Cheyne-Stokes respiration (CSR) may trigger ventricular arrhythmia in patients with heart failure with reduced ejection fraction (HFrEF) and central sleep apnoea (CSA). This study determined the prevalence and predictors of a high nocturnal ventricular arrhythmia burden in patients with HFrEF and CSA (with and without CSR) and to evaluate the temporal association between CSR and the ventricular arrhythmia burden.This cross-sectional ancillary analysis included 239 participants from the SERVE-HF major sub-study who had HFrEF and CSA, and nocturnal ECG from polysomnography. CSR was stratified in ≥20% and <20% of total recording time (TRT). High burden of ventricular arrhythmia was defined as >30 premature ventricular complexes (PVCs) per hour of TRT. A sub-analysis was performed to evaluate the temporal association between CSR and ventricular arrhythmias in sleep stage N2.High ventricular arrhythmia burden was observed in 44% of patients. In multivariate logistic regression analysis, male sex, lower systolic blood pressure, non-use of antiarrhythmic medication and CSR ≥20% were significantly associated with PVC >30/h (odds ratio [95% confidence interval]: 5.49 [1.51–19.91], p=0.010; 0.98 [0.97–1.00], p=0.017; 5.02 [1.51–19.91], p=0.001; and 2.22 [1.22–4.05]; p=0.009; respectively). PVCs occurred more frequently during sleep phases with versus without CSR (median [interquartile range]: 64.6 [24.8–145.7] versus 34.6 [4.8–75.2]/h N2 sleep; p=0.006).Further mechanistic studies and arrhythmia analysis of major randomised trials evaluating the effect treating CSR on ventricular arrhythmia burden and arrhythmia-related outcomes are warranted to understand how these data match with the results of the parent SERVE-HF study.
BackgroundThe SERVE-HF trial investigated the effect of treating central sleep apnoea (CSA) with adaptive servo-ventilation (ASV) in patients with heart failure with reduced ejection fraction (HFrEF).ObjectiveThe aim of the present ancillary analysis of the SERVE-HF major substudy (NCT01164592) was to assess the effects of ASV on the burden of nocturnal ventricular arrhythmias as one possible mechanism for sudden cardiac death in ASV-treated patients with HFrEF and CSA.MethodsThree hundred twelve patients were randomized in the SERVE-HF major substudy [no treatment of CSA (control) vs. ASV]. Polysomnography including nocturnal ECG fulfilling technical requirements was performed at baseline, and at 3 and 12 months. Premature ventricular complexes (events/h of total recording time) and non-sustained ventricular tachycardia were assessed. Linear mixed models and generalized linear mixed models were used to analyse differences between the control and ASV groups, and changes over time.ResultsFrom baseline to 3- and 12-month follow-up, respectively, the number of premature ventricular complexes (control: median 19.7, 19.0 and 19.0; ASV: 29.1, 29.0 and 26.0 events/h; p = 0.800) and the occurrence of ≥1 non-sustained ventricular tachycardia/night (control: 18, 25, and 18% of patients; ASV: 24, 16, and 24% of patients; p = 0.095) were similar in the control and ASV groups.ConclusionAddition of ASV to guideline-based medical management had no significant effect on nocturnal ventricular ectopy or tachyarrhythmia over a period of 12 months in alive patients with HFrEF and CSA. Findings do not further support the hypothesis that ASV may lead to sudden cardiac death by triggering ventricular tachyarrhythmia.
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