We asked whether thyroid hormone (T4) would improve heart function in left 
ventricular hypertrophy (LVH) induced by pressure overload (aortic banding). 
After banding for 10-22 wk, rats were treated with T4 or saline for 10-14 d. 
Isovolumic LV pressure and cytosolic [Ca2+] (indo-1) were assessed in perfused 
hearts. Sarcoplasmic reticulum Ca2+-ATPase (SERCA), phospholamban, and alpha- 
and beta-myosin heavy chain (MHC) proteins were assayed in homogenates of 
myocytes isolated from the same hearts. Of 14 banded hearts treated with saline, 
8 had compensated LVH with normal function (LVHcomp), whereas 6 had abnormal 
contraction, relaxation, and calcium handling (LVHdecomp). In contrast, banded 
animals treated with T4 had no myocardial dysfunction; these hearts had 
increased contractility, and faster relaxation and cytosolic [Ca2+] decline 
compared with LVHcomp and LVHdecomp. Myocytes from banded hearts treated with T4 
were hypertrophied but had increased concentrations of alpha-MHC and SERCA 
proteins, similar to physiological hypertrophy induced by exercise. Thus thyroid 
hormone improves LV function and calcium handling in pressure overload 
hypertrophy, and these beneficial effects are related to changes in myocyte gene 
expression. Induction of physiological hypertrophy by thyroid hormone-like 
signaling might be a therapeutic strategy for treating cardiac dysfunction in 
pathological hypertrophy and heart failure.