Studies Indicate Heart Can Repair Itself

New discoveries may improve heart attack treatments

MONDAY, April 14, 2003 (HealthDayNews) -- The human heart may have more ability to repair itself after a heart attack than previously believed, says a New York cardiovascular researcher.

If that ability bears out, heart attack treatment could change drastically, says Dr. Bernardo Nadal-Ginard of the New York Medical College, who will present his findings April 15 at the Experimental Biology 2003 meeting in San Diego.

Working with an animal model, Nadal-Ginard and his team successfully repaired hearts damaged by heart attacks. They did so by stimulating the stem cells -- the body's "master" cells that can turn into specialized cells -- to multiply and differentiate to repair the damaged heart muscle. The team has accomplished the repair without removing the stem cells, stimulating them in place by injecting a protein that helps communication between cells.

"We believe this might work in humans," Nadal-Ginard says. "But we must study it more in animals to see if there are any long-term [adverse] effects."

If the treatment works, it has the potential to change the current approach to the treatment of heart attacks, suffered by more than 1 million Americans each year. Currently, the emphasis is on increasing blood supply to the heart to preserve the surviving heart cells, using such approaches as clot-busting drugs or balloons to open up clogged vessels.

But that approach is based on the belief, challenged in recent years, that the heart has no ability to regenerate -- that once cells die during a heart attack, the heart can't make new ones.

Two years ago, Nadal-Ginard and his colleagues published a report in The New England Journal of Medicine, reporting evidence that cardiac myocytes, or heart muscle cells, regenerate after a heart attack.

And other researchers have taken stem cells from the bone marrow of animals and transplanted them into the damaged animals' hearts, succeeding in producing replacement cardiac muscle cells.

Now, Nadal-Ginard will report on his team's success in repairing animal hearts and on other observations in human hearts.

In the animal studies, they retrieved heart stem cells, grew them in the lab, cloned them and injected them back into the heart after a heart attack had been induced. The cells differentiated into myocytes, smooth muscle, and endothelial cells, he says, "and made a new myocardial wall."

"Then we showed you don't need to take the cells out," Nadal-Ginard says. "You can stimulate the cells in place with cytokines [proteins that help cells communicate] and the cells proliferate and differentiate and make a new [cardiac] wall."

In human studies, Nadal-Ginard's team took myocardial tissue out of patients who had died of an acute heart attack and examined it. "At the time they died, they were regenerating myocardium," he says.

Nadal-Ginard's team also examined, in the laboratory, myocardial tissue that was removed from more than 20 patients during a valve replacement operation. "These patients were making new heart cells from cells that looked like stem cells," Nadal-Ginard says. The studies support the fact that cells with stem cell characteristics do exist in the human heart. However, he was not prepared to call them full-blown stem cells.

"Until now, researchers have transplanted bone marrow stem cells to the heart [in animal studies]," says Dr. Valentin Fuster, director of the Cardiovascular Institute and Health Center at the Mount Sinai School of Medicine in New York City. But Nadal-Ginard's approach may be simpler and more effective, he says. What he has done is not to transplant cells, but stimulate cells already present in the heart to proliferate and differentiate, Fuster says.

Someday, Fuster adds, it may be possible to "inject a drug that may repair the heart by stimulating the cells that are there."

More information

For more information on stem cells, go to the National Institutes of Health. For information on heart attack treatments, try the American Heart Association.

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