Cardiac sympathetic overactivation is a critical driver in the progression of acute myocardial infarction (AMI). The left middle cervical ganglion (LMCG) is an important extracardiac sympathetic ganglion. However, the regulatory effects of LMCG on AMI have not yet been fully documented. In the present study, we detected that the LMCG was innervated by abundant sympathetic components and exerted an excitatory effect on the cardiac sympathetic nervous system in response to stimulation. In canine models of AMI, targeted ablation of LMCG reduced the sympathetic indexes of heart rate variability and serum norepinephrine, resulting in suppressed cardiac sympathetic activity. Moreover, LMCG ablation could improve ventricular electrophysiological stability, evidenced by the prolonged ventricular effective refractory period, elevated action potential duration, increased ventricular fibrillation threshold, and enhanced connexin43 expression, consequently showing antiarrhythmic effects. Additionally, compared with the control group, myocardial infarction size, circulating cardiac troponin I, and myocardial apoptosis were significantly reduced, accompanied by preserved cardiac function in canines subjected to LMCG ablation. Finally, we performed the left stellate ganglion (LSG) ablation and compared its effects with LMCG destruction. The results indicated that LMCG ablation prevented ventricular electrophysiological instability, cardiac sympathetic activation, and AMI-induced ventricular arrhythmias with similar efficiency as LSG denervation. In conclusion, this study demonstrated that LMCG ablation suppressed cardiac sympathetic activity, stabilized ventricular electrophysiological properties and mitigated cardiomyocyte death, resultantly preventing ischemia-induced ventricular arrhythmias, myocardial injury, and cardiac dysfunction. Neuromodulation therapy targeting LMCG represented a promising strategy for the treatment of AMI.

心脏交感神经过度激活是急性心肌梗死（AMI）进展的关键驱动因素。左颈中神经节（LMCG）是重要的心外交感神经节。然而，LMCG 对 AMI 的监管作用尚未得到充分记录。在本研究中，我们检测到 LMCG 受丰富的交感神经成分支配，并对心脏交感神经系统响应刺激产生兴奋作用。在 AMI 犬模型中，靶向消融 LMCG 降低了心率变异性和血清去甲肾上腺素的交感指数，导致心脏交感神经活动受到抑制。此外，LMCG消融可以改善心室电生理稳定性，表现为心室有效不应期延长、动作电位持续时间延长、心室颤动阈值增加和connexin43表达增强，从而显示出抗心律失常作用。此外，与对照组相比，接受 LMCG 消融的犬的心肌梗塞面积、循环心肌肌钙蛋白 I 和心肌细胞凋亡均显着减少，同时心脏功能得到保留。最后，我们进行了左星状神经节 (LSG) 消融，并将其效果与 LMCG 破坏进行了比较。结果表明，LMCG 消融可预防心室电生理不稳定、心脏交感神经激活和 AMI 诱发的室性心律失常，其效果与 LSG 去神经术相似。总之，本研究表明，LMCG 消融可抑制心脏交感神经活动，稳定心室电生理特性并减轻心肌细胞死亡，从而预防缺血引起的室性心律失常、心肌损伤和心功能不全。针对 LMCG 的神经调节疗法是治疗 AMI 的一种有前景的策略。