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Possible Trigger For Heart Failure Identified In Lab Animal Studies

DALLAS, April 14 -- Researchers have demonstrated in laboratory animals that tumor necrosis factor alpha, a protein produced in the heart, can lead to congestive heart failure. The finding may pave the way for a new treatment for the nation's fastest-growing heart disease. The studies, from two different research teams, appear in today's Circulation: Journal of the American Heart Association.

Released by the body to help heal injured tissue, tumor necrosis factor alpha (TNF), can initiate an "inflammatory cascade," or immune reaction, that may turn against the heart and weaken it, resulting in congestive heart failure, according to scientists at the University of Texas Southwestern Medical Center in Dallas and Baylor College of Medicine in Houston. One study also found that TNF is produced not just by white blood cells, but also by heart muscle cells called myocytes.

The Dallas scientists demonstrated that laboratory mice who were genetically altered so their heart cells produced an excess of TNF pumped less blood and developed an enlarged heart -- the primary features of congestive heart failure in humans.

Afflicting almost 5 million Americans, congestive heart failure is the single most frequent cause of hospitalizations for people age 65 or older, according to the American Heart Association. From 1979 to 1995, deaths from heart failure increased 115.7 percent.

In the study, researchers developed two lines of transgenic mice which expressed TNF in the heart. The two lines, which included 30 mice, died prematurely of heart failure. The progression of heart failure was directly related to the amount of TNF. Mice which did not express TNF in the heart proved to be free of disease, notes Deborah Bryant, B.S., the study's lead author. She is a senior research associate at U.T. Southwestern's department of pediatrics.

"Production of TNF by cardiac myocytes is sufficient to cause myocardit
'"/>

Contact: Carole Bullock
caroleb@amhrt.org
214-706-1279
American Heart Association
13-Apr-1998


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