Objective Transverse aortic constriction (TAC) was used to establish a stable and reliable model of heart failure in mice, and the pathological process of heart failure in mice was analyzed and observed. Methods The heart failure model of C57BL/ 6J mice was established by non-thoracotomy TAC. The heart function and degree of heart failure were evaluated by echocardiography, left ventricular mass index, and histopathological examination. Results The left ventricular mass index gradually increased overtime. Compared with that in the sham-operated group, there were significant differences in left ventricular mass index at 4, 8, and 12 weeks after operation (P< 0. 01). Echocardiography showed that the left ventricular anterior wall thickness, left ventricular corrected weight, heart rate, and cardiac output increased significantly 4 weeks after TAC compared with those in the sham operation group ( P < 0. 01). Left ventricular wall thickness, left ventricular corrected weight, and left ventricular end systolic volume increased significantly ( P< 0. 01), while ejection fraction and fractional shortening decreased significantly (P<0. 01). At 12 weeks after TAC, left ventricular enddiastolic diameter, left ventricular endsystolic diameter, left ventricular enddiastolicvolume, and left ventricular endsystolic volumeincreased significantly ( P< 0. 01), ejection fraction and fractional shortening decreased further ( P < 0. 01), and pathological examination showed that myocardial fibers were abnormal tovarying degrees and lesional. Conclusions The experimental result show that the establishment of a mouse heart failure model by non-thoracotomy TAC is stable and feasible, and can simulate the pathophysiological process from left ventricular hypertrophy to heart failure caused by human pressure overload