Selective ablation of ligament of Marshall reduces the prevalence of ventricular arrhythmias through autonomic modulation in a CsCl-induced long QT canine model

Abstract

Objective Previous studies have demonstrated that selective stimulation of sympathetic elements of ligament of Marshall(LOM), the distal segment of LOM that extends towards the left superior pulmonary vein(LOMLSPV), might induce ventricular arrhythmia(VA). The present study aimed to investigate the effect of selective ablation of LOMLSPV on VA. Methods In protocol 1, the blood pressure(BP)and ventricular effective refractory period(ERP)change as response to LOMLSPV stimulation and left stellate ganglion(LSG)stimulation were measured before and after LOMLSPV ablation in 8 anesthetized dogs.In protocol 2, 24 dogs were randomly divided into group 1(received CsCl alone, n=8), group 2(CsCl combined with LSG stimulation, n=8)and group 3(CsCl combined with LSG stimulation after LOMLSPV ablation, n=8). Early after-depolarization(EAD)amplitude, VA prevalence and the tachycardia threshold(measured according to the dose of CsCl administered)were compared among the three groups. Results In protocol 1, both LOMLSPV stimulation and LSG stimulation significantly increased BP and shortened ventricular ERP, both of which were significantly attenuated by LOMLSPV ablation.In protocol 2, compared with group 1, the prevalence of VA and EAD 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 group 1 and group 3(both 1.000 mmol/kg, P<0.05). Conclusion LOMLSPV ablation reduces the prevalence of VA induced by CsCl in combination with LSG stimulation in acquired long QT model, and the antiarrhythmic effect may involve the blockade of the sympathetic conduit between LSG and ventricles. Key words: Ligament of Marshall; Left stellate ganglion; Autonomic nervous system; Ventricular arrhythmia