Selective ablation of ligament of Marshall inhibits ventricular arrhythmias during acute myocardial infarction: Possible mechanisms.

Abstract

Our recent study found that selective ablation of the distal part of the ligament of Marshall (LOMLSPV ) could suppress ventricular arrhythmias (VAs) during acute myocardial infarction (AMI). This study was to investigate the possible underlying mechanisms. Dogs were randomly divided into the sham-operated group (SO; n = 6), AMI group (AMI; n = 8) and the group undergoing LOMLSPV ablation ahead of AMI (LOMD+AMI; n = 8). Incidence of VAs, serum levels of malondialdehyde (MDA) and superoxide dismutase (SOD), expression of connexin (Cx43), Bcl-2, Bax, caspase-3, tumor necrosis factor (TNF)-α, interleukin-6 (IL-6), and high mobility group box (HMGB)1 were compared. Anatomic and immunostaining examinations of LOM LSPV were performed. Compared with the AMI group, incidence of VAs was reduced in the LOMD+AMI group. Compared with the SO group, Cx43, SOD, and Bcl-2 were decreased, MDA, Bax, caspase-3, TNF-α, IL-6, and HMGB1 were increased in the MI group, and all the alterations were significantly restrained in the LOMD+AMI group. A visual nerve fiber communication between the left stellate ganglion (LSG) and LOM and abundant sympathetic nerve bundles distribution in LOMLSPV were revealed. LOMLSPV ablation could suppress VAs during AMI. The possible mechanism may be associated with disconnection of the sympathetic conduit from LSG to the ventricles. Preservation of Cx43, inhibition of cardiac oxidative stress, apoptosis, and inflammation may be involved.