New Hope for Fixing Broken Hearts

Research Shows Heart Damage Can Be Reversed

Medically Reviewed by Louise Chang, MD on July 23, 2009

July 23, 2009 - It has long been thought that damage to the heart is irreversible, but new research is challenging that assumption.

Investigators from Children's Hospital Boston were able to reverse heart damage in mice by stimulating the growth of new heart muscle cells.

They did this by injecting the mice with the growth factor neuregulin1, which is a key player in heart cell growth.

Until recently, most experts believed that the heart muscle could not repair itself, in part because the cells responsible for its development stop proliferating after birth.

But recent studies have shown that these heart muscle cells, known as cardiomyocytes, do have a limited ability to replace themselves.

The hope is that neuroregulin1 can one day be used to ramp up this process in humans and help heal damaged hearts, as it seems to do in mice, study co-author Bernhard Kuhn, MD, tells WebMD.

"Contemporary heart failure treatment is directed at making the remaining cardiomyocytes function better, and improvements in outcomes are harder and harder to achieve because these therapies have become so good," he says. "But despite this, heart failure is still a fatal disease. Therapies that replace lost heart muscle cells have the potential to greatly advance the field."

Injections Reversed Heart Attack Damage

Many other research teams are looking for ways to repair damaged heart muscle, but most of these efforts have focused on coaxing stem cells to become new heart cells.

The research by Kuhn and colleagues shows that stimulating heart muscle cells to proliferate in other ways may prove to be a viable alternative to stem cells, Duke cardiologist Richard C. Becker, MD, tells WebMD.

Becker, who is a spokesman for the American Heart Association, called the new research compelling.

"This is something that I suspect people in the field of cardiology will be very excited about, and I suspect this interest will stimulate additional research,” he says.

The mice in the study were treated with daily injections of neuregulin1 starting a week after experiencing laboratory-induced heart attacks.

Twelve weeks later, they showed evidence of better heart function, reductions in heart muscle scar size, and an increase in heart muscle cells, Kuhn says.

And unlike untreated controls, the treated mice showed no evidence of heart failure.

"Most of the [heart attack] related cell death had already occurred," he says. "When we began the injections we saw replacement of a significant number of cardiomyocytes resulting in significant structural and functional improvements in the heart muscle."

Researchers Studying Other Compounds

Neuregulin1 is not the first substance identified by the authors that promotes heart muscle cell growth.

In 2007, they reported that the protein periostin, found in the developing fetal heart and injured skeletal muscles, also induced cardiomyocyte production and improved heart function in rats.

Periostin cannot be injected, so the researchers developed patches infused with the compound, which were placed directly on the damaged area of the heart.

Kuhn says the two therapies may one day prove useful in the treatment of heart attack patients.

"During initial treatment patients might receive neuregulin injections, and once they are stable and out of the ICU they might be taken to the cath lab for a periostin patch," Kuhn says.

But before that happens, the two treatments must be proven safe and effective in large animal and human studies.

The researchers recently completed a study of periostin in pigs, but the findings have not been published.

Show Sources


Bersell, K. Cell, July 27, 2009; vol 138: pp 257-270.

Bernhard Kuhn, MD, pediatric cardiologist, Children's Hospital Boston; assistant professor of pediatrics, Harvard Medical School.

Richard C. Becker, MD, professor of medicine; director, Duke Cardiovascular Thrombosis Center, Duke Clinical Research Institute, Durham, N.C.

Kuhn, B. Nature Medicine, August 2007; vol 13: pp 962-969.

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