We examined the effects of thyroid hormones (THs) on left ventricular (LV) 
function and myocyte remodeling in rats with spontaneously hypertensive heart 
failure (SHHF). SHHF rats were treated with three different TH doses from 20-21 
mo of age. In terminal experiments, LV function (as determined by 
echocardiography and catheterization) and isolated myocyte shape were examined 
in SHHF rat groups and age-matched Wistar-Furth control animals. Compared with 
Wistar-Furth rats, the ratio of alpha- to beta-myosin was reduced in untreated 
SHHF rats. The alpha-to-beta-myosin ratio increased in all TH groups, which 
suggests a reversal of the fetal gene program. Low-dose TH produced no changes 
in LV myocyte size or function, but high-dose TH produced signs of 
hyperthyroidism (e.g., increased heart weight, tachycardia). The chamber 
diameter-to-wall thickness ratio declined with increasing dose due to reduced 
chamber diameter and increased wall thickness. This resulted in a 38% reduction 
in LV systolic wall stress in the middle- and high-dose groups despite sustained 
hypertension. Isolated myocyte data indicated that chamber remodeling and 
reduced wall stress were due to a unique alteration in myocyte transverse shape 
(e.g., reduced major diameter and increased minor diameter). Based on our 
present understanding of ventricular remodeling and wall stress, we believe 
these changes are likely beneficial. Results suggest that TH may be an important 
regulator of myocyte transverse shape in heart disease.