Abstract: Objective：To investigate the effect of type 2 diabetes mellitus (T2DM) on inflammatory reaction and long-term cardiac remodeling in patients with acute ST-elevation myocardial infarction (STEMI) underwent primary percutaneous coronary intervention (PCI). Methods：A total of 60 patients diagnosed with STEMI were selected, and 30 patients among whom also had T2DM (DM group). Creatinine kinase-MB (CK-MB), cardiac troponin T (cTnT), monocyte chemotactic protein-1 (MCP-1), matrix metalloproteinase-9 (MMP-9), tissue inhibitor of metalloproteinase-1 (TIMP-1), and osteopontin (OPN) were measured before PCI and 12 h, 36 h, and 60 h after PCI. All patients took echocardiogram measurements in one week and one year after PCI. The primary end point was one year incidence of major adverse cardiovascular events (MACE), including cardiac death, nonfatal myocardial infarction, and target vessel revascularization. Secondary end points were thrombolysis in myocardial infarction (TIMI) flow grade, laboratory markers, left ventricular ejection fraction (LVEF), left ventricular end diastolic volume (LVEDV), and left ventricular end systolic volume (LVESV). Results：Compared with non-DM group, DM group (n=30) had higher peak levels of both CK-MB and cTnT after PCI (P＜0.05). MCP-1 level and the ratio of MMP-9/TIMP-1 level were also higher in DM group 60 h after PCI (P＜0.05). There were no significant differences in LVEFs, LVEDVs, or LVESVs one week after PCI between the groups. However, DM group had lower LVEFs (P＜0.001) as well as larger LVEDVs and LVESVs (P＜0.05) versus non-DM group one year after PCI. Conclusions：The peak myocardial enzyme, MCP-1 level, and MMP-9/TIMP-1 ratio are higher in DM group after direct PCI, LVEF is lower, LVEDV and LVESV are higher one year after PCI, suggesting that patients with STEMI complicated with T2DM are more prone to long-term myocardial remodeling, and the mechanism may be related to more active inflammatory reactions.