Longstanding hyperthyroidism is associated with normal or enhanced intrinsic cardiomyocyte function despite decline in global cardiac function.
Thyroid hormones (THs) play a pivotal role in cardiac homeostasis. TH imbalances alter cardiac performance and ultimately cause cardiac dysfunction. Although short-term hyperthyroidism typically leads to heightened left ventricular (LV) contractility and improved hemodynamic parameters, chronic hyperthyroidism is associated with deleterious cardiac consequences including increased risk of arrhythmia, impaired cardiac reserve and exercise capacity, myocardial remodeling, and occasionally heart failure. To evaluate the long-term consequences of chronic hyperthyroidism on LV remodeling and function, we examined LV isolated myocyte function, chamber function, and whole tissue remodeling in a hamster model. Three-month-old F1b hamsters were randomized to control or 10 months TH treatment (0.1% grade I desiccated TH). LV chamber remodeling and function was assessed by echocardiography at 1, 2, 4, 6, 8, and 10 months of treatment. After 10 months, terminal cardiac function was assessed by echocardiography and LV hemodynamics. Hyperthyroid hamsters exhibited significant cardiac hypertrophy and deleterious cardiac remodeling characterized by myocyte lengthening, chamber dilatation, decreased relative wall thickness, increased wall stress, and increased LV interstitial fibrotic deposition. Importantly, hyperthyroid hamsters demonstrated significant LV systolic and diastolic dysfunction. Despite the aforementioned remodeling and global cardiac decline, individual isolated cardiac myocytes from chronically hyperthyroid hamsters had enhanced function when compared with myocytes from untreated age-matched controls. Thus, it appears that long-term hyperthyroidism may impair global LV function, at least in part by increasing interstitial ventricular fibrosis, in spite of normal or enhanced intrinsic cardiomyocyte function.
Department of Basic Biomedical Sciences, Sanford School of Medicine at the University of South Dakota, Sioux Falls, South Dakota, United States of America.
Nathan Y
NY
Weltman
Dajun
D
Wang
Rebecca A
RA
Redetzke
A Martin
AM
Gerdes
D000818:Animals; D006332:Cardiomegaly / Q000139:chemically induced / Q000378:metabolism; D002478:Cells, Cultured; D006224:Cricetinae; D004452:Echocardiography; D006980:Hyperthyroidism / Q000139:chemically induced / Q000378:metabolism*; D032383:Myocytes, Cardiac / Q000187:drug effects; D013963:Thyroid Hormones / Q000494:pharmacology; D020257:Ventricular Remodeling / Q000187:drug effects
D013963:Thyroid Hormones