2-Drug Treatment Reverses Heart Attack Damage

Therapy proves successful with rats, but human trials a long way off

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By Ed Edelson
HealthDay Reporter

MONDAY, Oct. 9, 2006 (HealthDay News) -- A two-drug treatment has healed heart muscle in animals after stimulated heart attacks, researchers report.

One drug blocks an enzyme that normally suppresses reproduction of heart cells, while the other encourages the growth of blood vessels, according to a study by researchers at Children's Hospital Boston, a Harvard facility.

But human trials of the treatment can't be expected in the immediate future, said study author Felix Engel, an instructor in pediatrics at the hospital, since work is still on the most basic level.

"I'm interested in the molecular mechanisms, how these drugs work," Engel said. "I'm trying to find other drugs, more efficient drugs, and to develop other therapies that would be capable of acting in humans."

Still, the study does show that it's possible to rescue heart muscle, something that does not occur naturally after a heart attack. Normally, the damaged heart muscle is replaced by scar tissue, which can impair the heart's pumping capacity and lead to life-threatening abnormal heart rhythms.

The findings will be published in next week's issue of the Proceedings of the National Academy of Sciences, and will be available online this week.

A first step in the new research -- a demonstration that heart cells could multiply in a petri dish if a drug blocked an enzyme designated p38 MAP kinase -- was reported last year by Engel and Dr. Mark Keating, who worked on the current experiment but has since left Children's Hospital.

The new trial added a molecule designated FGF1, which stimulates growth of blood vessels, to the treatment given to some of the 120 rats with stimulated heart attacks. Three months later, echocardiograms showed markedly improved heart function in rats who received both drugs. Muscle scarring was minimized, and blood-pumping ability was close to normal. Rats receiving a single drug showed lesser improvement.

One important step now is to develop a method of delivering the treatment to the proper location in the body, Engel said. FGF1 has the potential for serious side effects if it goes to places other than the heart, and the p38 MAP kinase inhibitor has been shown to damage the liver.

"I am working on delivery by using a kind of gel," Engel said. "We can mix the drug with nanofibers. It is a liquid when injected into the heart and then becomes a gel, diffusing over time."

An assessment of the therapy by Dr. Richard T. Lee, an associate professor of medicine at Brigham and Women's Hospital in Boston who did the actual work with the animals, was guardedly enthusiastic.

"There clearly was an effect," Lee said. "The kind of study we did can't prove exactly why there was an effect, but there certainly was a benefit on how the heart performs. It's a long way from doing an experiment to developing something for human use. But the field is young, so we are excited about things that look like they benefit long-term heart function."

What happens now, Lee said, "depends on people in industry and people in the academic world."

More information

Current treatments for a heart attack are described by the National Library of Medicine.

SOURCES: Felix Engel, Ph.D., instructor, pediatrics, Children's Hospital Boston; Richard T. Lee, M.D., associate professor, medicine, Brigham and Women's Hospital, Boston; Oct. 9-13, 2006, Proceedings of the National Academy of Sciences online

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