for their deployment can be advocated (Table). However, the promise of observational studies and randomized trials of small size and duration describing a beneficial effect of treating SDB in HF via positive airway pressure (PAP) was not realized in 2 recent randomized outcome-driven trials: SAVE, which evaluated the cardiovascular effect of treating OSA in a cohort without HF, 7 and SERVE-HF, which reported the results of a strategy of random allocation of minute-ventilation-triggered adaptive servo-ventilation (ASV) for HF patients with CSA. 3 Consequently, equipoise remains as to whether either OSA or CSA, once detected in a HF patient with reduced left ventricular ejection fraction (LVEF), should be therapeutically suppressed. The threefold purpose of this review was to: (1) summarize current knowledge concerning the prevalence, pathophysiology, and prognostic implications of SDB in HF in support of treatment; (2) examine and reflect upon the results of randomized controlled trials evaluating the effect of treating OSA or CSA on cardiovascular endpoints and mortality; and (3) illustrate how ADVENT-HF, a randomized controlled trial designed to determine the effect of treating HF patients with either CSA or nonsleepy OSA using a peak-airflow triggered ASV algorithm, could resolve the present clinical equipoise concerning the treatment of one or both forms of SDB.A fundamental and as yet unresolved question for the heart failure (HF) community is whether coexisting obstructive (OSA) or central sleep apnea (CSA) should be specific targets of therapy. For individuals without HF, the principal clinical indication to treat sleep apnea is to improve quality of life (QOL) and avert accidental injury or death by alleviating daytime hypersomnolence. However, this indication does not pertain to the majority of patients with reduced left ventricular systolic function and sleep-disordered breathing (SDB) as they are not burdened by excess daytime sleepiness. 1-3 In such individuals, the impetus to diagnosis and treatment is the hypothesis that attenuation or abolition of SDB will modify beneficially the natural history of HF.OSA and CSA interrupt breathing by different mechanisms but impose qualitatively similar autonomic, chemical, mechanical, and inflammatory burdens on the heart and circulation. 4-6 Because contemporary evidence-based drug and device HF therapies have little or no mitigating effect on the acute consequences of such stimuli or on the long-term structural and functional adaptations they induce within the atria and ventricles, the brain and the peripheral vasculature, there is a sound mechanistic rationale for targeting SDB to reduce cardiovascular event rates and prolong life. Importantly, effective treatment is presently available for both OSA and CSA and cogent reasons Sleep-disordered breathing (SDB) occurs in approximately 50% of patients with reduced left ventricular ejection fraction receiving contemporary heart failure (HF) therapies. Obstructive (OSA) and central sleep apneas (CSA) interrupt brea...