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European Journal of Heart Failure 2007 9(3):251-257; doi:10.1016/j.ejheart.2006.08.003
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© 2007 European Society of Cardiology

Sleep-disordered breathing in patients with symptomatic heart failure A contemporary study of prevalence in and characteristics of 700 patients

Olaf Oldenburga,*, Barbara Lampa, Lothar Fabera, Helmut Teschlerb, Dieter Horstkottea and Volker Töpfera

a Department of Cardiology, Heart and Diabetes Center North Rhine-Westphalia Georgstrasse 11, D-32545 Bad Oeynhausen, Germany
b Department of Pneumology and Sleep Medicine Ruhrlandklinik, University Duisburg-Essen, Essen, Germany

* Corresponding author. Tel.: +49 5731 97 0; fax: +49 5731 97 2194. E-mail address: ooldenburg{at}hdz-nrw.de


   Abstract
Top
 Abstract
1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Conclusion
 References
 
Aim: Evaluation of the prevalence and nature of sleep-disordered breathing (SDB) in patients with symptomatic chronic heart failure (CHF) receiving therapy according to current guidelines.

Methods and results: We prospectively screened 700 patients with CHF (NYHA class≥II, LV-EF≤40%) for SDB using cardiorespiratory polygraphy (EmblettaTM). Furthermore, echocardiography, cardiopulmonary exercise and 6-min walk testing were performed. Medication included ACE-inhibitors and/or AT1-receptor blockers in at least 94%, diuretics in 87%, β-blockers in 85%, digitalis in 61% and spironolactone in 62% of patients.

SDB was present in 76% of patients (40% central (CSA), 36% obstructive sleep apnoea (OSA)). CSA patients were more symptomatic (NYHA class 2.9±0.5 vs. no SDB 2.57±0.5 or OSA 2.57±0.5; p<0.05) and had a lower LV-EF (27.4±6.6% vs. 29.3±2.6%, p<0.05) than OSA patients. Oxygen uptake (VO2) was lowest in CSA patients: predicted peak VO2 57±16% vs. 64±18% in OSA and 63±17% in no SDB, p<0.05. 6-min walking distances were 331±111m in CSA, 373±108m in OSA and 377±118m in no SDB (p<0.05).

Conclusions: This study confirms the high prevalence of SDB, particularly CSA in CHF patients. CSA seems to be a marker of heart failure severity.

Key Words: Congestive heart failure • Sleep-disordered breathing • Sleep apnoea syndromes

Received April 1, 2006; Revised June 28, 2006; Accepted August 22, 2006


   1. Introduction
Top
 Abstract
 1. Introduction
2. Methods
 3. Results
 4. Discussion
 5. Conclusion
 References
 
Due to similarities in the pathophysiology of sleep-disordered breathing (SDB) and chronic heart failure (CHF), there is an emerging interest in the link between these two conditions. Two major types of SDB have been recognized in CHF: obstructive sleep apnoea (OSA) and central sleep apnoea (CSA). While OSA seems to be a cardiovascular risk factor per se [1-4], CSA appears to be a marker of CHF severity [5,6]. However, both OSA and CSA interfere with neuro-humoral systems and thus may worsen heart failure, e.g. by increasing sympathetic and renin-angiotensin-aldosterone activity, both targets of state of the art heart failure therapy. Several studies have demonstrated an increased mortality in CHF patients suffering from SDB in contrast to those without SDB [1,6,7].

Our knowledge about the prevalence and characteristics of SDB in CHF is based on only a few small scale studies. Reported prospective studies have only included 20 to 81 symptomatic or asymptomatic patients, with either acute or chronic heart failure, and systolic or diastolic left ventricular dysfunction [7-12]. One study described risk factors for OSA and in particular CSA in a larger cohort of CHF patients [13]. Risk factors for CSA were male gender, atrial fibrillation, age>60 years and hypocapnia with PaCO2<38 mm Hg during wakefulness. Unfortunately, this study was retrospective and CHF was not treated according to present guidelines [14,15]. Therefore, the effect of β-blocker treatment, which significantly improves outcome in CHF [16-19] and may impact the occurrence and severity of CSA [20], was not analysed in this cohort.

Treatment of heart failure has changed substantially since these early studies, and heart failure prognosis has improved [16-18,21]. This may have an impact on the prevalence and characteristics of SDB in CHF patients. The purpose of this study was therefore to prospectively investigate the prevalence and characteristics of SDB in symptomatic chronic heart failure in a large scale study.


   2. Methods
Top
 Abstract
 1. Introduction
 2. Methods
3. Results
 4. Discussion
 5. Conclusion
 References
 
Between January 2003 and April 2005, 700 consecutive patients with symptomatic stable CHF (NYHA class≥II) and impaired left ventricular systolic function (left ventricular ejection fraction≤40%) were screened prospectively for the presence of SDB. All patients had been referred to our hospital, a tertiary academic cardiac referral centre, for the investigation and management of CHF, which for the purpose of this study included a sleep study. None of the patients had been screened for SDB before. In 34 patients, a sleep study had been performed before admission; these patients were not included in this study. Exclusion criteria were decompensated heart failure, chronic obstructive pulmonary disease (COPD, documented by a forced expiratory volume per second [FEV1]<70%) or history of asthma, myocardial infarction within the last 3 months, history of stroke or clinical signs of peripheral or central nervous system disorders. Patients with a pacemaker, defibrillator or resynchronization device were included only 6 or more months after implantation.

2.1. Cardiorespiratory polygraphy
Sleep studies were performed by in-hospital unattended overnight cardiorespiratory polygraphy (Embletta–, Medcare, Island). Nasal air flow measured by nasal pressure, chest and abdominal effort, pulse oximetry, snoring and body position were recorded continuously. More than 85% of total recording time had to be of good quality. The temporary loss of not more than one channel (except nasal airflow) was accepted. Analyses were performed by a physician specially trained in SDB, who was not involved in the clinical treatment of patients. Standard definitions were used to describe and score SDB as follows. An apnoea was scored if the breathing signal decreased (by eye) to less than 10% of the recent average (5 min) for at least 10 s, in case of CSA without any abdominal or thoracic breathing efforts, in case of OSA with visible ribcage and abdominal respiratory impedance signals [11]. Hypopnoea was defined as decrease to ≥50% baseline lasting ≥10 s and accompanied by a ≥4% drop in oxygen saturation. Based on our experience of no substantial overlap of SDB type in most cases, patients were classified to have either predominately CSA or OSA. The apnoea hypopnoea index (AHI) is an established maker of SDB severity and can be reliably obtained with the Embletta–-System [22]. It describes the number of episodes of apnoea and hypopnoea per hour. SDB severity was graded according to guideline recommendations [23] and our clinical routine as mild (AHI 6-14/h), moderate (15-29/h) and severe (AHI≥30/h). Patients with an AHI≤5/h were considered to have no relevant SDB. Since there is no generally accepted guideline for respiratory treatment of CHF patients with SDB, we consider specific treatment (non-invasive ventilation) for symptomatic patients with an AHI of ≥ 15/h. For the purpose of this study, we characterized these patients separately.

2.2. Echocardiography
Two-dimensional echocardiography was performed to evaluate LV function in all patients. LV-EF was determined using apical four-chamber view and the Simpson's method. Whenever possible, parasternal M-mode and Doppler recordings were performed to complete the echocardiographic examination. All recordings were performed on Vingmed/GE ultrasound systems. The echocardiographers were blinded to sleep study data.

2.3. Spiroergometry
Symptom-limited bicycle exercise testing with spirometry was used whenever possible to evaluate exercise tolerance, peak oxygen consumption and oxygen consumption at the individual aerobic-anaerobic threshold (ZAN Ferraris, Germany). Exercise testing started with 0-10 W of workload with a continuous increase of 10 W/min. Maximum workload and total exercise time were recorded and predicted VO2-peak was calculated automatically taking sex and age into account. Exercise tests were not performed in patients with NYHA class>III, in patients unable to perform bicycle testing due to non-cardiac disorders and in patients unable to tolerate the face masks used for respiratory measurements.

2.4. Statistics
Continuous data are expressed as mean value±S.D. Statistical analyses were performed with SigmaStat– software (SPSS Inc., Chicago, Il, USA). Differences between groups were compared by ANOVA for repeated measures test and frequency of parameters by chi-square test. Correlation analysis was performed using Spearman rank correlation. P<0.05 was considered significant.


   3. Results
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
4. Discussion
 5. Conclusion
 References
 
3.1. Patient characteristics
The mean age of the 700 patients (561 men, 139 women) was 64.5±10.4 years. Underlying aetiology was angiographically documented coronary artery disease (CAD) in 323 patients (46.1%), dilated cardiomyopathy (DCM), defined as impaired left ventricular function in the absence of coronary artery disease, in 323 patients (46.1%), a combination of CAD and valvular heart disease (CAD+VHD) in 23 patients (3.3%), and VHD only in 31 patients (4.4%). Patients presented with an average NYHA class of 2.7±0.5 and a LV-EF of 28.3±6.8%. Regarding state of the art heart failure medication, 95% of patients were receiving ACE-inhibitors and/or AT-1-receptor blockers, 90% diuretics, 85% β-blockers, 62% digitalis and 64% spironolactone. Mean CPX duration was 6.61±2.8 min, workload 71.9±29 W, oxygen consumption at the individual anaerobic threshold (VO2AT) 11.9±3.6 ml/kg/min, peak VO2 14.4±4.2 ml/kg/min and predicted peak VO2 60.9±17%. Mean walking distance during the 6-min walk test was 358±114 m.

3.2. Prevalence of SDB in CHF
SDB was present in 531 of our CHF patients (76%), 40% of patients had CSA and 36% OSA. Only 24% of the entire cohort did not present with relevant SDB (AHI≤5/h). Considering the severity of SDB in these patients, a mild (AHI=6-14/h) form of CSA was present in 8% of all CHF patients and mild OSA in 17%. More than 50% of CHF patients had moderate to severe SDB with an AHI of ≥ 15/h (CSA 32%, OSA 19%).

Demographic and clinical data are summarized in Table 1. Patients with OSA or CSA were older than CHF patients without SDB. Male gender was predominant in OSA (86%) and CSA (87%) compared to no SDB (60%). In patients with OSA, a higher BMI and a trend towards a higher prevalence of diabetes was documented. Patients with CSA presented with more advanced heart failure symptoms: a significantly higher NYHA class, a higher frequency of nycturia and a markedly lower systolic blood pressure. In addition, the prevalence of atrial fibrillation was markedly higher in CSA (35%) than in OSA (21%) and patients without SDB (14%). Concerning the severity of SDB, CSA patients had a significantly worse AHI than OSA patients (30.2/h vs. 18.5/h). No differences between the groups were found regarding resting heart rate, diastolic blood pressure, standard heart failure medication and aetiology of CHF.


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  		Table 1 Demographic and clinical data for all 700 CHF patients

 
3.3. CPX testing
Maximum duration of standardized CPX testing was 6.81±2.8 min in patients without SDB, 6.98±2.9 min in patients with OSA and 6.14±2.6 min in CSA patients. Differences were not significant except a trend towards lower exercise time in the CSA group. Maximum workload was 72.44±27.8 watts in patients without SDB, 77.72±29.8 W in OSA and 65.94±27.5 W in CSA (p<0.05 compared to OSA) patients. Oxygen uptake at the individual anaerobic threshold was lower in CSA patients compared to patients with OSA. Peak oxygen uptake was significantly lower in CSA patients compared to OSA patients or those without SDB (Fig. 1). There was a negative correlation between VO2-peak and the individual AHI (Spearman correlation coefficient –0.2, p<0.001). In addition, predicted VO2 peak was significantly lower in CSA (56.7±15.8%) patients compared to patients with OSA (64.2±17.8%, p<0.05) or without SDB (63.4±16.5%, p<0.05).


Figure 01
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  		Fig. 1 Cardiorespiratory exercise results in patients without SDB, obstructive sleep apnoea (OSA) and central sleep apnoea (CSA). Graphs show oxygen uptake at the individual anaerobic threshold (VO2-AT) and the individual peak oxygen uptake (VO2-peak). VO2-AT was significantly lower in CSA patients compared to those without SDB ({dagger}p<0.05). VO2-peak was also lower in CSA patients compared to OSA patients ({ddagger}p<0.05) and those without SDB ({dagger}p<0.05).

 
3.4. 6-min walk test
Walking distance was more than 10% lower in patients with CHF and CSA compared to CHF patients with OSA or those without SDB (Fig. 2). There was a negative correlation between 6-min walking distance and the individual AHI (Spearman correlation coefficient –0.2, p<0.001). Maximum walking distance in 6 min was 331.1±111 m in the CSA group, 373.2±108 m in the OSA group and 376.8±118 m (p<0.05 vs. CSA) in patients without SDB (p<0.01 vs. CSA).


Figure 02
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  		Fig. 2 Result of a standardized 6-min walk test. Patients with CSA (331.2±111 m) had a more than 10% reduced walking distance compared to OSA patients (373.2±108 m, {ddagger}p<0.05) or those without SDB (376.8±118 m; {dagger}p<0.01).

 
3.5. Echocardiography
Evaluation of echocardiographic parameters (Table 2) showed a lower LV-EF in patients with CSA compared to OSA. There was a trend towards lower EF compared to patients without SDB but this did not reach significance. Left atrial diameter was significantly higher in CSA and OSA compared to patients without SDB. There were no differences in left ventricular diameters.


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  		Table 2 Echocardiographic parameters

 
3.6. Moderate and severe SDB
Patients with SDB and an AHI≥15/h may be considered for treatment with non-invasive ventilation [4,11]. Patients presenting with symptomatic CHF were mainly suffering from CSA (32.8% vs. 19.1% OSA). Demographic and clinical data are summarized in Table 3 and show more advanced heart failure symptoms (NYHA class, nycturia) and greater impairment of cardiopulmonary function (LV-EF, CPX results, 6-min walking distance; Table 4) in CSA patients as compared to OSA patients. In addition, mean AHI was significantly higher and minimal oxygen saturation significantly lower in the CSA group.


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  		Table 3 Demographic and clinical data for the CHF patients with moderate to severe SDB

 


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  		Table 4 Comparison of echocardiographic, cardiopulmonary exercise testing (CPX) and 6-min walking test results in patients with moderate to severe OSA and CSA

 

   4. Discussion
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
5. Conclusion
 References
 
We have demonstrated a surprisingly high prevalence of SDB in a large cohort of patients with symptomatic systolic heart failure receiving optimal CHF medication. About 75% of CHF patients investigated had either central (40%) or obstructive (36%) sleep apnoea (AHI>5/h). More than 50% of patients had an AHI≥15/h (32.8% CSA and 19.1% OSA). CSA appears to be a marker of heart failure severity; CSA patients had more advanced symptoms (NYHA class, nycturia), lower LV-EF and larger left atrial diameters. Poorer results on CPX testing and 6-min walking distance also corresponded to a higher AHI.

A high prevalence of SDB in male heart failure patients has been reported previously. Javaheri et al. investigated 81 out-patients with stable heart failure, defined as an LV-EF<45%. Most of these patients (75%) had CAD, the remainder had cardiomyopathies. Using an AHI threshold of ≥15/h, the authors found relevant SDB in 41 patients (51%) [11], which is consistent with our data. However, the vast majority of Javaheri's patients had CSA (40%), only 11% had OSA. In a large retrospective analysis of SDB in symptomatic CHF (AHI≥15/h, NYHA class≥II, LV-EF 27.3±15.6%), Sin et al. reported a 61% prevalence of SDB, including CSA in 29% and OSA in 32% [13]. Using the same AHI cut-off, about 33% of our patients had CSA and 20% presented with OSA.

In contrast to previous studies [5,11,13], the patients in our study were receiving current state of the art heart failure medication, including β-blockers (≥85%), ACE-inhibitors and/or AT-1-receptor blockers (≥94%), diuretics (≥87%) and spironolactone (≥62%). Despite optimal heart failure medication, the prevalence of SDB and in particular CSA remained remarkably high. However, it should be noted that the current study was not designed to test the effect of optimized heart failure treatment on CSA or SDB.

It is supposed that CSA is a consequence of heart failure. However, whether CSA is just a reflection of severely compromised cardiac function with elevated left ventricular filling pressure, or exerts unique and independent pathological effects in the failing heart, is a controversial issue [24,25]. This study was not intended to answer these questions, but it clearly demonstrates that CSA is a frequent concomitant finding in patients with severely impaired cardiac function (when compared to patients with OSA or those without SDB). CSA in CHF is typically associated with increased age, male gender, higher NYHA class, more frequent nycturia, a shorter 6-min walking distance, a lower oxygen uptake in CPX testing (VO2AT, VO2-peak, predicted VO2-peak), a lower resting blood pressure and a reduced LV-EF with large left atrial dimensions. In addition, there was also a trend to a higher prevalence of atrial fibrillation. This corresponds to the results of previous studies which have reported a higher incidence of atrial fibrillation and a more reduced systolic LV-function in CSA patients compared to OSA patients [12,13].

OSA is independently associated with metabolic syndrome in classical symptomatic SDB patients [3]. Therefore, a high body mass index and a trend towards a higher prevalence of diabetes would be expected for CHF patients with OSA as described previously [13]. However, our OSA patients presented with a BMI of 27.8 kg/m2, which is less than in typical patients with metabolic syndrome. On the other hand, our results are in line with those reported by Ferrier et al., who reported a BMI of 28.4 kg/m2 in heart failure patients with SDB and of 26.9 kg/m2 in heart failure patients without SDB [12]. With respect to cardiac function, OSA might be a cause of daytime systolic LV dysfunction, which may resolve following effective continuous positive airway pressure (CPAP) therapy [26-30]. Even in adults with normal resting LV function, OSA is associated with an impaired response (increase in cardiac output and stroke volume) to exercise, with CPAP therapy being able to reverse this response. This suggests that pathophysiological changes associated with OSA over the years might progress into structural ventricular damage and lead to symptomatic heart failure [31]. Therefore, OSA might be related to both, causation and progression of heart failure [32]. So far, it is proven that OSA is an independent risk factor for fatal and non-fatal cardiovascular events [33] and all-cause mortality [34].

In the present study, severity of SDB, when assessed by AHI or, in moderate and severe cases, by minimal oxygen saturation, was worse in CSA compared to OSA. This is consistent with data from Solin et al. which showed that, in spite of no significant differences in LV-EF, AHI was significantly higher in CSA patients compared to OSA. However, they found no differences in overnight oxygen saturation [35]. In this context, Sin et al. [13] reported differences in parameters indicative for central and obstructive sleep-disordered breathing events, but the overall mean AHI was not statistically different. In close agreement with their findings, we also found no differences in lowest oxygen saturation.

The higher AHI might have a relevant prognostic impact. Besides classic predictors of mortality like oxygen consumption [36], Lanfranchi et al. identified the AHI as a powerful and independent predictor for a poor prognosis in clinically stable CHF patients with Cheyne-Stokes respiration. In these patients, the presence of an AHI≥30/h identifies patients at high risk for subsequent cardiac death [7,37].

There are some potential limitations to our study. First, we evaluated SDB by cardiorespiratory polygraphy and not by polysomnography (PSG), which still represents the gold standard. Dingle et al. performed a comparative study in OSA to validate Embletta–-based cardiorespiratory polygraphy results. They found an extremely close correlation between the results obtained by PSG and Embletta– screening ({rho}=0.98, p<0.001). Mean difference in AHI was 2±5/h [22]. Theoretically, Embletta– results which are obtained from unattended patients can underestimate AHI because actual sleeping time might be shorter than the recorded time. As a consequence, the prevalence and degree of SDB might even be higher in our cohort of CHF patients. Second, periodic limb movements during sleep were reported to be associated with CHF. This disorder may contribute to sleep/wake complaints in CHF patients and even have an influence on cardiopulmonary function [38]. However, this cannot be detected accurately by cardiorespiratory polygraphy. Third, Bradley's group reported the possible coexistence of obstructive and central sleep apnoea in CHF patients. There may be an overnight shift from obstructive towards central apnoeas in these patients [39]. We classified SDB into OSA and CSA according to the majority of events during the night. In the vast majority of patients, more than 85% of events were either central or obstructive allowing for a clear classification.

Finally, another limitation may be the fact that the prevalence of SDB in our hospital, which is a tertiary academic cardiac referral unit, is different to outpatient facilities and community hospitals. On the other hand, this might also reflect the true prevalence of SDB in symptomatic and severe heart failure.


   5. Conclusion
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Conclusion
References
 
There is an unexpected high prevalence of SDB in patients with symptomatic CHF, despite state of the art heart failure medication including ACE-inhibitors, AT-1-receptor blockers, diuretics, β-blockers, spironolactone and digitalis. CSA is accompanied by more advanced symptoms and a more impaired cardiovascular function as compared to OSA. In view of its pathophysiological and especially prognostic significance and the availability of modern treatment options, sleep apnoea screening should be routinely implemented in the evaluation and follow-up of heart failure patients.


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

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