Songyun Wang1, Zhibing Lu1, Wenbo He1, Bo He1, Jing Xie1, Xiaomei Yu1, Hong Jiang2. 1. Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute of Wuhan University, Wuhan, Hubei, People's Republic of China. 2. Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute of Wuhan University, Wuhan, Hubei, People's Republic of China. Electronic address: hong-jiang@whu.edu.cn.
Abstract
OBJECTIVES: The goal of this study was to investigate the effect of selective ablation of the ligament of Marshall (LOM) on ventricular arrhythmias (VAs). BACKGROUND: Previous studies have shown that selective stimulation of sympathetic elements of the LOM, the distal segment of the ligament of Marshall that extends beyond the left superior pulmonary vein (LOMLSPV), might induce VAs. METHODS: In protocol 1, the blood pressure and ventricular effective refractory period changes as a response to LOMLSPV stimulation and left stellate ganglion (LSG) stimulation were measured before and after LOMLSPV ablation in 8 anesthetized dogs. In protocol 2, a total of 24 dogs were randomly divided into group 1 (cesium alone, n = 8), group 2 (cesium combined with LSG stimulation, n = 8), and group 3 (cesium combined with LSG stimulation after LOMLSPV ablation, n = 8). Early afterdepolarization amplitude, VA prevalence, and the tachycardia threshold (measured according to the dose of cesium administered) were compared among the groups. RESULTS: In protocol 1, both LOMLSPV stimulation and LSG stimulation significantly increased blood pressure and shortened the ventricular effective refractory period, both of which were significantly attenuated by LOMLSPV ablation. In protocol 2, compared with group 1, the prevalence of VAs and the early afterdepolarization amplitudes were significantly augmented in group 2 and were maintained at a comparable level in group 3. Furthermore, the tachycardia threshold in group 2 (0.625 mmol/kg) was significantly lower than that noted in groups 1 and 3 (both 1.000 mmol/kg; p < 0.05). CONCLUSIONS: LOMLSPV ablation reduced the prevalence of the VAs induced by cesium in combination with LSG stimulation, and the antiarrhythmic effect may involve the blockade of the sympathetic conduit between the LSG and the ventricles.
OBJECTIVES: The goal of this study was to investigate the effect of selective ablation of the ligament of Marshall (LOM) on ventricular arrhythmias (VAs). BACKGROUND: Previous studies have shown that selective stimulation of sympathetic elements of the LOM, the distal segment of the ligament of Marshall that extends beyond the left superior pulmonary vein (LOMLSPV), might induce VAs. METHODS: In protocol 1, the blood pressure and ventricular effective refractory period changes as a response to LOMLSPV stimulation and left stellate ganglion (LSG) stimulation were measured before and after LOMLSPV ablation in 8 anesthetized dogs. In protocol 2, a total of 24 dogs were randomly divided into group 1 (cesium alone, n = 8), group 2 (cesium combined with LSG stimulation, n = 8), and group 3 (cesium combined with LSG stimulation after LOMLSPV ablation, n = 8). Early afterdepolarization amplitude, VA prevalence, and the tachycardia threshold (measured according to the dose of cesium administered) were compared among the groups. RESULTS: In protocol 1, both LOMLSPV stimulation and LSG stimulation significantly increased blood pressure and shortened the ventricular effective refractory period, both of which were significantly attenuated by LOMLSPV ablation. In protocol 2, compared with group 1, the prevalence of VAs and the early afterdepolarization amplitudes were significantly augmented in group 2 and were maintained at a comparable level in group 3. Furthermore, the tachycardia threshold in group 2 (0.625 mmol/kg) was significantly lower than that noted in groups 1 and 3 (both 1.000 mmol/kg; p < 0.05). CONCLUSIONS:LOMLSPV ablation reduced the prevalence of the VAs induced by cesium in combination with LSG stimulation, and the antiarrhythmic effect may involve the blockade of the sympathetic conduit between the LSG and the ventricles.