Catheter Ablation of Cardiac Fat Pads Attenuates Bezold-Jarisch Reflex in Dogs

• Published in: Journal of cardiovascular electrophysiology Vol. 22; no. 5; pp. 573 - 578
• Main Authors: XIA, YANG, ZHAO, WEI, YANG, ZHI-JIAN, ZHANG, JIA-YOU, ZHAO, LIANG, GU, XING-JIAN, ZHAO, XUE, LÜ, FEI, WU, ZONG-GUI, LIAO, DE-NING
• Format: Journal Article
• Language: English
• Published: Malden, USA Blackwell Publishing Inc 01.05.2011
• Subjects: Adipose Tissue - innervation; Adipose Tissue - physiopathology; Adipose Tissue - surgery; Animals; Bezold-Jarisch reflex; cardiac fat pad; Cardiac Surgical Procedures - methods; catheter ablation; Catheter Ablation - methods; Dogs; Female; Heart - innervation; Heart - physiopathology; Male; neurally mediated syncope; Reflex; Treatment Outcome; vagus ganglion; Vagus Nerve - physiopathology; Vagus Nerve - surgery
• ISSN: 1045-3873; 1540-8167
• DOI: 10.1111/j.1540-8167.2010.01922.x

Ablation of Cardiac Fat Pads and BJR. Background: Bezold–Jarisch reflex (BJR) plays an important role in the pathophysiology of several cardiovascular disorders. Radiofrequency catheter ablation (RFCA) of the vagal ganglia in cardiac fat pads (FPs) may attenuate BJR. The purpose of this study was to examine the effects of RFCA of the cardiac FPs on veratridine‐induced BJR in dogs. Methods and Results: This study was performed in 30 pentobarbital‐anesthetized and open‐chest dogs: control group received no ablation (n = 15); and ablation group (n = 15) received epicardial ablation of the 3 FPs located near the right pulmonary vein, the inferior vena cava, and the aortic root. The BJR was induced by injection of veratridine (15 μg/kg) into the left ventricle. Before injection of veratridine, there were no significant differences in heart rate (HR), systolic arterial pressure (SAP), diastolic arterial pressure (DAP), mean arterial pressure (MAP), left ventricular systolic pressure (LVSP), left ventricle end‐diastolic pressure (LVEDP), left ventricular peak systolic and diastolic velocity (±dp/dtmax) between these 2 groups (P > 0.05). However, the veratridine‐induced decrease of HR in ablation group was significantly lower than that in control group (22.9 ± 8.5 bpm vs 93.3 ± 18.4 bpm, P < 0.01). There were no differences in the reduction of SAP, DAP, MAP, LVSP, LVEDP and dp/dtmax between both groups (P > 0.05). Conclusions: RFCA of the cardiac FPs significantly attenuated veratridine‐induced cardio‐vagal component but not the vasodepressor component of the BJR. This might have therapeutic implications in BJR‐related disorders such as cardio‐inhibitory vasovagal syncope. (J Cardiovasc Electrophysiol, Vol. 22, pp. 573‐578 May 2011)