Objective To assess left ventricular remodeling (LVRM) after acute myocardial in-farction (AMI) quantitatively by SPECT gated myocardial perfusion imaging (GMPI), and further explore its influencing factors. Methods Twelve Ba-Ma miniature swine were used to establish AMI model. GMPI was performed at the baseline (before AMI), 24 h, 1 and 4 weeks after AMI. Infarct expansion index, left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), left ventricular ejection fraction ( LVEF) and myocardial perfusion defect were measured. Meanwhile, creatine kinase isozyme MB (CK-MB) and hypersensitive cardiac troponin I (hs-cTn I) were detected. The changes of LVEDV and LVESV before and after AMI (ΔLVEDV and ΔLVESV) were calculated. Repeated measurement analy-sis of variance, the least significant difference t test and Pearson correlation analysis were performed. Re?sults Nine AMI swine were successfully created. LVRM was present 24 h after AMI. LVEDV and LVESV were significantly greater than those before AMI and aggravated within 1 week after AMI, then were down-wards at 4 weeks after AMI. Before AMI, 24 h, 1 and 4 weeks after AMI, the LVEDV was (34.44±7. 90), (47.56±22.66), (71.89±14.90) and (70.33±19.47) ml (F = 28.836, P<0.001), and the LVESV was (10.11±5.49), (25.33±11.62), (40.89±15.88) and (35.44±17.11) ml (F = 22.450, P<0. 001). In-farct expansion index increased progressively within 4 weeks after AMI (F= 16.054, P<0.001). LVEF was significantly lower after AMI than that before AMI (F = 18.267, P<0.001) and improved at 4 weeks after AMI compared to that at 1 week ((52.56±14.96)％ vs (45.11±15.80)％; t= 2.440, P<0. 05). There was a significant correlation between the change in perfusion defect and the ΔLVEDV or ΔLVESV (r values:0. 731 and 0.700, both P<0.05) at 1 week after AMI. In addition, hs-cTn I at 24 h was correlated withΔLVEDV at 24 h and 4 weeks after AMI, respectively (r values: 0.669 and 0.693, both P<0.05). Conclu?sions LVRM and cardiac dysfunction occur in the early period after AMI. LVRM and cardiac dysfunction are most severe at 1 week after AMI, and recover at 4 weeks after AMI, whereas infarct expansion is aggra-vated within 4 weeks. Infarct size and hs-cTn I are closely related to the degree of LVRM.