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University of Maryland School of Medicine Researchers Lead Multi-Center Heart Failure Studies Thanks to a $11.2 Million Grant

Wednesday, September 09, 2009

 William C. Stanley, PhD, will continue to study heart failure with his latest grant.

Research will evaluate dietary changes that may impact heart failure

A new $11.2 million, five-year grant from the National Institutes of Health (NIH) will enable researchers at the University of Maryland School of Medicine in Baltimore and three other centers to improve the treatment of chronic heart failure. This multifaceted research program is the largest effort of its kind to focus on a basic question in heart failure: how can nutritional changes impact heart function to help patients with a failing heart?

The heart needs fuel to work properly. In a process called metabolism, chemical energy from food is transformed into the electrical energy that causes the heart to pump. Impaired metabolism is both a cause and effect of heart failure. Cell structures known as mitochondria are at the center of the process.

“Years of untreated high blood pressure or loss of cardiac tissue and scarring after a heart attack cause certain mitochondria to develop defects,” says William C. Stanley, Ph.D., professor of medicine and director of cardiovascular sciences at the University of Maryland School of Medicine, who is leading the research program. “Different substances from food affect the mitochondria in different ways. We want to improve those defective mitochondria and prevent the mitochondria from going bad when they are constantly under stress.”

Dr. Stanley and investigators at three other institutions, Case Western Reserve in Cleveland, Henry Ford Hospital in Detroit, and New York Medical College, have been collaborating for 10 years. Their work, funded with a previous NIH grant, has already produced 85 peer-reviewed journal publications and has provided many insights into the causes and results of heart failure.

Dr. Stanley and his team will investigate new dietary changes to prevent and treat heart failure. Their hypothesis is that the electrical abnormalities that lead to heart failure can be reversed by consumption of a diet low in carbohydrates and sugar, and high in polyunsaturated fat. “We want to figure out how to improve this transfer of energy so the function of the heart is maintained in the early stages of heart failure or even before heart failure has been established,” he says.

Dr. Stanley’s study builds on the group’s previous research, which showed that a low-carbohydrate/high-fat diet can prevent or reduce some of the most serious aspects of heart failure. In addition, they found that dietary supplementation with omega-3 polyunsaturated fatty acids prevents development of heart failure, and a high-sugar diet further accelerates development of heart failure. “We have observed that high-sugar diets are toxic in animal models of high blood pressure, which can lead to heart failure. We’ll try to learn why that is. We will also evaluate why polyunsaturated fatty acids from fish oils are protective to the heart in heart failure.”

E. Albert Reece, M.D., Ph.D., M.B.A., vice president for medical affairs at the University of Maryland and dean of the University of Maryland School of Medicine, says, “Dr. Stanley’s research has the potential to advance a new model of treatment. An important aspect of heart failure treatment in the future may involve the targeting of changes in the way the heart receives its nourishment.”

“Therapy focused on improving cardiac energy metabolism could help the heart work smarter, not harder,” says Mandeep R. Mehra, M.B.B.S., professor of medicine, head of the Division of Cardiology at the University of Maryland School of Medicine and chief of cardiology at the University of Maryland Medical Center. “We believe this is a very important and promising area of research because it may be the key to simpler approaches, through the diet, to manage and even improve heart failure.”

The three other teams in this research program are studying related aspects of cardiac energy metabolism in heart failure. The Case Western Reserve team will design therapies to improve mitochondrial energy production, while investigators at Henry Ford Hospital will explore ways to reduce heart rate, a major regulator of energy utilization in heart failure. Researchers at New York Medical College will look at the relationship between altered energy metabolism and oxidative stress, which is the damage associated with unstable molecules called “free radicals.”

Each project will incorporate pre-clinical, animal models of heart failure to test approaches that can be translated into clinical treatments for humans. Heart failure affects nearly 5 million Americans. Five years after their initial diagnosis, fewer than 50 percent of heart failure patients are alive; at the 10-year mark, fewer than a quarter of patients survive. Risk factors that lead to heart failure include high blood pressure, a prior heart attack, abnormal heart valves and diabetes. In addition, a large number of patients have a form of heart failure called idiopathic cardiomyopathy, where no cause can be identified.
Heart failure develops when the heart is not able to pump enough blood to meet the body’s needs. The heart compensates for this loss in pumping capacity by growing larger, increasing muscle mass and pumping faster to increase the heart’s output. These changes typically occur over a long period of time, masking the problem. Eventually, the heart and the body cannot keep up with the demands, and the person begins to experience the fatigue and breathing problems that often are the first signs of the disease.

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