Sleep apnoea is a common and important co-morbidity in heart failure. It affects survival adversely by: (1) causing nocturnal hypoxia and oxidative stress; (2) raising nocturnal and daytime sympathetic activity and blood pressure and blunting vagal tone; and (3) increasing left ventricular transmural pressure (that is, afterload) and myocardial oxygen demand. Although its abolition by positive airway pressure counters these mechanisms of increased cardiovascular risk and augments ejection fraction, this device therapy has not been adopted widely in cardiovascular practice. An adequately powered outcome trial is required to determine whether sleep apnoea should be a specific therapeutic target in heart failure.
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Funding: The author holds the Canada Research Chair in Integrative Cardiovascular Biology and is a Career Investigator of the Heart and Stroke Foundation of Ontario. This article refers to original research funded by the Canadian Institutes of Health Research (MOP82731; MOP11607; UI-14909) and the Heart and Stroke Foundation of Ontario (PRG 5276; T4938; T4050).
Competing interests: In 2005 the author received an honorarium for speaking at a scientific symposium of the Japanese Circulation Society (Respironics Inc). The author is presently one of a group of investigators applying for Canadian Institutes of Health Research-University-Industry Grant funding for a clinical trial of positive airway pressure for sleep apnoea in heart failure. Respironics Inc is the industrial partner.
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