Effect of low-level electrical stimulation of the arotic root ven | 53497
Clinical & Experimental Cardiology

Clinical & Experimental Cardiology
Open Access

ISSN: 2155-9880

+44 1300 500008

Effect of low-level electrical stimulation of the arotic root ventricular ganglionated plexi on electrical and structural remodling in dogs with heart failure

8th Global Cardiologists & Echocardiography Annual Meeting

July 18-20, 2016 Berlin, Germany

Hong-Tao Wang, Fei-Fei Su, Di Zeng, Boyuan-Fan,Jun Li and Qiang-sun Zheng

Fourth Military Medical University, China

Posters & Accepted Abstracts: J Clin Exp Cardiolog

Abstract :

Background: Low-level electrical stimulation (LL-ES) of automomic nerve was reported to suppress atrial fibrillation (AF) by inhibiting the intrinsic cardiac autonomic nervous system and bring both anti- arrhythmia and anti-inflammation effect. However, it was still unknown whether LL-ES could reverse the structural remodeling of myocardial fibrosis and atrial enlargement following heart failure (HF) Aim: This study was designed to investigate the anti-cardiac remodeling effect of LL-ES of the aortic root ventricular GP. Method: Twenty dogs were randomly divided into control group and LL-ES group after rapid right ventricle pacing was performed to establish heart failure model. Following a week of LL-ES of the aortic root ventricular GP, bioactive factors for HF including angiotensin II, TGF-�?², mitogen-activated protein kinase (MAPK), matrix metalloproteinase (MMP) was assessed. Furthermore, ventricle size, cardiac fibrosis as well as left ventricular ejection fraction were also determined. Results: Compared by control group, expression of angiotensin II, TGF-�?², MAPK, and MMP were significantly down-regulated in LL-ES group (P<0.05). Moreover, the volume of left ventricle and cardiac fibrosis were markedly decreased, and LVEF in LL-ES group was significantly increased compared with those in control group (P<0.05). Conclusion: Long term LL-ES of the aortic root ventricular GP improved rapid pacing induced cardiac structural and functional remodeling by attenuating the sympathetic tone.

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