DALLAS, June 29 -- A drug that inactivates a protein in the body that worsens congestive heart failure could eventually lead to a new approach to treating this devastating disease. A preliminary clinical study involving the drug, called etanercept, is reported in today's issue of Circulation: Journal of the American Heart Association.
The drug, called etanercept, evaluated in 18 people with severe congestive heart failure (CHF), is designed to inactivate tumor necrosis factor (TNF), a protein produced by the body in response to cell and tissue damage.
TNF production is one of the three known biological avenues that lead to a worsening of heart failure. "Current CHF medications block the other two: adrenaline, which makes the heart pump faster, and angiotensin, which increases blood pressure, putting an additional strain on the heart. However this is the first clinical attempt to inactivate the third biological factor -- TNF," says Douglas Mann, M.D., the study's principal investigator and professor of medicine at Baylor College of Medicine and chief of cardiology at the Houston VA Medical Center.
New drug therapies to treat heart failure are needed because current medications, while alleviating symptoms and prolonging life, can slow, but don't always halt the progression of the disease, says Mann. He adds that heart failure is the only form of heart disease that is dramatically increasing in the population.
Mann says TNF may worsen heart failure because of its toxic effects on the heart and circulatory system. "TNF levels are seven to eight times higher in people with congestive heart failure than in those with normal hearts," he says. "Since in laboratory animals TNF alone can produce many of the symptoms of congestive heart failure, including dilation of the heart, a weakening of the heart's contraction force and a buildup of fluid in the lungs, it seems likely that it would play a major role in heart failure."
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Contact: Carole Bullock
caroleb@heart.org
214-706-1279
American Heart Association
28-Jun-1999