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Sleep-Disordered Breathing, Heart Failure, and Phrenic Nerve StimulationHeart Failure and Phrenic Nerve Stimulation FREE TO VIEW

Michelle Cao, DO, FCCP; Christian Guilleminault, MD
Author and Funding Information

From Division of Sleep Medicine, Stanford University School of Medicine.

Correspondence to: Michelle Cao, DO, FCCP, Division of Sleep Medicine, Stanford University School of Medicine, 450 Broadway St, Pavilion C, 2nd Floor, Redwood City, CA 94063; e-mail: michellecao@stanford.edu


Financial/nonfinancial disclosures: The authors have reported to CHEST 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. 2012;142(4):821-823. doi:10.1378/chest.12-0591
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Sleep disordered breathing (SDB), in particular obstructive sleep apnea (OSA) and central sleep apnea-Cheyne-Stokes respiration (CSA-CSR), are prevalent in patients with heart failure and are associated with poor outcome.1 OSA is characterized by repeated pharyngeal airway collapse during sleep despite ongoing respiratory effort. CSA-CSR (or periodic breathing) describes a distinct respiratory pattern characterized by crescendo-decrescendo changes in tidal volume alternating with central apneas or central hypopneas. In both disorders, repetitive cortical arousals and oxyhemoglobin desaturation are of consequence during sleep. CSA-CSR in heart failure is thought to be secondary to instability of the ventilatory system due to increased chemo-responsiveness to Paco2. OSA in heart failure is thought to be due to a narrow upper airway, obesity, possibly pharyngeal wall edema, and ventilatory control instability.

The prevalence of SDB is estimated to be 47% to 76% among patients with heart failure and reduced ejection fraction (<45%).2 The presence of SDB in heart failure is associated with poor quality of life, increased morbidity, mortality, and economic cost.

The first goal of SDB treatment in patients with heart failure is to medically optimize cardiac function and positive airway pressure (PAP) therapies are recommended. Nocturnal CPAP therapy may be helpful; however, studies have shown mixed results.3 More advanced forms of PAP therapy, such as bilevel with back-up rate or servo-ventilators (eg, adapt servo-ventilation and auto servo-ventilation), improve cardiac function and prognosis in patients with heart failure with comorbid SDB.4-8 A major limitation of the long-term use of PAP therapy is adherence. Cardiac resynchronization therapy, achieved by biventricular pacing, has shown improvements in apnea indexes (ie, central and obstructive apneas) in patients with heart failure.9

In this issue of CHEST (see page 927), Zhang and colleagues10 evaluated a novel method of treating CSA-CSR in patients with heart failure through the use of transvenous phrenic nerve stimulation (PNS). Patients with implantable devices (ie, pacemaker, defibrillator, resynchronization device) were excluded. The objective of the authors was to stimulate the diaphragm, thereby preventing central apnea and the associated hyperpnea phase. Sixteen patients underwent successful stimulation capture of the phrenic nerve during a single overnight sleep study (19 enrolled, three failed to capture). The subjects served as their own controls (prestimulation period). Compared with controls, there was a significant decrease in the apnea-hypopnea index (AHI) (33.8±9.3 vs 8.1±2.3; normal, <5; mild, 5-15; moderate, 16-30; severe, >30/h sleep). The study also showed improvements in the oxygen desaturation index (ODI) and increases in mean and minimal oxyhemoglobin saturation. Ventilatory parameters improved, with an increase in Paco2 and a corresponding decrease in respiratory rate. Of note, the AHI remained mildly elevated (8.2±2.3) during treatment. Neither cardiac arrhythmias nor hemodynamic instability were observed during this single night.

An earlier published and similar multicenter study by Ponikowski and colleagues11 also evaluated transvenous PNS for the treatment of CSA-CSR in heart failure. Unlike the study by Zhang and colleagues,10 in which patients underwent one overnight sleep study, in this study, 16 patients (31 enrolled, 11 failed to capture, four did not qualify) underwent two successive overnight studies: one control and one with PNS. All 16 patients had more severe SDB at baseline. Similar to the study by Zhang and colleagues,10 treatment with PNS showed improvements in apnea indexes, with a reduction in AHI (45 [39-59] vs 23 [12-27]), central apnea index (27 [11-38] vs 1 [0-5]), and ODI (31 [22-36] vs 14 [7-20]) compared with the control night. Although apnea indexes improved, AHI and ODI remained mild to moderately elevated: (23 [12-27] and 14 [7-20], respectively) during the treatment night. The obstructive hypopnea index remained elevated in the control and PNS-treated groups (10 [3-18] and 10 [7-14], respectively). Interestingly, the obstructive apnea index worsened with PNS treatment (1 [0-7] vs 4 [1-14]).

The application of PNS to support breathing and ventilation is not new; however, incorporating PNS to treat CSA-CSR in heart failure is a novel idea. Findings from the acute feasibility studies of Zhang and colleagues10 and Ponikowski and colleagues11 suggest the usefulness of transvenous PNS in the treatment of CSA-CSR in patients with heart failure. PNS seems to have a stabilizing effect on ventilator instability, with corresponding improvements in major indexes of SDB. However, based on the results of the studies by Zhang and colleagues10 and Ponikowski and colleagues,11 PNS does not effectively eliminate OSA, a sleep-related breathing disorder with a high prevalence in patients with heart failure.

With diaphragmatic pacing, there is discoordination between the forces applied and the consequent development of transpalatal pressure and contraction of the upper airway muscles: The contraction is not enough for the amount of applied negative pressure. As a result, PNS may increase diaphragmatic effort and consequently worsen upper airway collapse during sleep in patients with OSA. This phenomenon was observed with PNS in the treatment of congenital central alveolar syndrome in children during sleep that subsequently led to tracheostomy or treatment with CPAP.12 This known side effect was not mentioned in the above studies. In the presence of CSA-CSR and a normal upper airway tone, upper airway collapse will likely not happen. However, when considering a patient for PNS, we recommend careful screening to avoid worsening of the underlying OSA.

PNS may interfere with chronic implantable devices, which are common in patients with heart failure. Unsuccessful lead placement was a significant factor in both studies and needs to be evaluated further. Subjects tolerated PNS well; however, this was evaluated over 1 night and it would be worthwhile to evaluate subjects’ comfort level over the long term.

Long-term, randomized, controlled trials with PNS are necessary to evaluate the long-term practicality and clinical impact of this novel therapy. We favor treatment modalities that effectively eliminate both CSA-CSR and OSA and improve long-term cardiac function and prognosis. We recommend a multifaceted approach, involving lifestyle modification and pharmacologic therapy, in conjunction with PAP therapy, for the treatment of comorbid SDB in patients with heart failure.

References

Selim B, Won C, Yaggi HK. Cardiovascular consequences of sleep apnea. Clin Chest Med. 2010;31(2):203-220. [PubMed] [CrossRef]
 
Sharma B, Owens R, Malhotra A. Sleep in congestive heart failure. Med Clin North Am. 2010;94(3):447-464.
 
Arzt M, Floras JS, Logan AG, et al;; CANPAP Investigators 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.
 
Sharma B, McSharry D, Malhotra A. Sleep disordered breathing in patients with heart failure: pathophysiology and management. Curr Treat Options Cardiovasc Med. 2011;13(6):506-516.
 
Arzt M, Wensel R, Montalvan S, et al. Effects of dynamic bilevel positive airway pressure support on central sleep apnea in men with heart failure. Chest. 2008;134(1):61-66.
 
Teschler H, Döhring J, Wang YM, Berthon-Jones M. Adaptive pressure support servo-ventilation: a novel treatment for Cheyne-Stokes respiration in heart failure. Am J Respir Crit Care Med. 2001;164(4):614-619.
 
Yoshihisa A, Shimizu T, Owada T, et al. Adaptive servo ventilation improves cardiac dysfunction and prognosis in chronic heart failure patients with Cheyne-Stokes respiration. In Heart J. 2011;52(4):218-223.
 
Javaheri S, Goetting MG, Khayat R, Wylie PE, Goodwin JL, Parthasarathy S. The performance of two automatic servo-ventilation devices in the treatment of central sleep apnea. Sleep. 2011;34(12):1693-1698.
 
Simantirakis EN, Schiza SE, Siafakas NS, Vardas PE. Sleep-disordered breathing in heart failure and the effect of cardiac resynchronization therapy. Europace. 2008;10(9):1029-1033.
 
Zhang X-L, Ding N, Wang H, et al. Transvenous phrenic nerve stimulation in patients with Cheyne-Stokes respiration and congestive heart failure: a safety and proof-of-concept study. Chest. 2012;142(4):927-934.
 
Ponikowski P, Javaheri S, Michalkiewicz D, et al. Transvenous phrenic nerve stimulation for the treatment of central sleep apnoea in heart failure. Eur Heart J. 2012;33(7):889-894.
 
Chervin RD, Guilleminault C. Diaphragm pacing: review and reassessment. Sleep. 1994;17(2):176-187.
 

Figures

Tables

References

Selim B, Won C, Yaggi HK. Cardiovascular consequences of sleep apnea. Clin Chest Med. 2010;31(2):203-220. [PubMed] [CrossRef]
 
Sharma B, Owens R, Malhotra A. Sleep in congestive heart failure. Med Clin North Am. 2010;94(3):447-464.
 
Arzt M, Floras JS, Logan AG, et al;; CANPAP Investigators 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.
 
Sharma B, McSharry D, Malhotra A. Sleep disordered breathing in patients with heart failure: pathophysiology and management. Curr Treat Options Cardiovasc Med. 2011;13(6):506-516.
 
Arzt M, Wensel R, Montalvan S, et al. Effects of dynamic bilevel positive airway pressure support on central sleep apnea in men with heart failure. Chest. 2008;134(1):61-66.
 
Teschler H, Döhring J, Wang YM, Berthon-Jones M. Adaptive pressure support servo-ventilation: a novel treatment for Cheyne-Stokes respiration in heart failure. Am J Respir Crit Care Med. 2001;164(4):614-619.
 
Yoshihisa A, Shimizu T, Owada T, et al. Adaptive servo ventilation improves cardiac dysfunction and prognosis in chronic heart failure patients with Cheyne-Stokes respiration. In Heart J. 2011;52(4):218-223.
 
Javaheri S, Goetting MG, Khayat R, Wylie PE, Goodwin JL, Parthasarathy S. The performance of two automatic servo-ventilation devices in the treatment of central sleep apnea. Sleep. 2011;34(12):1693-1698.
 
Simantirakis EN, Schiza SE, Siafakas NS, Vardas PE. Sleep-disordered breathing in heart failure and the effect of cardiac resynchronization therapy. Europace. 2008;10(9):1029-1033.
 
Zhang X-L, Ding N, Wang H, et al. Transvenous phrenic nerve stimulation in patients with Cheyne-Stokes respiration and congestive heart failure: a safety and proof-of-concept study. Chest. 2012;142(4):927-934.
 
Ponikowski P, Javaheri S, Michalkiewicz D, et al. Transvenous phrenic nerve stimulation for the treatment of central sleep apnoea in heart failure. Eur Heart J. 2012;33(7):889-894.
 
Chervin RD, Guilleminault C. Diaphragm pacing: review and reassessment. Sleep. 1994;17(2):176-187.
 
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