EDITORIAL COMMENT
Seek and Treat Obstructive Sleep Apnea in Heart Failure*
Thierry H. Le Jemtel, MD ,* and
Sanja Jelic, MD
Section of Cardiology, Tulane University School of Medicine, New Orleans, Louisiana
Division of Pulmonary, Allergy, and Critical Care Medicine, Columbia University College of Physicians and Surgeons, New York, New York.
* Reprint requests and correspondence: Dr. Thierry H. Le Jemtel, Tulane University School of Medicine, Department of Medicine, Section of Cardiology, 1430 Tulane Avenue, SL-48, New Orleans, Louisiana 70112-2699. (Email: lejemtel{at}tulane.edu).
Obstructive sleep apnea (OSA) is a highly prevalent disorder. It affects 9% to 25% of the North American population (1–4). Intermittent cessation of breathing during sleep caused by occlusion of the upper airway followed by arousals from sleep defines OSA. The prevalence of OSA is even greater among patients with chronic heart failure (CHF). Approximately one-third to one-half of the 5 million Americans with CHF suffers from concomitant OSA, especially those with severe CHF (5–7). Notwithstanding the sheer number of patients with OSA and obesity as a common risk factor, repetitive episodes of hypoxia/reoxygenation, augmented intrathoracic pressure swings, and arousals from sleep promote arterial stiffness, hypertension, and increased sympathetic activity that account for the frequent coexistence of OSA and CHF (8–10). Patients with OSA are 2.2 times more likely to develop CHF than patients without OSA, and patients with CHF who develop OSA are thought to have a worse prognosis than patients with CHF alone (11).
In this issue of the Journal, Wang et al. (12) report their experience in the context of a single-center prospective observational study that compared the mortality of patients with coexistent CHF and OSA with that of patients with only CHF over an average period of 33 months. The mortality of patients with CHF and untreated OSA was nearly 2-fold greater than that of patients with CHF alone. In contrast, none of the patients with CHF and treated OSA died during the 39-month follow-up period.
These findings, although not unexpected and somewhat optimistic, are of great importance. Treatment with continuous positive airway pressure (CPAP) for 4 h per night does not improve survival in patients with CHF and central sleep apnea (CSA) (13). However, in contrast to CSA that is a consequence of CHF, OSA is on its own a risk factor for hypertension and stroke and is likely to impact negatively on left ventricular function (9,14). Patients with untreated severe OSA have a higher incidence of fatal cardiovascular events (1.06 vs. 0.35 per 100 person-years, p = 0.0008) and nonfatal cardiovascular events (2.13 vs. 0.64 per 100 person-years, p < 0.0001) than patients treated with CPAP after adjustment for pre-existing cardiovascular risk factors (15).
The observation by Wang et al. (12) that untreated OSA independently increases mortality in CHF is important because OSA remains frequently unrecognized in patients with CHF (7). The modest impact of OSA on subjective measurements of sleepiness or quality of life may explain why OSA is so often unrecognized in patients with CHF (16). To make things worse, even when recognized OSA remains often untreated, as was the case in the report by Wang et al. (12). Hopefully the positive findings in their report will encourage physicians and nurse practitioners who care for patients with CHF to be more vigilant about the diagnosis and treatment of OSA.
Wang et al. (12) contend that treatment with CPAP negates OSA-related increase in mortality in patients with CHF, but they do not definitively prove it. Patients with CHF and OSA were not randomly assigned to CPAP. Moreover, the majority of patients were not treated with CPAP for unclear reasons. Patients with CHF who are willing to comply with CPAP treatment may be more health conscious and thus more adherent to other treatment modalities and more likely to do well.
Treatment with CPAP has become the standard of care for moderate to severe OSA, and thus unbiased randomization of OSA patients to CPAP or no CPAP may no longer be feasible (17). Confronted with evidence that supports the use of CPAP in the management of OSA, physicians may not be willing to enroll patients with severe OSA into a randomized trial, thereby biasing the trial toward negative results. The use of a multivariate risk model to predict 1-, 2-, and 3-year mortality of patients with coexistent CHF and OSA who have accepted or refused treatment with CPAP may be a preferable and ethical approach for evaluating the effects of CPAP on clinical outcomes in this patient population (18).
Objective evaluation of the minimum CPAP adherence needed for reduction of mortality is also a worthwhile goal in patients with OSA and CHF. Wang et al. (12) reported CPAP adherence as self-reported "use" or "no use." Subjective or objective CPAP adherence data were not provided. Self reporting of CPAP adherence is notably unreliable (19). In a prospective study that covertly monitored objective CPAP adherence, 60% of patients claimed to use CPAP nightly; however, only 46% met criteria for regular use, and they overestimated CPAP use by more than 1 h (16). In the report by Wang et al. (12), the majority of patients with coexistent OSA and CHF did not receive CPAP treatment because they were not complaining of daytime sleepiness. Patients with moderate to severe OSA documented by nocturnal polysomnography should not be left untreated (17). One to three months of CPAP treatment increases left ventricular ejection fraction and improves quality of life in patients with coexistent CHF and OSA whether or not they complain of daytime sleepiness (20,21).
Lastly, CPAP therapy may not completely reverse the complications associated with OSA. Many patients with OSA continue to experience daytime sleepiness despite effective long-term CPAP therapy (22). Reduction of oxidative stress requires effective CPAP therapy for at least 3 months, whereas antioxidant defense remains partially impaired after 12 months of therapy in OSA patients (22–25). Adherence to treatment is hampered by the cumbersomeness of CPAP devices, and proper delivery of pressures is frequently impaired by ill-fitting facial interfaces and inadvertent leaks. Delayed diagnosis and poor adherence to CPAP treatment may contribute to the partial reversibility of OSA cardiovascular manifestations. Nevertheless, as observed in the study by Wang et al. (12), effective CPAP therapy may halt progression of the underlying cardiovascular condition. Therefore, early diagnosis of OSA and initiation of effective CPAP therapy are of paramount importance in patients with coexistent CHF and OSA. Future studies will establish the minimum duration of nightly CPAP therapy needed to offset the impact of OSA on morbidity and mortality in CHF.
In summary, the observational study by Wang et al. (12) points out the therapeutic usefulness of CPAP in patients with coexistent CHF and OSA. The findings of this observational study need to be confirmed by either a large randomized trial or a detailed registry of the use or lack of use of CPAP in patients with coexistent CHF and OSA. The latter approach seems preferable for ethical and practical reasons.
 |
Footnotes
|
|---|
* Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology. 
|
References
|
|---|
1. Young T, Peppard PE, Gottlieb DJ. Epidemiology of obstructive sleep apnea: a population health perspective Am J Respir Crit Care Med 2002;165:1217-1239.[Abstract/Free Full Text]2. Kapur V, Strohl KP, Redline S, Iber C, O’Connor G, Nieto J. Underdiagnosis of sleep apnea syndrome in U.S. communities Sleep Breath 2002;6:49-54.[CrossRef][Medline] 3. Ocasio-Tascon ME, Alicea-Colon E, Torres-Palacios A, Rodriguez-Cintron W. The veteran population: one at high risk for sleep-disordered breathing Sleep Breath 2006;10:70-75.[CrossRef][Web of Science][Medline] 4. Hedner J, Bengtsson-Bostrom K, Peker Y, Grote L, Rastam L, Lindblad U. Hypertension prevalence in obstructive sleep apnoea and sex: a population-based case-control study Eur Respir J 2006;27:564-570.[Abstract/Free Full Text] 5. Sin DD, Fitzgerald F, Parker JD, Newton G, Floras JS, Bradley TD. Risk factors for central and obstructive sleep apnea in 450 men and women with congestive heart failure Am J Respir Crit Care Med 1999;160:1101-1106.[Abstract/Free Full Text] 6. Ferrier K, Campbell A, Yee B, et al. Sleep-disordered breathing occurs frequently in stable outpatients with congestive heart failure Chest 2005;128:2116-2122.[CrossRef][Web of Science][Medline] 7. Rao A, Georgiadou P, Francis DP, et al. Sleep-disordered breathing in a general heart failure population: relationships to neurohumoral activation and subjective symptoms J Sleep Res 2006;15:81-88.[CrossRef][Web of Science][Medline] 8. Jelic S, Bartels MN, Mateika JH, Ngai P, DeMeersman RE, Basner RC. Arterial stiffness increases during obstructive sleep apneas Sleep 2002;25:850-855.[Web of Science][Medline] 9. Nieto FJ, Young TB, Lind BK, et al. Association of sleep-disordered breathing, sleep apnea, and hypertension in a large community-based studySleep Heart Health Study. JAMA 2000;283:1829-1836.[Abstract/Free Full Text] 10. Carlson JT, Hedner J, Elam M, Ejnell H, Sellgren J, Wallin BG. Augmented resting sympathetic activity in awake patients with obstructive sleep apnea Chest 1993;103:1763-1768.[CrossRef][Web of Science][Medline] 11. Shahar E, Whitney CW, Redline S, et al. Sleep-disordered breathing and cardiovascular disease: cross-sectional results of the Sleep Heart Health Study Am J Respir Crit Care Med 2001;163:19-25.[Abstract/Free Full Text] 12. Wang H, Parker JD, Newton GE, et al. Influence of obstructive sleep apnea on mortality in patients with heart failure J Am Coll Cardiol 2007;49:1625-1631.[Abstract/Free Full Text] 13. Bradley TD, Logan AG, Kimoff RJ, et al. Continuous positive airway pressure for central sleep apnea and heart failure N Engl J Med 2005;353:2025-2033.[Abstract/Free Full Text] 14. Yaggi HK, Concato J, Kernan WN, Lichtman JH, Brass LM, Mohsenin V. Obstructive sleep apnea as a risk factor for stroke and death N Engl J Med 2005;353:2034-2041.[Abstract/Free Full Text] 15. Marin JM, Carrizo SJ, Vicente E, Agusti AG. Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study Lancet 2005;365:1046-1053.[Web of Science][Medline] 16. Kribbs NB, Pack AI, Kline LR, et al. Objective measurement of patterns of nasal CPAP use by patients with obstructive sleep apnea Am Rev Respir Dis 1993;147:887-895.[Web of Science][Medline] 17. American Thoracic Society Indications and standards for use of nasal continuous positive airway pressure (CPAP) in sleep apnea syndromesOfficial statement adopted March 1944. Am J Respir Crit Care Med 1994;150:1738-1745.[Web of Science][Medline] 18. Levy WC, Mozaffarian D, Linker DT, et al. The Seattle Heart Failure Model: prediction of survival in heart failure Circulation 2006;113:1424-1433.[Abstract/Free Full Text] 19. Gay P, Weaver T, Loube D, Iber C. Evaluation of positive airway pressure treatment for sleep related breathing disorders in adults Sleep 2006;29:381-401.[Web of Science][Medline] 20. Kaneko Y, Floras JS, Usui K, et al. Cardiovascular effects of continuous positive airway pressure in patients with heart failure and obstructive sleep apnea N Engl J Med 2003;348:1233-1241.[Abstract/Free Full Text] 21. 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;169:361-366.[Abstract/Free Full Text] 22. Morisson F, Decary A, Petit D, Lavigne G, Malo J, Montplaisir J. Daytime sleepiness and EEG spectral analysis in apneic patients before and after treatment with continuous positive airway pressure Chest 2001;119:45-52.[Medline] 23. Carpagnano GE, Kharitonov SA, Resta O, Foschino-Barbaro MP, Gramiccioni E, Barnes PJ. 8-Isoprostane, a marker of oxidative stress, is increased in exhaled breath condensate of patients with obstructive sleep apnea after night and is reduced by continuous positive airway pressure therapy Chest 2003;124:1386-1392.[CrossRef][Web of Science][Medline] 24. Schulz R, Mahmoudi S, Hattar K, et al. Enhanced release of superoxide from polymorphonuclear neutrophils in obstructive sleep apneaImpact of continuous positive airway pressure therapy. Am J Respir Crit Care Med 2000;162:566-570.[Abstract/Free Full Text] 25. Barcelo A, Barbe F, de la Pena M, et al. Antioxidant status in patients with sleep apnoea and impact of continuous positive airway pressure treatment Eur Respir J 2006;27:756-760.[Abstract/Free Full Text]
Related Article
-
Influence of Obstructive Sleep Apnea on Mortality in Patients With Heart Failure
- Hanqiao Wang, John D. Parker, Gary E. Newton, John S. Floras, Susanna Mak, Kuo-Liang Chiu, Pimon Ruttanaumpawan, George Tomlinson, and T. Douglas Bradley
J. Am. Coll. Cardiol. 2007 49: 1625-1631.
[Abstract]
[Full Text]
[PDF]
This article has been cited by other articles:
|
|
|
|
 
J Amit Benjamin and K E Lewis
Sleep-disordered breathing and cardiovascular disease
Postgrad. Med. J.,
January 1, 2008;
84(987):
15 - 22.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
Obstructive Sleep Apnea and Heart Failure
Journal Watch (General),
May 8, 2007;
2007(508):
1 - 1.
[Full Text]
|
|
|
|
|
|
|
Untreated Obstructive Sleep Apnea Increases Mortality Risk in HF
Journal Watch Cardiology,
April 25, 2007;
2007(425):
3 - 3.
[Full Text]
|
|
|
|
Top
References