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1 University of South Dakota, Cardiovascular Research Institute-South Dakota Heath Research Foundation, Sioux Falls, SD, USA
* To whom correspondence should be addressed. E-mail: mgerdes{at}usd.edu.
Thyroid hormones (TH) enhance cardiac function and reverse gene changes typical of pathologic hypertrophy. However, reports in humans, but not animals, indicate that excess TH
can cause heart failure (HF). Also, the effects of TH on normal and cardiomyopathic hearts is likely to be different. The goal of this study was to characterize the effects of prolonged hyperthyroidism on cardiac function, chamber and cellular remodeling, and protein expression in
both normal and cardiomyopathic hearts. Hyperthyroidism was induced in 3 mo old normal BIO F1B and dilated cardiomyopathic BIO TO2 hamsters. After TH treatment for 10 days and 2 months, hemodynamics, echos, myocyte length, histology, and protein expression were assessed. After 10 days and 2 months, there were no differences between TO-2 treated (Tx) and TO-2 untreated (Untx) hamsters in chamber diameters or LV function. After 2 months of treatment,
however, F1B-Tx showed evidence of dilated heart failure vs F1B-Untx. Chamber diameters were increased and ejection fraction, +dP/dT, and -dP/dT were reduced. In F1B-Tx and TO-2-Tx hamsters, 
-myosin isoform expression was reduced while 
-myosin increased significantly in
F1B-Tx only. In TO-2-Tx hamsters, the percent of viable myocardium was increased and percent fibronecrosis was reduced vs TO-2-Untx. Myocyte length increased with TH treatment in both hamster strains. We conclude: (1) excess TH can induce HF in normal animals as observed in humans; (2) reversal of MHC expression does not necessarily improve heart function; and (3) excess TH altered cellular remodeling but did not adversely affect chamber function or
dimensions in TO-2 hamsters.
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