Objective To investigate the effect of angiotensin receptor/neprilysin inhibitor (ARNI) on ventricular arrhythmias in rats with heart failure (HF) after myocardial infarction and its possible mechanism. Methods SD rats with heart failure after myocardial infarction were established by ligation of left anterior descending coronary artery，and then divided into heart failure group (HF group)， angiotensin receptor/neprilysin inhibitor (ARNI) (HF+ARNI group) (68mg/kg/d，intragastric)，valsartan group (HF+ARB group) (30mg/ kg/d，intragastric)，and mitochondrial Ca2+ uniporter protein (MCU) inhibitor-ruthenium red group (HF+RR group) (2mg/kg/d，intraperitoneal injection). The sham operation group (Sham group) was also established. Continuous drug intervention lasted for 4 weeks. Echocardiography was performed before and after drug intervention. The induction rate of ventricular arrhythmia was detected by Burst stimulation. HE staining was used to observe the histopathological changes of rat heart. The expression of MCU in rat myocardium was detected by Western blot. Results Compared with the Sham group，the HF group had cardiac structural remodeling and significantly decreased cardiac function ((P < 0.05). Compared with HF group and HF+RR group，the cardiac structural remodeling and cardiac function of rats in HF + ARNI group were significantly improved (P < 0.05). Compared with HF + ARB group，the cardiac structural remodeling of rats in HF + ARNI group was significantly improved (P < 0.05)，but the cardiac function of rats in HF + ARNI group was not significantly improved (P > 0.05). Compared with HF group and HF+RR group，the induction rate of ventricular arrhythmia in HF+ARNI group was significantly decreased when the voltage was 6V and 12V with the Burst stimulation (P < 0.05). Compared with HF +ARB 0.05). Western blot results showed that compared with Sham group，the expression level of MCU protein in myocardium of rats in HF group was significantly increased (P < 0.05). Compared with HF group，the expression of MCU protein in HF+ARNI group，HF+RR group and HF + ARB group was decreased (P < 0.05). Compared with HF+ARB group，the expression of myocardial MCU in HF+ARNI group was significantly decreased ((P < 0.05). Compared with HF+ARNI group，the expression of myocardial MCU in HF+ RR group was significantly decreased (P < 0.05). Conclusion ARNI could significantly reduce the induction rate of ventricular arrhythmias in rats with heart failure after myocardial infarction，which might be through improving cardiac function and structural remodeling，and down-regulating the expression of MCU.