Effect of adaptive servo-ventilation for central sleep apnoea in systolic heart failure on muscle sympathetic nerve activity: a SERVE-HF randomised ancillary study.

Background: Adaptive servo-ventilation (ASV) effectively suppresses central sleep apnoea (CSA) but has been associated with increased all-cause and cardiovascular mortality in chronic heart failure patients with reduced ventricular ejection fraction (HFrEF). All-cause and, especially, cardiovascular mortality in chronic heart failure is highly correlated with sympathetic tone. This analysis of SERVE-HF data investigated the effect of ASV on sympathetic tone in patients with HFrEF and CSA.
Methods: HFrEF patients in the SERVE-HF trial (left ventricular ejection fraction (LVEF) ≤45%, apnoea-hypopnoea index (AHI) ≥15 events·h ^-1 with predominant CSA) were randomly assigned to receive guideline-based heart failure treatment alone (controls) or plus ASV. For this analysis, the primary outcome was change in muscle sympathetic nerve activity (MSNA) at 3-month follow-up. The effects of baseline MSNA and change in MSNA over time on mortality in the main study were also assessed.
Results: 40 patients with HFrEF were included in this analysis (age 71.3±11.7 years, LVEF 34.2±7.7%, 57.5% in New York Heart Association (NYHA) Functional Class II, 42.5% in NYHA Functional Class III, AHI 35.2±11 events·h ^-1 ). Sympathetic tone evolution during follow-up did not differ between groups (controls: 47.6±8.3 bursts·min ^-1 at baseline to 44.6±11.2 bursts·min ^-1 ; ASV group: 43.0±9.0 bursts·min ^-1 at baseline to 42.74±9.45 bursts·min ^-1 ). The reduction in sympathetic tone was associated with significantly increased cardiovascular mortality in the ASV group, whereas in the control group reduced sympathetic tone appeared to be protective.
Conclusions: Suppression of CSA with ASV did not seem to have a significant effect on chronic heart failure-related sympathetic activation. Simultaneous suppression of CSA and reduction in MSNA was associated with increased cardiovascular mortality.
Competing Interests: Conflict of interest: R. Tamisier reports lecture fees from ResMed, grant support through his institution from ResMed, Agiradom and Philips, and travel grants from Agiradom. J-L. Pépin reports grant support through his institution from ResMed, Agiradom, Vutalaire and Philips, and travel grants from Agiradom. H. Woehrle reports no conflict of interest. M. Salvat reports no conflict of interest. G. Barone-Rochette reports research grants from Merck Sharp and Dohme, Fondation de France, INSERM, Fédération Française de Cardiologie and Société Française de Cardiologie, and consulting fees from Bayer. C. Rocca reports no conflict of interest. E. Vettorazzi reports institutional research grants from ResMed. H. Teschler reports no conflict of interest. M. Cowie reports no conflict of interest. P. Lévy reports no conflict of interest.
(Copyright ©The authors 2023.)