MONDAY, July 16, 2007 (HealthDay News) -- A special patch placed on a damaged area of the heart regenerates cardiac cells after heart attack and improves heart function, a new study finds.
Success with the patch in rats may lead the way to new methods of repairing damaged human hearts and possibly spare some patients the need for a heart transplant, according to researchers reporting in the July 15 online edition of Nature Medicine.
"Normally, adult human hearts do not regenerate because the heart doesn't make more cardiomyocytes (heart muscle cells) after injury," explained lead researcher Dr. Bernhard Kuhn, from the Department of Cardiology at Children's Hospital Boston. "It would be desirable to induce the heart to make new cardiomyocytes after injury."
To that end, Kuhn's team created a patch that contains a compound called periostin, which helps cardiomyocytes divide and multiply. "If you do that over a number of cycles, you do get an increase in cardiomyocytes," he said. "So, the cardiomyocytes you have lost are replaced."
Periostin is a natural component of tissue surrounding cells. It comes from the skin lying around bone and helps stimulate cells to divide.
During a heart attack, cardiac cells die from lack of blood and oxygen. This damage prevents the heart from working normally. Typically, lost or damaged cardiac tissue cannot regrow.
In their experiments, Kuhn's team made patches from a material called Gelfoam and soaked the patches with periostin. They placed the patches on the damaged heart muscle of rats in which they had induced a heart attack.
After 12 weeks, the rats treated with the periostin patch experienced a 16 percent improvement in their heart's cardiac pumping ability. They also had less scarring of heart tissue, a reduction in the size of the damaged area of the heart, and more blood vessels feeding the area. In contrast, rats that received a patch without periostin showed no change in their heart function.
The hearts of rats treated with periostin showed a 100-fold increase in the number of heart cells and an average of 6 million more heart cells, far outnumbering the amount of dying cells.
The advantage of this technique is that it doesn't require new cells, such as stem cells, to coax the growth of new heart cells. Stem cells might also migrate to other parts of the body, with unknown consequences, Kuhn said. The patch is "also not gene-based, so it's not gene therapy," he said.
It is possible that this same technique could be used in people who have severe heart disease, Kuhn said. Although the technique might not restore heart function back to normal, there could be significant improvement, he said.
"At this point, the only biologically proven myocardial [heart] replacement therapy is heart transplant," Kuhn said. "But with this method, if you were on a transplant list, you may be able to come off it," he said. "This could be a revolutionary approach to treating heart failure."
One expert was impressed by the findings.
"The work is important in at least two ways: It helps improve our understanding of the molecular pathways regulating cell cycle reentry in adult cardiomyocytes, and it can form a basis for novel heart therapies based on the mobilization of [the heart's own] cells," said Gordana Vunjak-Novakovic, a professor of biomedical engineering at Columbia University Medical Center in New York City and co-director of the Tissue Engineering Resource Center at the U.S. National Institutes of Health.
"It will be interesting to see the extensions of this work to human cells and other cell types, including cardiogenic stem cells that could also be affected by periostin," Vunjak-Novakovic said.
Another expert echoed those sentiments.
"This research nicely demonstrates that periostin induced cardiomyocytes' reentry into the cell cycle," said Dr. Gregg C. Fonarow, director of the Ahmanson-UCLA Cardiomyopathy Center at the University of California Los Angeles.
Rather than needing to introduce brand new cells into the damaged heart, it may be possible to induce existing cardiomyocytes to grow and thus regenerate normal functioning heart muscle, said Fonarow, who is also professor of clinical medicine at UCLA.
"The ability to enhance cardiac regeneration holds great promise as novel treatment strategies for [heart attack] complicated by left ventricular dysfunction and for chronic heart failure," he said.
But rat studies can only tell scientists so much, Fonarow added. "Additional studies with adult human cardiomyocytes, and ultimately clinical trials, are needed," he said.
To learn more about how the heart works, head to the American Heart Association.