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Heart Disease Symptoms Worsen When Body Tries To Adapt

Mouse Model Provides Window into How the Disease Progresses

For years doctors have debated whether the progressively destructive course of genetic heart disease is due principally to the altered genes that set it in motion, or to the body's ceaseless efforts to compensate for and cope with the initial damage. Now results of a Johns Hopkins-led study in mice, published in the March issue of Nature Medicine, show that many of the disease's common features are better explained by the latter theory.

Using a miniaturized catheter developed at Hopkins, researchers compared the heart pumping action of healthy young and old mice to those of same-age mice harboring a defective gene that causes familial hypertrophic cardiomyopathy (FHC) -- a potentially fatal form of inherited heart disease in which the heart wall thickens and obstructs blood flow.

Hypertropic cardiomyopathy is associated with changes in the proteins principally responsible for the capacity of heart muscle to contract and relax as it pumps blood throughout the body. As a result, the wall of the left ventricle -- the heart's main pumping chamber -- thickens, leaving little room inside the chamber for blood to fill. The wall also can stiffen, further impairing the heart's ability to contract.

While the hearts of both younger and older mice with FHC had the identical gene defect, they performed differently. Both contracted faster but relaxed abnormally slowly. However, the hearts of the older FHC mice squeezed much harder only to pump less blood. The higher pressure, reduced volume, and accompanying stiffness were seen only in the older, FHC mice, indicating evolving responses do the damage over time. The same traits are hallmarks of the disease in humans.

"This study provides a major new window to the development of this disease," says David A. Kass, M.D., senior author of the study and professor of medicine and biomedical enginee
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Contact: Karen Infeld
kinfeld@jhmi.edu
410-955-1534
Johns Hopkins Medical Institutions
4-Mar-1999


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