Martin Gerdes, New York Institute of Technology – Heart Failure

Martin Gerdes1Reducing heart failures in the U.S. could save millions of people.

Martin Gerdes, professor of biomedical sciences at the New York Institute of Technology, delves into a new treatment that could help us live longer and better lives.

Martin Gerdes completed his Ph.D. at the University of Texas Medical Branch at Galveston in 1978 and was recently recognized as the 2013 Distinguished Alumnus of the Graduate School of Biomedical Sciences. Throughout his career, work has focused on understanding the cellular and molecular mechanisms of maladaptive ventricular remodeling in heart failure and potential treatments. He has published over 100 peer reviewed journal articles and has been the PI on ~$30M in NIH funding during his career. He has identified key cellular mechanisms involved in dilated heart failure, including a maladaptive change in myocyte shape.

Heart Failure

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More than five million Americans suffer from heart failure, a condition that occurs when the heart can’t pump enough oxygen and blood through the body to support other organs. The American Heart Association reports that about half of the people who develop heart failure die within five years of diagnosis. The disease costs our nation an estimated $32 billion annually.

In the past few years, a series of animal studies have shown that heart health can improve with low doses of thyroid hormones. It’s very likely such improvements will occur in human hearts too – but we need clinical trials to provide clear evidence.

The animal studies are a crucial foundation on which to build.

In the latest study, we administered thyroid hormones to aging female rats with high blood pressure.

High blood pressure is a major contributor to a form of heart failure that affects the way the heart relaxes between contractions. About half of human patients with heart failure suffer this condition.

In our study, the rats’ cardiac health improved despite the continued presence of severe hypertension. Depressed thyroid hormone levels in the rats’ heart were restored to normal. Their hearts also did not accumulate scar tissue, a typical result of high blood pressure. And, heart function was enhanced.

We’ve done similar studies showing links between improvements in thyroid hormone levels and heart health in rats and mice.

Unfortunately, medical opinion on thyroid treatment for human patients with heart disease is largely shaped by outdated studies that used toxic doses of thyroid hormones.

Our animal studies show the effect of safe doses. Human clinical trials with similar, safe treatments and monitoring programs may lead to advances in heart failure treatment and savings in health care costs.

 

 

 

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