心肌梗死（MI）后室性心动过速（VT）诱发心室颤动是心源性猝死的主要原因。过去一直认为MI后心肌纤维化使心电传导异常是VT的主要原因。但最近有研究发现约84%的MI患者存在心肌内脂肪的异常增多，认为MI后梗死区边缘的心肌内脂肪的异常增生，改变了心电传导，才可能是诱发VT发生的主要原因。C/EBPα是脂肪细胞分化的重要转录因子，泛素连接酶E6AP可下调C/EBPα蛋白的表达及其转录，因而具有抑制脂肪分化的作用。稳心颗粒对MI后室性心律失常有良好疗效，但作用机制尚未完全清楚。本项目拟用结扎左前降支方法联合程序电刺激建立大鼠MI后VT模型，并在体外培养大鼠前脂肪细胞，采用RNAi技术、血清药理等方法，探讨E6AP负性调节C/EBPα对MI后心肌脂肪化生的作用以及抑制脂肪化生后对VT发生的影响，并观察稳心颗粒对MI后VT的作用及其机制。为MI后VT的防治提供新的理论基础、实验依据和可能的治疗手段。

Ventricular tachycardia (VT) after myocardial infarction (MI) prone to ventricular fibrillation is the major cause of sudden cardiac death. Postinfarction of myocardial collagen fbers leading to abnormalities of cardiac electrical transmission was considered to be the main reason of VT in the past. But the recent research found that 84% patients with MI were abnormalities in the amount of intramyocardial adipose, which was deemed to be the major cause of VT by the change of cardiac electrical transmission. CCAAT/Enhancer Binding Protein Alpha (C/EBPα) is a key transcription factor involved in the adipocyte differentiation. E6AP, an ubiquitin ligase may down-regulate C/EBPα’s expression and transcription, and then it will restrain the intramyocardial adipogenic differentiation. Wenxin grannle has good curative effect in VT After MI. Unfortunately, the mechanism of this drug is unidentified. This study, we will build up the rat model of VT after MI, we ligated their left anterior descending coronary associating with electrical stimulating, and nurtured the adipose cells in vitro by RNAi and serum pharmacology ect. We probed the negatively regulates of E6AP effacing on the intramyocardial adipose after MI and the inhibition of adipose effacing on for VT after MI. We also observed the effectiveness and its mechanism of Wenxin grannle on the VT. This study will offer the new evidence and the lab data to the treatment of VT after myocardial infarction.