Circulation. 2003;107:1671-1678
doi: 10.1161/01.CIR.0000061757.12581.15
doi: 10.1161/01.CIR.0000061757.12581.15
(Circulation. 2003;107:1671.)
© 2003 American Heart Association, Inc.
Special Review |
Sleep Apnea and Heart Failure
Part I: Obstructive Sleep Apnea
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 • sleep apnea
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
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Introduction |
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Heart failure (HF) affects 5 to 6 million North Americans and is increasing in prevalence.1 Mortality remains high. In Ontario, for example, between 1994 and 1997, approximately 33% of patients diagnosed with HF on first admission to hospital died within 1 year.2 Reductions in mortality demonstrated in randomized clinical trials of pharmacological agents, such as ß-receptor blockers3 and angiotensin-converting enzyme inhibitors,4 have been slow to translate into substantial reductions in death and hospitalization rates in community-based HF populations. These figures have remained relatively constant between 1948 and 1997.2,5–7 In more recent clinical trials, the addition of newer agents has had a marginal, neutral, or even adverse impact on the high residual mortality of optimally treated patients.8,9 Accordingly, investigators such as Massie10 have raised the concern that there may be limits to the benefits achievable through conventional pharmacological strategies. Resource-intensive interventions, such as left ventricular assist devices or heart transplantation, are available to only a small minority of patients. Therefore, there remains a need to develop novel, widely applicable, and cost-effective approaches to the therapy of HF.
An important limitation to the current guidelines for the evaluation and management of chronic HF is their focus on the patient as he/she presents while awake.1 This approach presupposes that any mechanisms that might contribute to the pathophysiology or progression of HF are quiescent during sleep. Our objective in this review, therefore, is to highlight the pathophysiological and therapeutic implications of co-existing sleep apnea in patients with HF.
There are 2 major forms of
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