July 14, 1998 CHAPEL HILL, N.C. -- Because scientists and physicians don't know enough about the cause of sudden death during heart attacks, researchers at the University of North Carolina at Chapel Hill have developed a unique new laboratory tool that promises to provide some useful answers.
Resulting discoveries eventually could reduce the death rate from the more than 300,000 sudden deaths in the United States each year, the researchers say.
"Our new method, which is an experimental model system, should contribute significantly to understanding internal changes in heart muscle cells and their interaction during heart attacks," said Dr. Wayne E. Cascio, associate professor of medicine at the UNC-CH School of Medicine. "That is key information for heart researchers and possibly the pharmaceutical industry, and we are excited about it."
A report on the development appears in the June issue of the American Journal of Physiology. Besides Cascio, authors are Christopher J. Hyatt, graduate assistant in biomedical engineering; and Drs. John J. LeMasters, professor of cell biology and anatomy; Barbara J. Muller-Borer, research associate in medicine; and Timothy A. Johnson, research associate professor of biomedical engineering.
Cascio said the new method simulates in a thin layer of cultured heart cells the conditions that exist between normal cells and those starved for oxygen during a heart attack. That region, known as the border zone, is the source of many abnormal rhythms during attacks.
As a result, the system should be especially helpful in studying arrhythmias -- heartbeat irregularities often resulting from reduced blood flow through the coronary arteries. Arrhythmias, which begin in the border zone, sooner or later degenerate into ventricular fibrillation -- wild, erratic heartbeats that can result in death within minutes if not controlled.
"Trying to understand the mechanism by which these arrhythmias form is very difficult," Cascio said. "Traditional experimental models rely on large animals or isolated single cells. The complicated structure of the animal models makes study of cell-to-cell interactions and the border zone nearly impossible. Cell-to-cell interaction doesn't exist in isolated single cells. With our new method, we have been able to simplify the complex three-dimensional structure of heart tissue into two dimensions and simulate in cell culture the interaction between normal and abnormal zones."
The two-dimensional structure is very stable, lasts for hours and will allow use of the most sophisticated methods for studying cells, he said.
"For the first time, we now will be able to really look at the interaction between the normal and damaged tissues and address cells of why these arrhythmias occur," the scientist said. "Once one understands mechanisms, then you can start thinking rationally about strategies that prevent rhythm disturbances. You also may be able to design drugs that will target cells in the border zone."
The National Heart, Lung and Blood Institute, the Office of Naval Research, the UNC Board of Governors and the N.C. affiliate of the American Heart Association supported the research.
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