【Background】The adult response to myocardial infarction results in inflammation, scar formation, left ventricular dilatation, and loss of regional and global function. Regenerative scarless healing has been demonstrated in fetal dermis and tendon and is associated with diminished inflammation. We hypothesized that following fetal MI there would be minimal inflammation, regenerative healing, and preservation of function. 【Methods and Results】Anteroapical MI encompassing 20% of the LV were created in adult or early gestation fetal sheep. Myocardial function was serially assessed using quantitative echocardiography. Infarct architecture was examined histologically. Cellular inflammation, cellular proliferation, and apoptosis were assessed using immunohistochemistry. In the adult 4 weeks following MI there was a significant decline in ejection fraction and the akinetic myocardial segment increased in size. In contrast, there was no decline in the fetal EF and no akinetic fetal myocardial segment 4 weeks post-infarction. The fetal infarcts also lacked an inflammatory cell infiltrate and healed without fibrosis or scar formation, compared to the adults. Fetal infarcts also demonstrated BrdU + proliferating cells within the infarct and migration of administered progenitor cells to the infarct. 【Conclusions】The fetal response to MI is dramatically different than the adult and is characterized by minimal inflammation, lack of fibrosis, myocardial proliferation, cellular recruitment, and restoration of cardiac function.