Peer-review started: August 30, 2018
First decision: Octorber 26, 2018
Revised: December 13, 2018
Accepted: January 5, 2019
Article in press: January 5, 2019
Published online: January 17, 2019
Processing time: 140 Days and 17.5 Hours
Heart failure (HF) is known to be associated with sleep-disordered breathing (SDB). In addition to disturbing patients’ sleep, SDB is also associated with a deterioration in the cardiac function and an increased mortality and morbidity. Central sleep apnea (CSA), typically characterized by Cheyne-Stokes breathing (CSB), is increasingly found in patients with HF compared to the general population. An important pathogenetic factor of CSA seen in HF patients is an instability in the control of the respiratory system, characterized by both hypocapnia and increased chemosensitivity. Sympathetic overactivation, pulmonary congestion and increased chemosensitivity associated with HF stimulate the pulmonary vagal irritant receptor, resulting in chronic hyperventilation and hypocapnia. Additionally, the repetitive apnea and arousal cycles induce cyclic sympathetic activation, which may worsen the cardiac prognosis. Correcting CSB may improve both patient’s quality of life and HF syndrome itself. However, a treatment for HF in patients also experiencing CSA is yet to be found. In fact, conflicting results from numerous clinical studies investigating sleep apnea with HF guide to a troubling question, that is whether (or not) sleep apnea should be treated in patients with HF? This editorial attempts to both collect the current evidence about randomized control trials investigating CSA in patients with HF and highlight the effect of specific CSA treatments on cardiovascular endpoints.
Core tip: Central sleep apnea (CSA) is commonly comorbid with heart failure (HF). In fact, sleep apnea is associated with a worsening of the cardiac prognosis and an increasing mortality. However, treatment for CSA remains to be elucidated due to the numerous conflicting results of clinical trials. This review attempts to both clarify the current evidence from randomized control trials investigating CSA in patients with HF and highlight the effect of specific CSA treatments on cardiovascular endpoints.