Sleep-disordered breathing in heart failure.

PURPOSE OF REVIEW: This review addresses the evolving intersection of sleep-disordered breathing (SDB) and heart failure, a topic of increasing clinical significance due to the high prevalence of SDB in heart failure patients and its impact on morbidity and mortality. It reflects recent advancements in diagnostic methodologies and therapeutic strategies. It emphasizes the need for heightened awareness among healthcare providers about the complex relationship between SDB and various forms of heart failure. RECENT FINDINGS: Recent studies underscore the high incidence of SDB in heart failure patients, varying with the cause of heart failure. Emerging diagnostic tools, including home sleep tests and advanced inpatient screening methods, have improved the early detection and accurate diagnosis of SDB. Novel treatment modalities, like hypoglossal and phrenic nerve stimulation, are promising, especially where conventional therapies are inadequate. The review also discusses the complexities of managing SDB in the context of different heart failure subtypes. SUMMARY: Findings from recent literature suggest that improved screening, diagnosis, and innovative treatment of SDB in heart failure patients can reduce morbidity, mortality, and healthcare costs. This review emphasizes the need for personalized treatment approaches tailored to individual patient profiles, highlighting the potential of new technologies and multidisciplinary strategies in clinical practice.

Ventricular assist devices and sleep-disordered breathing-A mechanical heart stimulating a sleepy brain.

Sleep-disordered breathing, including obstructive sleep apnea (OSA) and central sleep apnea (CSA), is common in severe heart failure (HF) patients. There is limited data on the effect of left ventricular assist devices (LVAD) on sleep apnea. We performed a retrospective review of 350 durable LVAD patients and found 5 with a history of pre- and post-LVAD sleep studies. All five patients had OSA, and three had concomitant CSA. We observed reduced apnea-hypopnea index following LVAD placement. This was due to a near abolishment of CSA in three mixed sleep apnea patients-as seen by a central apnea index improvement from an average of 25.9 ± 13.1 to 1.4 ± 2.5 events per hour (p = 0.063). LVAD placement was associated with an increase in thermodilution cardiac output from 2.7 ± 0.6 to 4.1 ± 1.1 L/min (p = 0.014). These findings support chemoreception physiology seen in patients with poor circulation and the effect of restoring this circulation with LVAD support.