Anti‐arrhythmic and anti‐heart failure effects of low‐level electrical stimulation on aortic root ventricular ganglionated plexi

• Published in: Pacing and clinical electrophysiology Vol. 44; no. 11; pp. 1817 - 1823
• Main Authors: Wang, Hong‐Tao, Sun, Hong‐Ke, Jin, Ai‐Ping, Jiang, Wei, Zhang, Yan, Su, Fei‐Fei, Zheng, Qiang‐sun
• Format: Journal Article
• Language: English
• Published: United States Wiley Subscription Services, Inc 01.11.2021
• Subjects: Angiotensin; Angiotensin II; Animals; Aorta; aortic root ventricular ganglionated plexi; Arrhythmia; Arrhythmias, Cardiac - physiopathology; Arrhythmias, Cardiac - prevention & control; Biomarkers - blood; Cardiac arrhythmia; Congestive heart failure; Disease Models, Animal; Dogs; Electric Stimulation; Electrical stimuli; Extracellular signal-regulated kinase; Ganglia, Autonomic - physiology; Heart Atria - physiopathology; Heart failure; Heart Failure - physiopathology; Heart Failure - prevention & control; Heart Ventricles - innervation; Heart Ventricles - physiopathology; Inflammation; Kinases; low‐level electrical stimulation; Matrix metalloproteinase; Metalloproteinase; Placebos; Stroke Volume; Tachycardia; Transforming growth factor-b; Ventricle; heart failure; low-level electrical stimulation; aortic root ventricular ganglionated plexi; arrhythmia
• ISSN: 0147-8389; 1540-8159
• DOI: 10.1111/pace.14261

Background It remains uncertain whether low‐level electrical stimulation (LL‐ES) of the ventricular ganglionated plexi (GP) improves heart function. This study investigated the anti‐arrhythmic and anti‐heart failure effects of LL‐ES of the aortic root ventricular GP (ARVGP). Methods Thirty dogs were divided randomly into control, drug, and LL‐ES groups after performing rapid right ventricular pacing to establish a heart failure (HF) model. The inducing rate of arrhythmia; levels of bioactive factors influencing HF, including angiotensin II type I receptor (AT‐1R), transforming growth factor‐beta (TGF‐β), matrix metalloproteinase (MMP), and phosphorylated extracellular signal‐regulated kinase (p‐ERK1/2); left ventricular stroke volume (LVSV), and left ventricular ejection fraction (LVEF)were measured after treatment with placebo, drugs, and LL‐ES. Results The inducing rate of atrial arrhythmia decreased from 60% in the control group to 50% in the drug group and 10% in the LL‐ES group (p = .033 vs. drug group) after 1 week of treatment. The ventricular effective refractory period was prolonged from 139 ± 8 ms in the drug group to 166 ± 13 ms in the LL‐ES group (p = .001). Compared to the drug group, the expressions of AT‐1R, TGF‐β, and MMP proteins were down‐regulated in the LL‐ES group, whereas that of p‐ERK1/2 was significantly increased (all p = .001). Moreover, in the LL‐ES group, LVSV increased markedly from 13.16 ± 0.22 to 16.86 ± 0.27 mL, relative to that in the drug group (p = .001), and LVEF increased significantly from 38.48% ± 0.53% to 48.94% ± 0.57% during the same time frame (p = .001). Conclusion Short‐term LL‐ES of ARVGP had both anti‐arrhythmic and anti‐inflammatory effects and contributed to the treatment of tachycardia‐induced HF and its associated arrhythmia.