Objective To establish a Juema minipig model of myocardial infarction, to evaluate the clinical indices in the model pigs, and to explore the relationship between gene expression and metabolic decompensation. Methods 13 male Juema minipigs were randomly divided into control (Sham, n=5), myocardial infarction (MI, n=5) and normal control (for evaluating the recovery condition after surgery, n=3) groups. In the MI group, the ligation was done at the left descending coronary artery around the 1/3 distance to heart apex. Four weeks after the surgery, the cardiac function and serum biochemistry was analyzed. The histological changes and gene expression profiles in the myocardium in the peri-infarct area were exanimated. Results Ultrasonic images showed that the infarction was formed, the ejection fraction and fraction shortening were significantly reduced in the MI group (~32% and ~40% less than those of the sham group). Histological examination showed that myocardial fibers at the peri-infarct area were broken, dissolved, and there was connective tissue hyperplasia with increased neutrophil and lymphocyte infiltration. Microarray analysis revealed that two myocardial remodeling and pathology mediating pathways, three inflammation-related pathways, and 8 metabolic pathways (including fatty acid, amino acid, and glucose metabolic pathways) were significantly changed. Conclusions We have successfully established a Juema minipig model of myocardial infarction. The less branches of the left descending coronary artery allow us to establish a stable model by surgery with comparable characteristics in the clinic indices. The results of this study provides useful reference characteristics of an animal model with characteristic changes in the peri-infarct area.