Tel.: +49 5731 97 1258; fax: +49 5731 97 2194 E-mail address: akohlstaedt{at}hdz-nrw.de.


   Abstract
Top
 Abstract
1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Limitations
 6. Conclusion
 References
 
Aims: This study investigates the influence of cardiac resynchronisation therapy (CRT) on sleep disordered breathing (SDB) in patients with severe heart failure (HF).

Methods and results: Seventy-seven patients with HF (19 females; 62.6±10 years) eligible for CRT were screened for presence, type, and severity of SDB before and after CRT initiation (5.3±3 months) using cardiorespiratory polygraphy. NYHA class, frequency of nycturia, cardiopulmonary exercise, 6-minute walking test results, and echocardiography parameters were obtained at baseline and follow-up.

Central sleep apnoea (CSA) was documented in 36 (47%), obstructive sleep apnoea (OSA) in 26 (34%), and no SDB in 15 (19%) patients. CRT improved clinical and haemodynamic parameters. SDB parameters improved in CSA patients only (apnoea hypopnoea index: 31.2±15.5 to 17.3±13.7/h, p<0.001; SaO2min: 81.8±6.6 to 84.8±3.3%, p=0.02, desaturation: 6.5±2.3 to 5.5±0.8%, p=0.004). Daytime capillary pCO2 was significantly lower in CSA patients compared to those without SDB with a trend towards increase with CRT (35.5±4.2 to 37.9±5.7 mm Hg, ns). After classifying short term clinical and haemodynamic CRT effects, improved SDB parameters in CSA occurred in responders only.

Conclusions: In patients with severe HF eligible for CRT, CSA is common and can be influenced by CRT, this improvement depends on good clinical and haemodynamic response to CRT.

Key Words: Heart failure • Cardiac resynchronisation therapy • Sleep disordered breathing • Central sleep apnoea

Received August 10, 2006; Revised February 16, 2007; Accepted March 22, 2007


   1. Introduction
Top
 Abstract
 1. Introduction
2. Methods
 3. Results
 4. Discussion
 5. Limitations
 6. Conclusion
 References
 
Sleep disordered breathing (SDB) is common in patients with heart failure (HF) and is associated with a further increase in mortality in these patients [1-5].

Continuous positive airway pressure (CPAP) ventilation in patients with obstructive (OSA) as well as central sleep apnoea (CSA) had positive effects on cardiovascular parameters in various studies [6-9], however a recent controlled multicentre trial failed to demonstrate a positive effect on mortality in HF patients with CSA [10]. Atrial pacing has also been suggested to improve SDB in patients with bradycardia [11], although this hypothesis has not been supported by recent studies [12,13].

Cardiac resynchronisation therapy (CRT) has been shown to improve haemodynamics, functional parameters, and mortality in patients with advanced congestive heart failure (NYHA≥III) and a wide QRS complex [14,15]. Sinha et al. reported a beneficial effect of CRT on CSA and Cheyne-Stokes respiration (CSR) in a total of 24 patients with chronic HF [16]. However, the effects of CRT on OSA and patients without significant SDB were not investigated.

This prospective trial was initiated to study the effects of CRT on different types of SDB.


   2. Methods
Top
 Abstract
 1. Introduction
 2. Methods
3. Results
 4. Discussion
 5. Limitations
 6. Conclusion
 References
 
2.1. Patients
A total of 77 consecutive patients eligible for CRT were tested for the presence and type of SDB before CRT device implantation (between January 2003 and January 2005) and after a mean follow-up of 5.3±3.3 months. Data were collected in a registry. The study was conducted in accordance with institutional guidelines, and all patients gave written informed consent. Centre-specific criteria for CRT have been reported previously [17,18], in summary patients had to present with dyspnoea according to the NYHA class III or IV, a left bundle branch block (LBBB) with a QRS width of ≥150 ms, a left ventricular enddiastolic diameter (LVEDD) of ≥60 mm, a left ventricular ejection fraction (LVEF) of ≤35%, and a peak oxygen uptake (peak VO2) during standardised cardiopulmonary exercise testing of ≤18 ml/kg/min. In addition, during an initial testing of several LV-lead positions (posterolateral veins), RV-stimulation sites (apex vs. RVOT) and LV vs. biventricular pacing, pulse pressure as a surrogate parameter of haemodynamic acute response had to increase by more than 10%. In some respects, these institutional criteria are more conservative compared to international guidelines. For example, we chose a minimum QRS width of 150 ms to increase the number of patients with asynchronous ventricular contraction. In order to get a more reliable parameter for dyspnoea than just NYHA functional class, we included a maximum value of 18 ml/kg/min for peak VO2.

2.2. Tailored CRT
The method of "tailored CRT" was described before in detail by Vogt et al. [17,18]. In summary, before CRT device implantation several LV-lead positions (posterolateral veins), RV-stimulations sites (apex vs. RVOT) and LV vs. biventricular pacing are tested in every patient to gain the optimal haemodynamic response. In addition, AV-delay optimisation according to an optimal fusion of intrinsic conduction in patients with sinus rhythm and stimulated excitation is performed. As a surrogate parameter, pulse pressure is used to verify haemodynamic acute response.

2.3. Cardiorespiratory polygraphy
Sleep studies were performed by in-hospital unattended cardiorespiratory polygraphy (Embletta–, Embla, Amsterdam, The Netherlands) as described before [1]. In summary, nasal air flow, chest and abdominal effort, pulse oxymetry, and body position were recorded continuously. Analyses were performed by Somnologica for Embletta software (Embla, Amsterdam, The Netherlands) and reviewed and corrected by two independent SDB specialists, not involved in further clinical 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, in case of CSA without any abdominal or thoracic breathing efforts and in case of OSA with typical efforts. Classification into OSA or CSA was done on the basis of the predominant type of SDB. The apnoea hypopnoea index (AHI) describes the number of apnoea and hypopnoea episodes per hour sleeping time, and is an established marker of SDB severity. According to current recommendations, an AHI of >5/h was chosen as a pathological cut-off [19]. Graduation of SDB was performed according to AHI values, SDB was considered mild if AHI was 6-14/h, moderate if AHI was 16-29/h, and severe if AHI was at least 30/h.

2.4. Echocardiography
Two-dimensional echocardiography was performed to evaluate LV function in all patients. LVEF was determined using apical 4- and 2-chamber views and the Simpson method. All recordings were performed on Vingmed/GE ultrasound systems. The echocardiographers were blinded to the patient's sleep study results.

2.5. 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 with a workload of 0-10 W with a continuous increase of 10 W every minute. Maximum workload and total exercise time were recorded, predicted VO2 peak was calculated automatically taking sex and age into account.

2.6. 6-minute walk testing
A standardised hallway 6-minute walk test was performed on days with no other strenuous activities or exercise testing.

2.7. Determination of haemodynamic response
Changes in NYHA class, CPX testing, echocardiographic parameters and 6-minute walking distance were obtained and scored as described in Table 1. A score of 1 or less was considered to reflect no relevant improvement after CRT, a score of 2 or 3 was considered to be a moderate improvement, and 4 or 5 to be a good response.


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  		Table 1 Scoring of CRT response in patients with CSA according to changes in symptoms, and haemodynamic and echocardiographic parameters

 
2.8. Statistics
Continuous data are expressed as the mean value±SD. Statistical analyses were performed with SigmaStat– software (SPSS Inc., Chicago, Illinois, USA). In continuous data, paired t-tests or Wilcoxon signed-rank tests were used to check for differences before and after treatment. Analysis of differences within the CSA group was done by ANOVA. The chi-square test was used for nominal variables. A value of p<0.05 was considered significant for all comparisons.


   3. Results
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
4. Discussion
 5. Limitations
 6. Conclusion
 References
 
Patients' characteristics are given in Table 2. There were no statistically significant differences in the baseline characteristics of patients with CSA, OSA, or those without SDB: Patients without SDB tended to be younger, more frequently female, with lower body weight, were less often diabetic, and presented less often with atrial fibrillation. Mean follow-up was 5.3±3.3 months (range: 3-9 months) after CRT initiation, without any statistically significant difference between the groups (Table 3). CRT significantly improved almost all heart failure parameters within this period of time. Patients with CSA presented with a more impaired cardiopulmonary function, seen especially in CPX duration and peak oxygen consumption, when compared with patients without SDB.


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  		Table 2 Baseline patient characteristics and medication

 


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  		Table 3 Symptoms, haemodynamic, echocardiographic, and laboratory parameters at baseline and follow-up

 
Significant changes in SDB parameters only occurred in patients with preexisting CSA (Table 4). There was a substantial decrease in total apnoea hypopnoea episodes (Fig. 1), as well as in maximum apnoea and hypopnoea duration, and an increase in minimal oxygen saturation. Baseline AHI in CSA was higher than in OSA, both, per definition, were higher than in patients without SDB. Daytime pCO2 concentration tended to be lowest in CSA patients, reaching significance only when compared to patients without SDB.


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  		Table 4 Sleep study and blood gas analysis results at baseline and follow-up

 


Figure 01
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  		Fig. 1 Apnoea hypopnoea index (AHI) in patients with central sleep apnoea (CSA), obstructive sleep apnoea (OSA) or patients without significant sleep disordered breathing (noSDB) at baseline and follow-up. Significant changes occurred in CSA patients only (p<0.001).

 
Further analysis of changes in SDB parameters in CSA patients revealed a positive influence depending on clinical and haemodynamic response to CRT. AHI improved only in patients with moderate or good response to CRT (Fig. 2) and daytime pCO2 concentration increased only in patients with good response to CRT (Fig. 3). In addition, minimum nocturnal oxygen saturation and oxygen desaturation improved only in moderate or good CRT responders (Table 5).


Figure 02
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  		Fig. 2 Changes in apnoea hypopnoea index (AHI) in patients with central sleep apnoea (CSA) according to their response to cardiac resynchronisation therapy (CRT).

 


Figure 03
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  		Fig. 3 Changes in daytime capillary pCO2 in patients with central sleep apnoea (CSA) according to their response to cardiac resynchronisation therapy (CRT).

 


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  		Table 5 Sleep disordered breathing parameters in CRT patients with CSA according to their clinical and haemodynamic response

 

   4. Discussion
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
5. Limitations
 6. Conclusion
 References
 
This study confirms a high prevalence of SDB in HF patients eligible for CRT. Potential positive effects of CRT on SDB were seen in HF patients with preexisting CSA, but not in those with OSA, and were limited to those with a good clinical and haemodynamic response to CRT. Patients without preexisting SDB did not show a substantial change in their sleep study results.

Recently, Sinha et al. reported a beneficial effect of CRT on CSA and CSR in patients with chronic heart failure [16]. Definition of CSA and the cut-off AHI of 5/h were comparable to ours and as recommended by guidelines [19]. In their study, CSA and CSR were found in 14 of 24 (58%) consecutive patients, in whom CRT was initiated. The prevalence of CSA in the present study was 47% which is less than Sinha reported, but still a high number compared to published prevalence data. In a previous prevalence study, we found SDB to be present in 76% of patients with symptomatic heart failure (LVEF≤40%, NYHA class≥II), 36% had OSA and 40% CSA [1]. Javaheri et al. reported a CSA prevalence of 40% in a cohort of 81 outpatients with stable heart failure [2]. In a retrospective analysis of 450 patients with HF, using an AHI cut-off of 10/h, Sin et al. found SDB to be present in 72% of all patients, 33% presenting with CSA and 38% presenting with OSA [3]. Assuming that CSA and CSR reflect heart failure severity at least to some extent, a higher prevalence can be expected in patients qualifying for CRT, because heart failure is usually more advanced in these patients.

Sinha et al. demonstrated an improvement in AHI in every patient with CSA after CRT (n=14) after a follow-up of 17±7 weeks. Patients without SDB at CRT initiation did not develop SDB during follow-up, however further analysis on OSA is not presented in this study [16]. The present study allows further insights into SDB and CRT. Tailored CRT in our patients led to an excellent improvement in cardiac function after a mean follow-up of 5.3 months. However, recovery of cardiac function is not homogeneous, and, at least in the present study, improvement of SDB did not manifest in every patient.

First, improvement in SDB was seen in the group of CSA patients only. There was no significant change in AHI, mean or minimal nocturnal oxygen saturation, maximal apnoea or hypopnoea duration in OSA patients. In accordance with Sinha et al. [16], patients without SDB at baseline did not develop SDB after CRT. Second, improvement in CSA was dependent on clinical response to CRT. For this purpose, we modified a scoring system introduced by Packer [20]. This score is not designed to verify reverse remodelling, but is introduced to capture clinical, morphological, and functional data during CRT. Considerable effects on SDB parameters were observed only in CSA patients with a moderate or good response to CRT. Exclusively in these patients AHI, minimum nocturnal oxygen saturation, and desaturation improved, and daytime capillary pCO2 increased.

In a recently published study, Gabor et al. screened 28 patients eligible for CRT for the presence and type of SDB [21]. By using an AHI cut-off value of 10/h, no relevant SDB was found in 12 patients (43%), OSA in 4 patients (14%), and CSA in 12 patients (43%). They were able to follow 10 of these 12 patients with CSA over a period of 27±7 weeks of CRT. In this small cohort of CSA patients, the AHI decreased from 42.7±9.1 at baseline to 30.8/h±18.7/h (p<0.05) at follow-up. This decrease in AHI was restricted to 6 of these patients in whom central AHI decreased; the four other patients did not experience a decrease. By analysing changes in cardiac function, no significant improvement in LVEF, LV size, mitral regurgitation, and 6-minute walking distance was found in these four patients. The present study and the data from Gabor indicate that an improvement in CSA under CRT depends on the haemodynamic response to CRT. However, this hypothesis still needs to be proven by controlled studies.

In an early study on the effect of atrial pacing on SDB, Garrigue et al. claimed a remarkable influence of atrial overdrive pacing on CSA and OSA without reduction in total sleep time [11]. In 13 out of 15 patients with symptomatic sinus bradycardia, atrial pacing at a rate of 15 beats per minute faster than the mean nocturnal heart rate resulted in a significant reduction in the number of episodes of all types of apnoea. In the present study, heart rate before and during CRT was not systematically investigated, but CRT pacing was not intended in an overdrive manner and recent studies have not confirmed Garrigue's results [22,23]. In addition, Garrigue did not document significant effects of atrial overdrive pacing on OSA in a recent study performed in 17 unselected patients with symptomatic bradyarrhythmia [13]. The results presented by Garrigue might be divergent, but further analysis might resolve the problem. In the first study, Garrigue [11] showed a greater reduction in the apnoea index in CSA patients when compared to OSA patients. Like others [24], we favour the hypothesis that atrial overdrive pacing in patients with symptomatic bradycardia led to an improvement in cardiac output. In terms of the present study this may also imply that these beneficial effects are missing in patients showing only mild or even no haemodynamic response to CRT and therefore no effect on CSA can be observed. Most likely, the improvement of CSA is not specifically due to CRT but to a general effect of improved heart failure.

Several experimental studies have demonstrated deleterious effects of OSA [25-27] and CSA [28-30] on cardiac function and prognosis leading to or worsening HF. The present data further support the theory that CSA is also a marker of HF severity: The prevalence of CSA in our cohort of severe HF patients qualifying for CRT is high and can be reduced by improving cardiac function.

Pulmonary congestion and stimulation of pulmonary vagal irritant J-receptors may be a consequence of severe HF [31]. Experimental studies demonstrate hyperventilation with subsequent decrease in blood pCO2 as a consequence. In combination with an enhanced receptor sensitivity to CO2 [32], an altered apnoea threshold [33] at night and an increased circulatory delay [34], this may lead to CSA and CSR. Moreover, the hyperventilatory state may be maintained while patients are awake and be expressed by a progressive ventilatory instability [29,35]. As a consequence, the presence of low pCO2 during the day should raise the suspicion for the presence of CSR and CSA, which is clearly associated with a worse prognosis [5], and should result in an intensified treatment.


   5. Limitations
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Limitations
6. Conclusion
 References
 
Categorisation of haemodynamic response was based on a novel scoring system not yet prospectively validated. Nevertheless, each parameter used in this scoring system has been proven to be a prognostic marker or a reliable parameter of CHF progression, remodelling or reverse remodelling. Another limitation is that we prospectively followed our CRT patients without calculating the statistical power needed to show results for patients without SDB, those with OSA, or CSA in advance. Therefore, as mentioned above, presented effects of CRT on SDB are indicative but not yet proven.


   6. Conclusion
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Limitations
 6. Conclusion
References
 
SDB is common in HF patients eligible for CRT. Both types of SDB, OSA and CSA, may worsen HF and its prognosis, but CSA especially seems to be a marker of heart failure severity. Improvement of CSA depends on a positive clinical and haemodynamic response to CRT. OSA is not influenced by CRT.


   References
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Limitations
 6. Conclusion
 References
 

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