[Renal sympathetic denervation suppresses ventricular substrate remodeling in a canine high-rate pacing model]

To explore the role of renal sympathetic denervation (RSD) on ventricular substrate remodeling in dogs with pacing-induced heart failure (HF).

A total of 19 dogs were randomized into 3 groups of sham-operated control (n = 7), right ventricular pacing induction of HF (n = 6) and RSD (n = 6). After 8-week pacing induction of HF. Hemodynamic variables were monitored at baseline and after HF. Masson's trichrome staining, enzyme-linked immunosorbent assay (ELISA) and Western blot were used to measure ventricular interstitial fibrosis, brain natriuretic peptide (BNP), angiotensin II (Ang II), aldosterone and transforming growth factor-beta (TGF-β).

All dogs in HF and HF+RSD groups showed increased left and right ventricular diastolic dimensions [left ventricle: (27.0 ± 2.4) vs (37.0 ± 2.8) mm, P < 0.01 and (30.0 ± 2.5) vs (36.0 ± 2.8) mm, P < 0.05; right ventricle: (11.0 ± 1.5) vs (14.0 ± 1.7) mm, P = 0.03 and (12.0 ± 1.1) vs (14.0 ± 1.2) mm, P < 0.05]. Compared with HF + RSD dogs, HF dogs had higher left ventricular end-diastolic pressure (LVEDP) [(25.0 ± 3.7) vs (3.3 ± 1.6) mmHg, P < 0.01] and more fibrous tissue (left ventricle:24.1% ± 4.8% vs 8.5% ± 1.9%, P < 0.01; right ventricle:17.2% ± 5.2% vs 11.8% ± 3.9%, P < 0.01). The levels of BNP, Ang II, aldosterone and TGF-β in ventricular tissue increased in HF dogs compared to sham-operated and HF+RSD dogs.

RSD could suppress ventricular substrate remodeling induced by long-term rapid ventricular pacing.