Thyroid hormone treatment administered to rats at the time of a heart attack (myocardial infarction) led to significant reduction in the loss of heart muscle cells and improvement in heart function, according to a study published by a team of researchers led by A. Martin Gerdes and Yue-Feng Chen from New York Institute of Technology College of Osteopathic Medicine.
The findings, published in the Journal of Translational Medicine, have bolstered the researchers' contention that thyroid hormones may help reduce heart damage in humans with cardiac diseases.
"I am extremely excited about the prospects of improving heart disease outcomes in patients by restoring normal thyroid function in the heart," says Gerdes, professor and chair of biomedical sciences at New York Institute of Technology College of Osteopathic Medicine. "Since thyroid hormones are inexpensive, significant health care savings could also result."
In the study, funded by the National Institutes of Health's National Heart, Lung, and Blood Institute and the American Heart Association, scientists treated rats with thyroid hormones after myocardial infarction and examined changes at the cellular level. After eight weeks of treatment, researchers saw significant improvements in heart function and a reduction in the loss of cardiac myocytes, the cells responsible for the heart's pumping ability.
"Reducing the loss of cardiac myocytes is a major therapeutic target after a heart attack since this should lead to improved patient survival and reduced disability," Gerdes said.
Gerdes, who has conducted heart failure research for 35 years, has focused on the two major forms of thyroid hormones known as T3 and T4. Previous animal studies have shown that myocardial infarction leads to reduced cardiac levels of T3, a change that animal studies have demonstrated can eventually cause heart failure by itself. However, blood hormone levels may not always reflect this cardiac tissue deficiency. Although tissue T3 levels have not yet been measured in human hearts, available evidence suggests the same hormone loss likely occurs after myocardial infarction.