Viable myocardium undergoes several changes in the course of cardiac remodeling following myocardial infarction aiming to adapt the heart to the hemodynamic compromise. This response is characterized by reactivation of the fetal transcriptional program and results in cardiac dysfunction. Changes in thyroid hormone (TH)-TH receptors (TRs) axis occur in the course of post-infarction cardiac remodeling and seem to contribute to cardiac fetal phenotype. TH can "rebuild" the post-infarcted heart by preventing the fetal-like pattern of contractile proteins expression, normalizing wall tension, and optimizing cardiac chamber geometry. This effect seems to be attributed to TH pleiotropic cellular actions; TH promotes tissue growth and differentiation and favorably remodels cardiac cell while increases cellular survival upon stress. TH may constitute a new therapeutic option for mending the ischemic myocardium.