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Circulation. 2007;115:3140-3142
doi: 10.1161/CIRCULATIONAHA.107.709303
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(Circulation. 2007;115:3140-3142.)
© 2007 American Heart Association, Inc.


Editorial

Treating Central Sleep Apnea in Heart Failure

Outcomes Revisited

Lyle J. Olson, MD; Virend K. Somers, MD, PhD

From the Division of Cardiovascular Diseases, Department of Internal Medicine, Mayo Clinic College of Medicine, Rochester, Minn.

Correspondence 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 somers.virend@mayo.edu


Key Words: Editorials • heart failure • sleep


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

A 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.1,2


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Figure 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 3173

Of 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 . . . [Full Text of this Article]




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CirculationHome page
V. K. Somers, D. P. White, R. Amin, W. T. Abraham, F. Costa, A. Culebras, S. Daniels, J. S. Floras, C. E. Hunt, L. J. Olson, et al.
Sleep Apnea and Cardiovascular Disease: An American Heart Association/American College of Cardiology Foundation Scientific Statement From the American Heart Association Council for High Blood Pressure Research Professional Education Committee, Council on Clinical Cardiology, Stroke Council, and Council on Cardiovascular Nursing In Collaboration With the National Heart, Lung, and Blood Institute National Center on Sleep Disorders Research (National Institutes of Health)
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J Am Coll CardiolHome page
V. K. Somers, D. P. White, R. Amin, W. T. Abraham, F. Costa, A. Culebras, S. Daniels, J. S. Floras, C. E. Hunt, L. J. Olson, et al.
Sleep Apnea and Cardiovascular Disease: An American Heart Association/American College of Cardiology Foundation Scientific Statement From the American Heart Association Council for High Blood Pressure Research Professional Education Committee, Council on Clinical Cardiology, Stroke Council, and Council on Cardiovascular Nursing In Collaboration With the National Heart, Lung, and Blood Institute National Center on Sleep Disorders Research (National Institutes of Health)
J. Am. Coll. Cardiol., August 19, 2008; 52(8): 686 - 717.
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