Gene Profiling: A New Tool To Combat Heart Failure

UR Scientist Investigates How Damaged Heart Repairs Itself

March 25, 2004

The University of Rochester Medical Center is involved in a new type of cutting-edge heart research, by studying the genes in damaged heart tissue that switch on and off when, sometimes inexplicably, a bad heart begins to heal itself. This path might lead to treatments that could induce the repair, or to a simple blood test that would give a more informed diagnosis.

It’s a new approach in cardiology, where scientists are still trying to solve the underlying causes of the nation’s No. 1 killer, according to Burns C. Blaxall, Ph.D., who recently joined the UR faculty from Duke University. Blaxall was part of a scientific team at Duke that pioneered the use of microarray technology to analyze gene patterns in heart tissue. (The UR leads a statewide consortium of universities and companies doing advanced gene analysis.)

Blaxall’s research has a direct link to better patient care at the Strong Health Program in Heart Failure and Transplantation, the only program in upstate New York to perform cardiac transplants. For example, one focus of his research is on Left Ventricle Assist Devices, or LVADs, and how they impact the failing heart. Patients often receive an LVAD while they await a donor heart and a transplant. With the patient’s consent, Blaxall retrieves small bits of heart tissue during the surgical implant of the LVAD, and again when the device is removed at the time of the transplant.

The LVAD essentially takes over the left ventricle’s pumping action, giving the heart a vacation, Blaxall says. Interestingly, many hearts begin to repair themselves during this “vacation” period. Doctors refer to this as a “mechanical rescue,” and Blaxall is investigating why it happens, and is looking for gene patterns that explain and predict the repair action.

“If you know which patients have the genes that will most likely trigger a repair, it would certainly help physicians decide if a transplant is the only option,” says Blaxall, assistant professor of Medicine, and of Pharmacology and Physiology, in the UR Center for Cellular and Molecular Cardiology.

“Rochester is unique because most transplant centers do not also have top-rate scientists to study failing hearts,” says Mark B. Taubman, M.D., chief of Strong’s Cardiology Unit and director of the UR Center for Cellular and Molecular Cardiology. “While technology and treatments are always improving, we believe basic science will ultimately answer the big questions that may lead to a dramatic improvement in the way we treat heart failure.”

Doctors diagnose heart failure more than a half-million times each year in the United States. It is a leading cause of hospitalizations, with about five million patients under treatment at any given time. Individuals are classified as having varying degrees of heart failure, from mild, Class I, to severe, Class IV. As Blaxall and others have shown, the next wave of cardiology research involves gene-risk identification, which not only predicts response to treatment, but also can lead to novel targets for better therapy.

Already, UR cardiologists and scientists have made great strides in understanding cholesterol and plaque buildup, inflammation, blood vessel damage, the development of atherosclerosis, and the risks associated with arrhythmias and sudden death due to other electrical malfunctions. Blaxall’s laboratory is also investigating mouse genes that play a key role in heart function to see if they correspond with the same human genes, and the different gene expressions that occur in two types of heart failure -- ischemic, due to lack of blood flow, versus idiopathic dilation, due to an enlarged organ.

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