Chronic ischemia or pressure overload decreases thyroid hormone (TH) signaling 
and activates the fetal gene program in the heart. While these features are of 
physiologic importance in the developing heart, their respective roles in the 
postnatal heart are debated. Administration of TH can prevent the changes of the 
fetal gene program and rebuild the heart after an "index event" such as 
ischemia. TH affects cardiac remodeling by limiting reperfusion injury, and, at 
later states, by inducing distinct changes in cardiac chamber geometry in a 
time-dependent manner. Furthermore, administration of TH can convert pathologic 
to physiologic hypertrophy. These effects are the result of favorable cellular 
remodeling. While preliminary clinical studies provide encouraging results, the 
potential and efficacy of TH in the treatment of heart disease still await 
evaluation in large clinical trials.