Antifibrillatory effects of renal denervation on ventricular fibrillation in a canine model of pacing-induced heart failure

Abstract

This study investigated the effects of renal denervation (RDN) on vulnerability to ventricular fibrillation (VF) and ventricular electrical properties in a canine model of pacing-induced heart failure (HF). Eighteen beagles were divided into the following three groups: control (n = 6), HF (n = 6) and HF+RDN (n = 6). HF was induced by rapid right ventricular pacing. RDN was performed simultaneously with the pacemaker implantation in the HF+RDN group. A 64-unipolar basket catheter was used to perform global endocardial mapping of the left ventricle. The restitution properties and dispersion of refractoriness were estimated from the activation recovery intervals (ARI) by a pacing protocol. The VF threshold (VFT) was defined as the maximal pacing cycle length required to induce VF using a specific pacing protocol. The defibrillation threshold (DFT) was measured by an up-down algorithm. RDN partially restored left ventricular (LV) systolic function and attenuated the process of HF. Compared to the control group, the VFT in the HF group was decreased by 27% (106 ± 8.0 ms vs. 135 ± 10 ms, P < 0.01). However, RDN increased the VFT by 13% (135 ± 10 ms vs. 118 ± 7.5 ms, P < 0.05) and decreased the DFT by 27% (30 ± 6.3 J vs. 21.8 ± 4.7 J, P < 0.05) in the treated hearts compared to the failing hearts. RDN significantly flattened the ventricular ARI restitution curve by 15% (1.48 ± 0.2 vs. 1.26 ± 0.11, P < 0.05) and decreased the dispersion of ARI by 25% (0.08 ± 0.02 vs. 0.06 ± 0.01, P < 0.01) in the treated group compared to the HF group. The findings of this study suggest that RDN can attenuate ventricular electrical remodeling and exert potential antifibrillatory action on VF in a canine model of pacing-induced HF.

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