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1 Cardiovascular Research Institute, University of South Dakota, Sioux Falls, SD, USA; Internal Medicine, University of South Dakota, Sioux Falls, SD, USA
2 Cardiovascular Research Institute, University of South Dakota, Sioux Falls, SD, USA
* To whom correspondence should be addressed. E-mail: mgerdes{at}usd.edu.
Growing evidence suggests that thyroid dysfunction may contribute to progression of cardiac disease to heart failure. We investigated the effects of a therapeutic dose of thyroid hormones (TH) on cardiomyopathic (CM) hamsters from 4 to 6 months (M) of age. CM hamsters had sub-clinical hypothyroidism (normal T4, elevated TSH). Left ventricular (LV) function was determined by echo and hemodynamics. Whole tissue pathology and isolated myocyte size and number were assessed. TH treatment prevented the decline in heart rate and +dP/dT, and improved LV ejection fraction. The percentage of fibrosis/necrosis in untreated 4 M old CM (4CM, 15.5±2.2%) and 6 M old CM (6CM, 21.5±2.4%) was pronounced and was reversed in treated CM (TCM, 11.9±0.1%). Total ventricular myocyte number was the same between 4M and 6M controls, but was reduced by 30% in 4CM and 43% in 6CM. TH treatment completely prevented further loss of myocytes in TCM hamsters. Compared to age-matched controls, resting and maximum coronary blood flow were impaired in 4CM and 6CM hamsters. Blood flow was completely normalized by TH treatment. We conclude that TH treatment of CM hamsters with subclinical hypothyroidism normalized impaired coronary blood flow which prevented the decline in LV function and loss of myocytes.
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