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EDITORIAL

Does pressure affect performance? Continuous positive airway pressure for sleep-disordered breathing in heart failure Key words: continuous positive airway pressure, heart failure, hypotension, sleep apnoea syndrome.

Sleep-disordered breathing is very common in patients with congestive heart failure. Either obstructive sleep apnoea (OSA) or central sleep apnoea (CSA) have been reported to occur in > 50% of this population, often with both coexisting in the same patient.1 In OSA, there is repetitive respiratory effort against an obstructed airway, whereas in CSA there is waxing and waning ventilatory drive leading to periods of apnoea alternating with hyperpnoea. The type of respiratory event has important haemodynamic implications in heart failure. OSA leads to exaggerated negative intrathoracic pressure swings, which increase left ventricular (LV) transmural pressure and therefore LV afterload. This has been shown to reduce stroke volume and cardiac output in awake and, more importantly, sleeping heart failure patients.2 Furthermore, severe OSA has been associated with an increased risk of developing heart failure and portends a poor long-term prognosis in those with both conditions.3 With this in mind, it is not surprising that continuous positive airway pressure (CPAP) treatment for OSA in heart failure prevents these adverse haemodynamic effects and has been shown to improve LV function in two randomized controlled trials.4,5 Although these trials were not large or long enough to address mortality, observational studies have suggested improved survival in those heart failure patients with CPAP-treated OSA compared with untreated OSA.6 In contrast, CSA leads to much smaller intrathoracic pressure swings than OSA. Thus, LV afterload is not greatly increased, and a recent study has in fact shown a small increase in stroke volume during central events in sleeping heart failure patients.2 From a clinical perspective, whether CSA is independently associated with mortality or is merely a marker of heart failure severity remains controversial.7 Furthermore, CPAP is only effective at resolving CSA approximately half of the time, and a large randomized controlled trial did not show any survival advantage to treating CSA with CPAP.8 CPAP is generally considered to be a very safe treatment. After widespread clinical use over the past 30 years, there have not been any clearly documented

Conflict of interest statement: G.S.H. has received research funding and equipment for research from Resmed, Philips and Compumedics. © 2013 The Authors Respirology © 2013 Asian Pacific Society of Respirology

long-term harmful effects in general populations. Nevertheless, the application of CPAP leads to positive intrathoracic pressure, which theoretically may have detrimental consequences for cardiac haemodynamics in some heart failure patients. Higher intrathoracic pressures oppose venous return (reducing preload) and reduce the LV transmural pressure gradient (reducing afterload). Those patients with low filling pressures are at risk of a reduction in cardiac output if the drop in preload is proportionally greater than the reduction in afterload. An intriguing observation from the continuous positive airway pressure for central sleep apnea and heart failure study was that in the first 18 months after randomization, transplantfree survival was worse in the CPAP-treated group compared with the control arm, before survival curves became similar by the end of the study.8 Was this a statistical anomaly or could this have been due to an early adverse haemodynamic effect of CPAP such as a reduction in systemic blood pressure or cardiac output affecting a subset of patients? Literature addressing the acute haemodynamic effects of CPAP in heart failure populations has been inconsistent. Studies have all been small and some have shown no effect on mean blood pressure, whereas others have demonstrated that CPAP reduces blood pressure and/or cardiac output.9,10 It has been suggested that the pulmonary capillary wedge pressure is important, with an improvement in cardiac output seen in those with high LV filling pressures and a reduction in cardiac output in those with normal filling pressures.11 In this edition of Respirology, Schroll et al. provide further data to help clarify the haemodynamic safety of CPAP in heart failure.12 In their study, the authors administered incremental levels of CPAP (up to 10 cm H2O) in 37 heart failure patients with severe sleep-disordered breathing (49% with predominantly CSA), defined by Apnoea Hypopnoea Index > 20 per hour. The majority of patients (97%) had a small and not clinically significant drop in mean blood pressure. One patient had a prespecified significant reduction in mean blood pressure of >15 mm Hg, but without any clinical symptoms. There was no effect of cardiac rhythm (atrial fibrillation or sinus), and there were no changes in cardiac output across different CPAP levels albeit in a small subset (n = 11). How should we interpret this study in the context of previous literature? Although the numbers were small, the study by Schroll and colleagues reassures us that any blood pressure reductions from CPAP use in heart failure are generally small and likely to be clinically insignificant. Large reductions in blood Respirology (2014) 19, 3–4 doi: 10.1111/resp.12216

4 pressure certainly appear to be rare. Does this mean that CPAP is safe for patients with heart failure? In general, we think so, but as with any treatment it is important to weigh the potential benefits against risks for individual patients. In this setting, the type of sleep-disordered breathing is important. Heart failure patients who have significant OSA should be treated with CPAP. There is strong evidence that moderate-severe OSA is deleterious to cardiac function in heart failure,2,3 and this is of far greater concern than the possible risk of hypotension or reduced cardiac output from CPAP itself. Treatment with CPAP effectively reverses these haemodynamic consequences of OSA, and the bulk of clinical evidence to date suggests outcomes in heart failure are improved with treatment of OSA.4–6 For heart failure patients who predominantly have CSA, things are not so clear. CSA might not be directly deleterious to cardiac haemodynamics, and it remains unproven whether the presence of CSA independently worsens prognosis.2,7 Moreover, CPAP treatment is not reliably effective at resolving CSA. Thus, in such patients, where CPAP benefit is inconsistent, important questions remain: Should CPAP be avoided in patients with CSA whose apnoea resolves, but cardiac output falls (e.g. CPAP responders with low filling pressures)? Do CPAP non-responders have a worse survival than CPAP responders13 due to differences in the hemodynamic effects of CPAP? What is the effect on haemodynamics of CPAP levels above 10 cm H2O? Do acute CPAP effects during wakefulness translate into longer-term effects during sleep? Given the breadth of unanswered questions, we advise clinicians to remain especially attentive when using CPAP long-term for patients with CSA (without significant coexisting OSA), ensuring first that heart failure management itself is optimized, that CPAP has indeed suppressed CSA (otherwise the potential benefit is presumably absent) and that the CPAP level used to suppress OSA/CSA does not appear to induce acute hemodynamic compromise. Garun S. Hamilton, MBBS, FRACP, PhD,1,2 Bradley A. Edwards, PhD3 and Scott A. Sands, PhD2,3 1 Monash Lung and Sleep, Monash Health, 2Monash University, Clayton, Victoria, Australia, and 3Division of Sleep Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA

Respirology (2014) 19, 3–4

Editorial

REFERENCES 1 Schulz R, Blau A, Börgel J, Duchna HW, Fietze I, Koper I, Prenzel R, Schädlich S, Schmitt J, Tasci S et al. Sleep apnoea in heart failure. Eur. Respir. J. 2007; 29: 1201–5. 2 Yumino D, Kasai T, Kimmerly D, Amirthalingam V, Floras JS, Bradley TD. Differing effects of obstructive and central sleep apneas on stroke volume in patients with heart failure. Am. J. Respir. Crit. Care Med. 2013; 187: 433–8. 3 Gottlieb DJ, Yenokyan G, Newman AB, O′Connor GT, Punjabi NM, Quan SF, Redline S, Resnick HE, Tong EK, Diener-West M et al. Prospective study of obstructive sleep apnea and incident coronary heart disease and heart failure: the sleep heart health study. Circulation 2010; 122: 352–60. 4 Kaneko Y, Floras JS, Usui K, Plante J, Tkacova R, Kubo T, Ando S, Bradley TD. Cardiovascular effects of continuous positive airway pressure in patients with heart failure and obstructive sleep apnea. N. Engl. J. Med. 2003; 348: 1233–41. 5 Mansfield DR, Gollogly NC, Kaye DM, Richardson M, Bergin P, Naughton MT. Controlled trial of continuous positive airway pressure in obstructive sleep apnea and heart failure. Am. J. Respir. Crit. Care Med. 2004; 169: 361–6. 6 Wang H, Parker JD, Newton GE, Floras JS, Mak S, Chiu KL, Ruttanaumpawan P, Tomlinson G, Bradley TD. Influence of obstructive sleep apnea on mortality in patients with heart failure. J. Am. Coll. Cardiol. 2007; 49: 1625–31. 7 Naughton MT. Cheyne-Stokes respiration: friend or foe? Thorax 2012; 67: 357–60. 8 Bradley TD, Logan AG, Kimoff RJ, Sériès F, Morrison D, Ferguson K, Belenkie I, Pfeifer M, Fleetham J, Hanly P et al. Continuous positive airway pressure for central sleep apnea and heart failure. N. Engl. J. Med. 2005; 353: 2025–33. 9 Kaye DM, Mansfield D, Aggarwal A, Naughton MT, Esler MD. Acute effects of continuous positive airway pressure on cardiac sympathetic tone in congestive heart failure. Circulation 2001; 103: 2336–8. 10 Kiely JL, Deegan P, Buckley A, Shiels P, Maurer B, McNicholas W. Efficacy of nasal continuous positive airway pressure therapy in chronic heart failure: importance of underlying cardiac rhythm. Thorax 1998; 53: 957–62. 11 De Hoyos A, Liu PP, Benard DC, Bradley TD. Haemodynamic effects of continuous positive airway pressure in humans with normal and impaired left ventricular function. Clin. Sci. (Lond.) 1995; 88: 173–8. 12 Schroll S, Sériès F, Lewis K, Benjamin A, Escourrou P, Luigart R, Pfeifer M, Arzt M. Acute hemodynamic effects of continuous positive airway pressure in awake patients with heart failure. Respirology 2013; 19: 47–52. 13 Arzt M, Floras JS, Logan AG, Kimoff RJ, Series F, Morrison D, Ferguson K, Belenkie I, Pfeifer M, Fleetham J, Hanly P, Smilovitch M, Ryan C et al. 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: 3173–80.

© 2013 The Authors Respirology © 2013 Asian Pacific Society of Respirology

Does pressure affect performance? Continuous positive airway pressure for sleep-disordered breathing in heart failure.

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