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Treating Central Sleep Apnea in Heart Failure

2007; Lippincott Williams & Wilkins; Volume: 115; Issue: 25 Linguagem: Inglês

10.1161/circulationaha.107.709303

1524-4539

Lyle J. Olson, Virend K. Somers,

Sleep and Wakefulness Research

HomeCirculationVol. 115, No. 25Treating Central Sleep Apnea in Heart Failure Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBTreating Central Sleep Apnea in Heart FailureOutcomes Revisited Lyle J. Olson and Virend K. Somers Lyle J. OlsonLyle J. Olson From the Division of Cardiovascular Diseases, Department of Internal Medicine, Mayo Clinic College of Medicine, Rochester, Minn. and Virend K. SomersVirend K. Somers From the Division of Cardiovascular Diseases, Department of Internal Medicine, Mayo Clinic College of Medicine, Rochester, Minn. Originally published26 Jun 2007https://doi.org/10.1161/CIRCULATIONAHA.107.709303Circulation. 2007;115:3140–3142A recent enhanced appreciation of sleep–cardiovascular interactions, particularly in patients with congestive heart failure (CHF), has prompted careful consideration of the relevance of sleep-disordered breathing to CHF pathophysiology, progression, and treatment.1 Sleep-disordered breathing may be broadly classified as either obstructive sleep apnea (OSA) or central sleep apnea (CSA).1 The former is characterized by repetitive collapse of the upper airway, whereas in patients with CHF, the latter is most often due to periodic alternation of diminished ventilatory drive and compensatory hyperventilation typical of Cheyne-Stokes respiration (Figure 1). CSA is likely a consequence rather than a cause of CHF. Although the mechanisms that underlie CSA/Cheyne-Stokes respiration in patients with CHF are not well understood, pulmonary congestion with increased lung J-receptor stimulation and greater chemosensitivity may play a role in the genesis of the periodic breathing that characterizes this disorder.1,2Download figureDownload PowerPointFigure 1. Ventilation during sleep from a patient with CHF and CSA. The ventilatory pattern is characteristic of Cheyne-Stokes respiration: apnea followed by crescendo-decrescendo breathing followed by apnea. The cycle may be repeated throughout sleep.Article p 3173Of 5 million North Americans with CHF, an estimated 50% may have coexistent sleep apnea. Although the prevalence of OSA is much higher than CSA in the general population,3 it appears that this relationship may be reversed among patients with systolic heart failure. Case series have reported frequencies of CSA exceeding 40% for stable, ambulatory patients with CHF in a ratio >2:1 relative to the frequency of OSA. Indeed, the frequency of OSA in these same series was similar to that observed in the general population, whereas the frequency of CSA was strikingly higher.4,5 Furthermore, in patients with CHF, CSA has been associated with increased morbidity and mortality,5–7 increased neurohormonal activation,1 increased ventricular arrhythmia,8 decreased exercise capacity,5,9 and more advanced New York Heart Association class.5 However, whether these associations merely reflect more advanced CHF or whether repetitive apneas with hypoxia and sympathetic neural activation10 independently promote disease progression and adverse outcomes remains unknown.Because OSA and CSA have different primary causes, optimal therapy may differ for these 2 distinct disorders. However, for patients with CHF, a paucity of data exists from prospective, randomized, controlled trials addressing the potential benefits of treatment for either OSA or CSA. Such studies have generally been limited to evaluation of the short-term effects of continuous positive airway pressure (CPAP) on left ventricular ejection fraction in patients with OSA.11,12 An exception is the Canadian Continuous Positive Airway Pressure for Patients With Central Sleep Apnea and Heart Failure (CANPAP), described later.13As yet, no consensus exists on management strategies for the treatment of sleep apnea associated with CHF that have been endorsed by either sleep medicine or CHF specialists.14 Because CSA is likely secondary to CHF, it follows that optimization of heart failure therapy may resolve CSA.1 In observational studies, therapies that appear to attenuate or eliminate CSA include diuretics,15 β-blockers,16 biventricular pacing,17 and cardiac surgery.1 For those patients with persistent CSA, potential adjunctive treatment includes nocturnal oxygen,1 adaptive servoventilation, and CPAP,6 each of which may reduce the frequency of central apneas in selected patients. Originally devised for the treatment of OSA, CPAP acts as a pneumatic stent to promote upper airway patency. The benefit to cardiac function in patients with OSA may be mediated by improved nocturnal oxygen saturation, reduced sympathetic neural activation, and increased intrathoracic pressure.11 However, in contrast to OSA, the mechanisms by which CPAP may yield benefit for CSA are not intuitive; by definition, no upper airway obstruction is present in this disorder. One proposed mechanism of benefit has been that CPAP may favorably modulate left ventricular function by promoting an increase in intrathoracic pressure, which in turn decreases transmural left ventricular pressure.1 Hence, CPAP may in theory act as both a short-term and a long-term hemodynamic intervention for CHF by functioning as an external, noninvasive appliance that reduces left ventricular afterload and thereby lowers cardiac filling pressures with resolution of CSA.The CANPAP trial was a prospective, randomized, controlled study that attempted to establish the efficacy of CPAP for the treatment of CSA/Cheyne-Stokes respiration associated with CHF by evaluation of the primary end point of transplant-free survival.13 Subjects with optimally managed CHF with left ventricular ejection fraction 15 were randomized to receive either CPAP or continued conventional therapy.13 On average, the AHI was reduced from 40 to 19 after 3 months of CPAP, and this reduction was associated with improved left ventricular ejection fraction, decreased norepinephrine concentration, increased nocturnal oxygen saturation, and increased 6-minute walk time.13 However, CPAP had no effect on the primary end point of transplant-free survival compared with conventional therapy alone.13 In fact, there was a suggestion of early poorer outcomes in the CPAP-treated group. The study was terminated because of lower-than-expected subject recruitment and better-than-anticipated survival regardless of randomization.13 Although lack of benefit from CPAP in the main analysis of CANPAP was unequivocal, in this issue of Circulation, Arzt and colleagues18 present data from this same trial describing the apparent benefits of suppression of CSA by CPAP in a subset of subjects from the original study cohort. In this post hoc analysis, subjects were stratified into 3 subgroups: control subjects, those treated with CPAP with suppression of CSA (defined as AHI 15). The investigators hypothesized that suppression of the AHI to 15).13 In addition, the mean duration of CPAP therapy per night was ≈4 hours over 3 months of follow-up and <4 hours at the 12-month follow-up. These observations indicate that, in the CANPAP trial, on average only a fraction of the burden of CSA was suppressed by CPAP.19 Hence, CPAP is less than ideal for reducing the AHI with obvious potential for suboptimal therapeutic outcomes. In contrast, the present study by Arzt and colleagues provides some optimism that CSA may be a worthy therapeutic target provided that treatment effectively suppresses the AHI, whether by standard pharmacotherapy, various modalities of positive airway pressure, or other emerging devices.20Better clarification of optimal management strategies for CHF patients with CSA will require prospective, suitably controlled and adequately powered studies evaluating cardiovascular end points in well-characterized subjects to identify which patients to target for specific interventions and what the intermediate and long-term benefits of such treatment may be. We agree with Arzt and colleagues18 that in the interim, given the possibility of early adverse outcomes associated with CPAP as reported in the primary results of the CANPAP trial,13 it does not seem prudent to recommend that clinicians routinely implement CPAP as a standard of care for patients with CHF and CSA.The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.Sources of FundingDr Olson is supported by National Institutes of Health grants HL-65176 and M01-RR00585 and by the Mayo Foundation. Dr Somers is supported by National Institutes of Health grants HL-65176, HL-70302, HL-73211, and M01-RR00585 and by the Mayo Foundation.DisclosuresDr Olson has received grant support from Medtronic for studies of CSA in CHF. Dr Somers is a consultant for Cardiac Concepts Inc, Respironics, Res Med, and Sepracor.FootnotesCorrespondence to Virend K. Somers, MD, PhD, Professor of Medicine, Consultant, Division of Cardiovascular Diseases, Department of Internal Medicine, Mayo Clinic College of Medicine, Rochester, MN 55905. E-mail [email protected] References 1 Bradley TD, Floras JS. Sleep apnea and heart failure, part II: central sleep apnea. Circulation. 2003; 107: 1822–1826.LinkGoogle Scholar2 Javaheri S. A mechanism of central sleep apnea in patients with heart failure. N Engl J Med. 1999; 341: 949–954.CrossrefMedlineGoogle Scholar3 Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med. 1993; 328: 1230–1235.CrossrefMedlineGoogle Scholar4 Javaheri S, Parker TJ, Liming JD, Corbett BS, Nishiyama H, Wexler L, Roselle GA. Sleep apnea in 81 ambulatory male patients with stable heart failure: types and their prevalences, consequences, and presentations. 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Ann Intern Med. 1998; 128: 204–207.CrossrefMedlineGoogle Scholar9 Arzt M, Harth M, Luchner A, Muders F, Holmer SR, Blumberg FC, GRiegger GAJ, Pfeifer M. Enhanced ventilatory response to exercise in patients with chronic heart failure and central sleep apnea. Circulation. 2003; 107: 1998–2003.LinkGoogle Scholar10 van de Borne PJH, Oren R, Abouassaly C, Anderson E, Somers VK. Effect of Cheyne-Stokes respiration on muscle sympathetic nerve activity in severe congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy. Am J Cardiol. 1998; 81: 432–436.CrossrefMedlineGoogle Scholar11 Kaneko Y, Floras JS, Usui K, Plante J, Tkacova R, Kubgo 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: 1233–1241.CrossrefMedlineGoogle Scholar12 Mansfield D, Gollogly NC, Kaye DM, Richardson M, Bergin P, Naughton MT. 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ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure): developed in collaboration with the American College of Chest Physicians and the International Society for Heart and Lung Transplantation: endorsed by the Heart Rhythm Society. Circulation. 2005; 112: e154–e235.LinkGoogle Scholar15 Solin P, Bergin P, Richardson M, Kaye DM, Walters EH, Naughton MT. Influence of pulmonary capillary wedge pressure on central apnea in heart failure. Circulation. 1999; 99: 1574–1579.CrossrefMedlineGoogle Scholar16 Tamura A, Kawano Y, Naono S, Kotoku M, Kadota J. Relationship between beta-blocker treatment and the severity of central sleep apnea in chronic heart failure. Chest. 2007; 131: 130–135.CrossrefMedlineGoogle Scholar17 Sinha AM, Skobel EC, Breithardt OA, Norra C, Markus KU, Breuer C, Hanrath P, Stellbrink C. Cardiac resynchronization therapy improves central sleep apnea and Cheyne-Stokes respiration in patients with chronic heart failure. J Am Coll Cardiol. 2004; 44: 68–71.CrossrefMedlineGoogle Scholar18 Arzt M, Floras JS, Logan AG, Kimoff RJ, Series F, Morrison D, Ferguson K, Belenkie I, Pfeifer M, Fleetham J, Hanley P, Smilovitch M, Ryan C, Tomlinson G, Bradley TD, for the 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: 3173–3180.LinkGoogle Scholar19 Somers VK. Sleep: a new cardiovascular frontier. N Engl J Med. 2005; 353: 2070–2073.CrossrefMedlineGoogle Scholar20 Philippe C, Stoica-Herman M, Drouot X, Raffestin B, Escourrou P, Hittinger L, Michel P-L, Rouault S, d'Ortho M-P. Compliance with and effectiveness of adaptive servoventilation versus continuous positive airway pressure in the treatment of Cheyne-Stokes respiration in heart failure over a six month period. Heart. 2006; 92: 337–342.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Martynowicz H, Czerwińska K, Wojakowska A, Januszewska L, Markiewicz-Górka I, Więckiewicz M, Mazur G, Pawlas K, Poręba R and Gać P (2020) Renalase and hypertension—demographic and clinical correlates in obstructive sleep apnea, Sleep and Breathing, 10.1007/s11325-020-02157-3, 25:2, (669-675), Online publication date: 1-Jun-2021. 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Vanhecke T, Franklin B, Ajluni S, Sangal R and McCullough P (2014) Cardiorespiratory fitness and sleep-related breathing disorders, Expert Review of Cardiovascular Therapy, 10.1586/14779072.6.5.745, 6:5, (745-758), Online publication date: 1-Jun-2008. Redeker N (2008) Sleep Disturbance in People With Heart Failure, Journal of Cardiovascular Nursing, 10.1097/01.JCN.0000305094.20012.76, 23:3, (231-238), Online publication date: 1-May-2008. June 26, 2007Vol 115, Issue 25 Advertisement Article InformationMetrics https://doi.org/10.1161/CIRCULATIONAHA.107.709303PMID: 17592088 Originally publishedJune 26, 2007 Keywordssleepheart failureEditorialsPDF download Advertisement SubjectsCongenital Heart Disease