Objective To establish a stable mouse model of chronic myocardial ischemia, and to preliminarily elaborate the electrophysiological principle of T-wave flattening under ischemic state. Methods 1. C57BL/6 J mice were used as control group with normal diet for 3 months. APOE-/- mice were randomly divided into a model group and a Lipid-lowering Drug (LLD) group, and were fed a high-fat diet for 3 months; 2. Plaque condition was assessed by Hematoxylin-eosin staining (HE) and oil red staining; 3. Electrocardiograms of the mice before and after modelling; and 4. Recordings of the ventricular myocytes' action potentials. Results 1. Cholesterol (CHO) and low-density lipoprotein (LDL-C) were significantly elevated in the model group, and lipid plaques appeared in the aorta of the model mice after modelling, while the lesions in the LLD group were significantly reduced, and no plaques were found in the control group; 2. There was no significant change in the T/QRS wave (T/QRS) in the ECG after modelling in the control group, whereas a significant reduction in T/QRS was observed in the model and LLD groups. 3. There was a significant positive correlation between the degree of T/QRS depression and the levels of lipids and the degree of atherosclerosis (AS) pathology. 4. The inner layer of the cardiomyocyte action potential repetitions more slowly than the outer layer of cardiomyocytes, whereas the repetitive rate was accelerated by the ischemic inner layer of cardiomyocytes. cardiomyocytes accelerated the repolarisation rate. Conclusions APOE-/- mice can be used as a mouse model of chronic myocardial ischemia, and the increased repolarisation rate of the inner myocardium in ischemia may be the main reason for the depression of the electrocardiographic "T wave" in ischemia.