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 (i.e., 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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