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1 Cardiovascular Research Institute, University of South Dakota, Sioux Falls, SD, USA; College of Pharmacy, Florida A&M University, Tallahassee, FL, USA
2 Cardiovascular Research Institute, University of South Dakota, Sioux Falls, SD, USA
3 College of Pharmacy, Florida A&M University, Tallahassee, FL, USA
* To whom correspondence should be addressed. E-mail: mgerdes{at}usd.edu.
We examined the effects of thyroid hormones (TH) on left ventricular (LV) function and myocyte remodeling in Spontaneously Hypertensive Heart Failure (SHHF) rats. SHHF rats were treated with 3 different TH doses from 20-21 months of age. In terminal experiments, LV
function (echo and catheter) and isolated myocyte shape was examined in SHHF rat groups and age-matched Wistar Furth (WF) controls. Compared to WF rats, 
/
myosin ratio was reduced in untreated SHHF rats. The ratio of / myosin increased in all TH groups suggesting a reversal of the fetal gene program. Low dose TH produced no changes in LV myocyte size or function but high dose produced signs of hyperthyroidism (e.g.
heart weight, tachycardia). Chamber diameter/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 current 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.
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