Researchers have found that a drug can heal heart muscles in mice. Earlier it was considered that this damage to the heart is permanent but this new findings refutes earlier beliefs.
The study was published in the journal Nature, showed the drug, thymosin beta 4, if used in advance of a heart attack, was able to “prime” the heart for repair. Professor Jeremy Pearson, associate medical director of the British Heart Foundation, said, “To repair a damaged heart is one of the holy grails of heart research. This ground breaking study shows adult hearts contain certain cells that, given the right stimulus, can mobilize and turn into new heart cells that might repair a damaged heart.”
Due to advances in health care the number of people dying from coronary heart disease is falling say experts. But those living with heart failure are on the rise - more than 750,000 people have the condition in the UK alone.
For this study the researchers at University College London looked at a group of cells which are able to transform into different types of heart tissue in an embryo. In adults epicardium-derived progenitor cells line the heart, but they lie dormant. Scientists used a chemical, thymosin beta 4, to “wake them up”.
Professor Paul Riley, from the University College London, said, “The adult epicardial cells which line the muscle of the heart can be activated, move inward and give rise to new heart muscle. We saw an improvement in the ejection fraction, in the ability of the heart to pump out blood, of 25%.”Apart from this the scar tissue was reduced and the walls of the heart became thicker he said.
Peter Weissberg, medical director of the British Heart Foundation, said he was “very excited” about the research but warned the scale of improvement seen in animals was rarely seen in humans. However, he argued that even a small improvement would have a dramatic impact on people's quality of life. “A normal heart has lots of spare capacity. In patients with heart failure it is working flat out just to sit down [and] it's like running a marathon. You could turn a patient from somebody who's gasping while sitting in a chair to somebody who can sit comfortably in a chair,” he said.
Since the drug needs to be taken before heart failure, Professor Riley said, “I could envisage a patient known to be at risk of a heart attack - either because of family history or warning signs spotted by their GP - taking an oral tablet, which would prime their heart so that if they had a heart attack the damage could be repaired.” He said this could be available in 10 years.
Steve Houser, director of the Cardiovascular Research Center at Temple University, who wasn't involved in the study, said other teams have also reported potential repair cells in the heart, including some cells being tested in humans. He also cautioned that “very little in the cardiac world has translated from mice to man.” Yet, he said the new research was well done and will “stir the field” of heart regeneration studies.