In the post-reperfusion era, molecular and genetic mechanisms of 
cardioprotection and regeneration represent new therapeutic challenges to limit 
infarct size and minimize post-ischemic remodeling after acute myocardial 
infarction (AMI). Activation of cell survival mechanisms can be promoted by the 
administration of external drugs, stimulation of internal mechanisms, and 
genetic manipulation to delete or replace pathological genes or enhance gene 
expression. Among internal cardiovascular regulatory mechanisms, thyroid 
hormones (THs) may play a fundamental role. TH has a critical role in 
cardiovascular development and homeostasis in both physiological and 
pathological conditions. In experimental AMI, TH has been shown to affect 
cardiac contractility, left ventricular (LV) function, and remodeling. Several 
experimental studies have clearly shown that THs participate in the regulation 
of molecular mechanisms of angiogenesis, cardioprotection, cardiac metabolism, 
and ultimately myocyte regeneration, changes that can reverse left ventricular 
remodeling by favorably improving myocyte shape and geometry of LV cavity, thus 
improving systolic and diastolic performance. This review is focused on the role 
of thyroid on AMI evolution and on the potential novel option of thyroid-related 
treatment of AMI.