Elsevier

Sleep Medicine

Volume 9, Issue 6, August 2008, Pages 660-666
Sleep Medicine

Original Article
Cardiac function after CPAP therapy in patients with chronic heart failure and sleep apnea: A multicenter study

https://doi.org/10.1016/j.sleep.2007.06.018Get rights and content

Abstract

Background and purpose

Continuous positive airway pressure (CPAP) is an effective treatment for sleep apnea (SA), although the evidence for improving chronic heart failure (CHF) is inconclusive. Our aim was to evaluate the effect of CPAP treatment on the left ventricle ejection fraction (LVEF) among other cardiological variables in a randomized, multicenter, placebo (sham-CPAP)-controlled study.

Methods

After the selection procedure, 60 patients with CHF with LVEF < 45% and SA with an apnea–hypopnea index (AHI) > 10/h were evaluated at baseline, and after 3 months of treatment with optimal CPAP or sham-CPAP. The assessment was based on the LVEF, hypertension, daytime sleepiness (Epworth sleepiness scale [ESS]), quality of life (SF-36), New York Heart Scale (NYHA score), dyspnea (by using the Borg scale) and exercise tolerance (6-min walk test).

Results

The mean AHI was normalized in the optimal CPAP group but not in the sham-CPAP group. The LVEF showed a significant improvement in the group of patients treated with CPAP (2.5; 95% CI: 0.6 to 4.3), which was not observed in the sham-CPAP group (0.0; 95% CI: −2.1 to 2.1). However, the change in the LVEF from baseline to 3 months was not significantly greater in the whole group (obstructive and Cheyne–Stokes events) treated with CPAP than in the control group (p: 0.07). In patients with only obstructive sleep apnea (OSA), who account for 83% of the total population, there was a significant improvement in the LVEF in the group of patients treated with CPAP but no such improvement in the sham-CPAP group. In this OSA group, the change in the LVEF from baseline to 3 months was significantly greater in the group treated with CPAP than in the sham-CPAP group (p: 0.03). The other variables studied were not modified. When the patients were divided according to the severity of the LVEF (a LVEF cut-off of 30%), improvement was observed in those with a LVEF > 30. No changes were found in the other cardiological variables.

Conclusions

CPAP therapy proved to be useful in patients with associated sleep-disordered breathing and CHF. The improvement was more marked in patients with a LVEF > 30%. However, the increased LVEF in the CPAP group was not accompanied by changes in the other cardiological variables.

Introduction

Chronic heart failure (CHF) is a common disease with a prevalence between 0.3% and 2%, up to more than 10% in subjects over 70 years of age [1]. The 5-year survival rate is 25% for men and 38% for women [2]. In developed countries, this survival rate is lower than the corresponding figures for known cancer disease [3]. Advances in pharmacological treatments have led to changes in cardiac function. Data derived from prevalence studies [4], [5], [6], [7] estimate a variable degree of Cheyne–Stokes apneas (CSA) and obstructive sleep apnea (OSA). The presence of CSA may be related to the progression of cardiac disease and is a prognostic factor even with the same degree of CHF [6], [7]. OSA may lead to deterioration in CHF [8], [9], [10], [11]. Suppression of these sleep events becomes a major therapeutic end-point together with the pharmacologic treatment of CHF [9]. It is well established that OSA and CSA often coexist in patients with CHF. Both probably contribute to CHF and mortality on a short-term basis [7], [8]. However, it has not been confirmed that long-term mortality is increased [12]. These patients may share a number of factors such as obesity, gender, metabolic and genetic markers [13], triggering further controversy. The role of continuous positive airway pressure (CPAP) in cardiac function in patients with CSA and OSA has been studied with varying results [7], [8], [11], [14]. It is not clear whether CPAP treatment for respiratory sleep disorders in CHF could slow down deterioration or improve cardiovascular function [9], [10], [11], [12], [13], [14], [15].

In an attempt to yield further insight into this subject, we undertook a multicenter study to analyse the role of CPAP therapy (optimal vs sham) in the left ventricular ejection fraction (LVEF) and in other cardiac measurements in patients with CHF.

Section snippets

Subjects

CHF patients were referred to the Sleep Units from the department of cardiology at eight university hospitals on the sole condition of having LVEF < 45%. After an interview and some clinical explorations, 127 out of 245 fulfilled the rigid inclusion and exclusion criteria (see flowchart in Fig. 1). These subjects underwent full polysomnography (PSG). Fifty-seven percent (n: 73) had an apnea–hyponea index (AHI) > 10. Forty-three percent (n: 54) had an AHI < 10. Only 17% of the patients had CSA. The

Results

Table 1 shows the anthropometric and clinical data at baseline of the 60 subjects that completed the study. No differences were observed in the whole CPAP or sham group. After removing the patients with CSA (17%), the OSA patients (83%) did not present any significant differences either. The nature of the cardiomyopathy was ischemic in 67.6% of the cases. Table 2 shows PSG parameters. A significant improvement in most of the PSG parameters was observed in the CPAP group but not in the sham

Discussion

Our study shows that CPAP therapy is of value in patients with associated SA and CHF. However, the increased LVEF in the CPAP group was not accompanied by improvements in the other cardiological variables. This improvement in the LVEF was more pronounced in patients with LVEF > 30%.

The study was performed using a true placebo. Given that the proportion of CSA was low (17%), we analysed all the patients with SA and those with only OSA. The reason for the low CSA proportion with respect to other

Acknowledgements

We are grateful to the Computer Services of Osakidetza and Txagorritxu Hospital for designing and maintaining the webpage. We also thank the Research Unit and the Research Commission at Txagorritxu Hospital (Vitoria) for supporting this project.

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    This work was supported by the Fondo de Investigación Sanitaria (01-01009), the Sociedad Vasco-Navarra de Patología Respiratoria 2002, Red RESPIRA RTIC (C03/011) (SAF 2004-00684).

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