Renal sympathetic denervation suppresses ventricular substrate remodelling in a canine high-rate pacing model

This study sought to assess whether renal sympathetic denervation (RSD) could suppress ventricular substrate remodelling and attenuate heart failure (HF) progression.

Nineteen dogs were randomised into three groups - seven sham-operated controls, six with right ventricular pacing to induce HF, and six with RSD followed eight weeks later by pacing induction of HF. Haemodynamic variables were monitored at baseline and after HF. Levels of ventricular interstitial fibrosis, BNP, Ang II, aldosterone and TGF-β were measured. All the dogs in the HF and HF﹢RSD groups showed increased left and right ventricular diastolic dimensions, but the dogs in the HF﹢RSD group had a higher left ventricular ejection fraction (LVEF) than the HF dogs (0.42±0.05 vs. 0.35±0.04, p<0.01). Compared with the dogs with HF alone, the HF+RSD dogs had lower left ventricular end-diastolic pressure (LVEDP) (3.3±1.6 vs. 25±3.7 mmHg, p<0.01) and less fibrous tissue. The levels of BNP, Ang II, aldosterone and TGF-β expression in ventricular tissue were higher in the HF dogs than in the sham-operated and HF﹢RSD dogs.

RSD suppressed ventricular substrate remodelling induced by long-term rapid ventricular pacing.