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.