心衰室性心律失常是心血管学科面临的难点，现代研究认为心衰时CaMKII介导的晚钠电流增大导致异常触发活动是其发生的主要机制之一，但缺乏有效药物可供临床选择。参连复脉颗粒能够有效防治室性心律失常，前期研究证实能够减少异常触发活动和室性心律失常的发生，君药党参能够降低心衰心肌细胞CaMKII激活水平，减少异常触发活动，其机制可能与抑制晚钠电流有关。据此提出参连复脉颗粒可能通过调节心肌细胞CaMKII激活水平，抑制晚钠电流，减少异常触发活动，从而干预心衰室性心律失常发生机制的假说。拟复制压力负荷心衰小鼠模型，使用参连复脉颗粒进行干预，以胺碘酮为西药对照；运用全细胞膜片钳检测系统、荧光离子成像系统和分子生物学技术等，从整体、细胞、分子层面研究，为参连复脉颗粒防治心衰室性心律失常提供科学依据，为阐释中药抗心律失常药理作用提供实验证据，为室性心律失常患者提供新的治疗策略。

Ventricular arrhythmia in heart failure is a hot point of cardiovascular research. CaMKII-mediated enhanced late sodium current induced trigger activity is regarded as one of the major mechanisms, but there is no related effective medicine option in clinic until now. SLFM granule is an effective TCM therapy for ventricular arrhythmia. Our previous research has showed that SLFM granule could reduce the risk of triggered activity and ventricular arrhythmia. Codonopsis, the principal drug of SLFM granule, could lower the activity of CaMKII and reduce the risk of triggered activity in heart failure myocardial, which may related to the late sodium current. There for we make a hypothesis that SLFM granule can prevent ventricular arrhythmia in heart failure by a mechanism of lowering the activity of CaMKII, reducing late sodium current and the risk of triggered activity. Pressure overload induced heart failure mouse models will be used to test this hypothesis. After surgery, animals will be treated with SLFM granule or amiodarone as positive control. The techniques of whole-cell patch clamp system, fluorescence micro-imaging system and molecular biology will be used in this protocol, and there for to reveal the mechanism of SLFM granule in animal, cell, and molecular level. The object of this project is to provide evidence for the clinical therapy of SLFM granule in ventricular arrhythmia with heart failure, to reveal the anti-arrhythmia pharmacological effect of Chinese medicine, to provide a new therapeutic option for ventricular arrhythmia patients.