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Circulation. 2003;107:1822-1826
doi: 10.1161/01.CIR.0000061758.05044.64
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(Circulation. 2003;107:1822.)
© 2003 American Heart Association, Inc.


Special Review

Sleep Apnea and Heart Failure

Part II: Central Sleep Apnea

T. Douglas Bradley, MD; John S. Floras, MD, DPhil

From the University of Toronto Centre for Sleep Medicine and Circadian Biology (T.D.B., J.S.F.), the Cardiopulmonary Sleep Disorders and Research Centre of the Toronto General Hospital/University Health Network (T.D.B.) and the Toronto Rehabilitation Institute (T.D.B.), and the Departments of Medicine of the University Health Network and Mount Sinai Hospital (T.D.B., J.S.F.), Toronto, Ontario, Canada.

Correspondence to T. Douglas Bradley, MD, Toronto General Hospital/University Health Network, NU 9-112, 200 Elizabeth St, Toronto, ON, M5G 2C4, Canada. E-mail douglas.bradley@utoronto.ca


Key Words: heart failure • respiration • morbidity


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


*    Introduction
 
In the first part of this 2-part review, we provided a synopsis of the cardiovascular effects of normal sleep and an overview of the diagnostic, pathophysiological, and therapeutic implications of obstructive sleep apnea (OSA) in the setting of heart failure (HF). In this second part, we turn our attention to central sleep apnea (CSA), commonly referred to as Cheyne-Stokes respiration. This breathing disorder has a strikingly higher prevalence in patients with HF as compared with the general population with normal left ventricular function, and when present appears to have adverse prognostic implications. Our objective in Part II of this review is to provide a broad perspective of the pathophysiological and clinical significance of CSA in HF.


*    Pathophysiology
 
CSA associated with Cheyne-Stokes respiration is a form of periodic breathing in which central apneas and hypopneas alternate with periods of hyperventilation that have a waxing-waning pattern of tidal volume. Figure 1 illustrates the proposed mechanisms that underlie periodic oscillations in ventilation in HF. Unlike OSA, CSA likely arises as a consequence of HF. Thus, the presence of CSA may alert the physician to the necessity of intensifying HF therapy. The current debate is whether CSA is simply a reflection of severely compromised cardiac function with elevated left ventricular filling pressures, or whether, for the same degree of cardiac dysfunction, CSA exerts unique and independent pathological effects on the failing myocardium. Although there are not yet sufficient data to resolve this controversy within the confines of this review, we will discuss evidence on both . . . [Full Text of this Article]




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