Objective To investigate the alteration of energy metabolism and oxidative injury in the myocardia suffering from lethal ventricular tachyarrhythmia (LVTA). Methods Two LVTA-SCD SD rat models, induced by aconitine injection or coronary artery ligation (CAL), respectively, were developed. Rats that died from over-anaesthesia or CAL-induced heart failure were served as their controls, respectively. Mitochondrial membrane potential (MMP), reactive oxygen species (ROS), malonaldehyde (MDA), phosphocreatine (PCr) in the ventricular myocardia, and serum troponin I (cTnI) were detected, and compared between LVTA rats and their controls. Results Fourteen ACO-LVTA and six CAL-LVTA rats were successfully developed. As compared to their controls, ACO-LVTA and CAL-LVTA rats had higher ROS and MDA content, and lower concentration of PCr in the ventricular myocardia. MDA content in ACO-LVTA group is signiifcantly higher than that of its control (P<0.05). MMP in myocardia of ACO-LVTA is lower than that of its control, but is higher than those of two CAL groups. Serum cTnI in rats of both LVTA models is higher than those of their controls and pre-treated control. Specially, serum cTnI in CAL-LVTA was signiifcantly higher than that of ACO-LVTA and its control (P<0.01). The myocardial ROS content is correlated with the duration of VT and VF (P<0.05), with correlation coefifcients being 0.44 and 0.46, respectively. Conclusions After LVTA, the ventricular myocardia had lower MMP and PCr content, higher concentration of ROS, MDA, as well as higher serum cTnI than their controls, indicative of oxidative injury and alteration of energy metabolism under LVTA-SCD.