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Winfried J. Randerath, MD, FCCP; Marcel Treml, PhD
Author and Funding Information

From the Institute of Pneumology at the University Witten/Herdecke, Clinic for Pneumology and Allergology, Center of Sleep Medicine and Respiratory Care, Bethanien Hospital.

Correspondence to: Winfried J. Randerath, MD, FCCP, Institute of Pneumology at the University Witten/Herdecke, Clinic for Pneumology and Allergology, Center of Sleep Medicine and Respiratory Care, Bethanien Hospital, Aufderhöherstraße 169-175, 42699 Solingen, Germany; e-mail: randerath@klinik-bethanien.de


Funding/Support: This study was supported in part by Philips Respironics (Murrysville, PA).

Financial/nonfinancial disclosures: The authors have reported to CHEST the following conflicts of interest: Dr Randerath has received travel grants and speaking fees from Philips Respironics. Dr Treml has reported that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2013;143(6):1834. doi:10.1378/chest.13-0499
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Published online
To the Editor:

We thank Dr Jaffuel and colleagues for their stimulating discussion of the heterogeneous effects of positive airway pressure on breathing disturbances and cardiovascular parameters. They hypothesized that higher levels of CPAP or expiratory positive airway pressure may impair hemodynamics, increase the ventilatory loop gain, and, thus, aggravate Cheyne-Stokes respiration. Our study1 confirmed previous findings, showing a 50% reduction of central sleep apnea under CPAP, whereas auto-servoventilation (ASV) normalized both obstructive and central disturbances. To address the idea of Jaffuel et al, we analyzed responders and nonresponders irrespective of their treatment mode. We asked whether a reduction of the apnea-hypopnea index to ≤10/h and by ≥50% was associated with different CPAP/expiratory positive airway pressure levels. The mean pressures differed significantly between responders (9.2 ± 1.7 cm H2O; n = 32) and nonresponders (10.3 ± 2.2; n = 19; P =.045). However, the absolute difference was mild and even smaller than the pressure difference between the complete CPAP and ASV groups. Most importantly, this difference was related almost exclusively to ASV responders (Table 1), whereas no pressure difference in CPAP responders vs nonresponders was found. These findings are not surprising because we aimed to apply a homogenous CPAP level of 10 cm H2O. Thus, the data do not support the idea that higher pressures are responsible for differences in efficacy. The heterogeneous response is associated with a homogeneous pressure profile.

Table Graphic Jump Location
Table 1 —Analysis of Responders and Nonresponders Irrespective of Treatment Mode

Data are presented as mean ± SD unless indicated otherwise. ASV = auto-servoventilation; BNP = brain natriuretic peptide; CSA = central sleep apnea; EPAP = expiratory positive airway pressure; NS = nonsignificant; OSA = obstructive sleep apnea.

a 

Proportion of obstructive/central disturbances at baseline in the combined (CPAP +ASV) responder vs nonresponder groups.

The second hypothesis by Jaffuel et al focused on the distribution of central disturbances during the night. Although the present data cannot answer this question directly, we found similar portions of obstructive (45%) and central events (55%) in responders and nonresponders. The relatively high amount of central sleep apnea and the even distribution make substantial differences throughout the night improbable.

The difference in brain natriuretic peptide levels between responders and nonresponders appears marked to us. There was a clear tendency toward improvement in the combined CPAP and ASV responders (Table 1). This nonsignificant finding (the study was actually not powered for this subanalysis) might help to explain the significant improvement of this parameter in the main study.1 Optimal suppression of respiratory disturbances seems to be more relevant for cardiac outcome than for pressure profiles or distribution of disturbances. These aspects are in line with the survival benefit of those patients with sufficient suppression of respiratory disturbances in the CANPAP (Canadian Continuous Positive Airway Pressure for Patients with Central Sleep Apnea and Heart Failure Trial) trial.2,3 The question remains: Which aspect of the cardiopulmonary interaction explains the phenomenon? Improvement of intermittent hypoxemia, reduction of oxygen demand of the breathing muscles, and reduction of breathing effort, which all influence oxygen supply or oxygen demand of the heart, can be discussed.4,5

Acknowledgments

Role of sponsors: The sponsor had no role in the design of the study, the collection and analysis of the data, or in the preparation of the manuscript.

Randerath WJ, Nothofer G, Priegnitz C, et al. Long-term auto-servoventilation or constant positive pressure in heart failure and coexisting central with obstructive sleep apnea. Chest. 2012;142(2):440-447. [CrossRef] [PubMed]
 
Arzt M, Floras JS, Logan AG, et al; CANPAP Investigators. Suppression of central sleep apnea by continuous positive airway pressure and transplant-free survival in heart failure: a post hoc analysis of the Canadian Continuous Positive Airway Pressure for Patients with Central Sleep Apnea and Heart Failure Trial (CANPAP). Circulation. 2007;115(25):3173-3180. [CrossRef] [PubMed]
 
Kourouklis SP, Vagiakis E, Paraskevaidis IA, et al. Effective sleep apnoea treatment improves cardiac function in patients with chronic heart failure [published online ahead of print October 2, 2012]. Int J Cardiol. doi:10.1016/j.ijcard.2012.09.101.
 
Foster GE, Brugniaux JV, Pialoux V, et al. Cardiovascular and cerebrovascular responses to acute hypoxia following exposure to intermittent hypoxia in healthy humans. J Physiol. 2009;587(pt 13):3287-3299. [CrossRef] [PubMed]
 
Krachman SL, Crocetti J, Berger TJ, Chatila W, Eisen HJ, D’Alonzo GE. Effects of nasal continuous positive airway pressure on oxygen body stores in patients with Cheyne-Stokes respiration and congestive heart failure. Chest. 2003;123(1):59-66. [CrossRef] [PubMed]
 

Figures

Tables

Table Graphic Jump Location
Table 1 —Analysis of Responders and Nonresponders Irrespective of Treatment Mode

Data are presented as mean ± SD unless indicated otherwise. ASV = auto-servoventilation; BNP = brain natriuretic peptide; CSA = central sleep apnea; EPAP = expiratory positive airway pressure; NS = nonsignificant; OSA = obstructive sleep apnea.

a 

Proportion of obstructive/central disturbances at baseline in the combined (CPAP +ASV) responder vs nonresponder groups.

References

Randerath WJ, Nothofer G, Priegnitz C, et al. Long-term auto-servoventilation or constant positive pressure in heart failure and coexisting central with obstructive sleep apnea. Chest. 2012;142(2):440-447. [CrossRef] [PubMed]
 
Arzt M, Floras JS, Logan AG, et al; CANPAP Investigators. Suppression of central sleep apnea by continuous positive airway pressure and transplant-free survival in heart failure: a post hoc analysis of the Canadian Continuous Positive Airway Pressure for Patients with Central Sleep Apnea and Heart Failure Trial (CANPAP). Circulation. 2007;115(25):3173-3180. [CrossRef] [PubMed]
 
Kourouklis SP, Vagiakis E, Paraskevaidis IA, et al. Effective sleep apnoea treatment improves cardiac function in patients with chronic heart failure [published online ahead of print October 2, 2012]. Int J Cardiol. doi:10.1016/j.ijcard.2012.09.101.
 
Foster GE, Brugniaux JV, Pialoux V, et al. Cardiovascular and cerebrovascular responses to acute hypoxia following exposure to intermittent hypoxia in healthy humans. J Physiol. 2009;587(pt 13):3287-3299. [CrossRef] [PubMed]
 
Krachman SL, Crocetti J, Berger TJ, Chatila W, Eisen HJ, D’Alonzo GE. Effects of nasal continuous positive airway pressure on oxygen body stores in patients with Cheyne-Stokes respiration and congestive heart failure. Chest. 2003;123(1):59-66. [CrossRef] [PubMed]
 
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