Stem cell therapy creates heart cells capable of partially repairing damage to the organ, although more work needed before human trials can take place 
 
 Scientists have taken a step towards a radical new treatment for heart attacks with a stem cell therapy that can partially repair damage to the organ. 
 
 The treatment uses heart cells which are created in the lab from the skin of a donor who is chosen to be a good genetic match for the recipient. 
 
 
 
 Tests in monkeys showed that injections of freshly-made heart cells were quickly incorporated into damaged areas of the heart and helped the organ to pump more vigorously. 
 
 
 
 Stem cell trial suggests damaged heart tissue could be regenerated Read more 
 
 But monkeys that had the procedure also developed unusual heart rhythms, leading the researchers to concede that far more work is needed before the treatment can be considered safe enough for human trials. 
 
 
 
 Heart attacks are one of the leading causes of death in the developed world. In the UK alone, hospitals deal with nearly 200,000 cases each year. While 70% of patients survive, many are left with tissue damage that stops their hearts from working properly. 
 
 
 
 One idea scientists have had to treat heart attack survivors is to take skin cells from the patient and convert them into pumping heart cells. The hope is that, when injected into the heart, these cells take hold and help the heart pump more effectively. The advantage is that the heart cells will not be rejected by the immune system, but the procedure is time consuming and expensive to do for individual patients. 
 
 
 
 In the latest work, researchers in Japan took a different tack. They induced heart attacks in five macaques and then treated the damage with heart cells created from the skin of a donor monkey. The donor was selected to be a close genetic match, but the recipients still need drugs to stop their bodies rejecting the cells. 
 
 
 
 Yuji Shiba and others at Shinshu University injected the monkeys with 400m lab-made heart cells and found that they replaced about 16% of the damaged tissue. The new cells were wired up with healthy ones in the heart and over 12 weeks started to help the organ to pump more strongly. Tests revealed, however, that all of the monkeys developed unusual heart rhythms after the therapy. Details appear in the journal Nature. 
 
 
 
 The scientists are now trying to understand the precise cause of the abnormal heart rhythms, but Shiba told the Guardian: “I think we can manage the post-transplant arrhythmia.” 
 
 
 
 Sam Boateng, who studies the mechanisms of heart failure at Reading University, said the work was exciting because it was a step towards the possibility of repairing a damaged heart following a heart attack. 
 
 
 
 Stem cell treatment repairs damaged hearts in monkeys Read more 
 
 “Currently, the only long term option for these patients is heart transplantation, but there are not enough donors to meet the current demand,” he said. 
 
 
 
 But he added that many challenges remain. “Ideally, immune rejection would be eliminated if the cells could be derived from the same patient, but this is costly and time consuming at a time when the patient requires immediate treatment. Another concern is that the incomplete integration of the transplanted cells could result in irregular heart beats which can be deadly,” he said. 
 
 
 
 Sian Harding, director of the British Heart Foundation cardiovascular regenerative medicine centre at Imperial College London, said the Japanese team’s work was a significant step forward. “They strengthen the case that a bank of pre-prepared matched [cells] could be used to treat patients, without relying on the long process of reprogramming and differentiating the patient’s own cells.” 
 
 
 
 “The arrhythmias were seen in a previous similar study, but in neither study did they prove fatal and both suggested that they would decrease with time. Clinical strategies for preventing sudden cardiac death from arrhythmia, such as implantable cardiodefibrillators, may therefore be necessary as adjunct therapy for some months after implantation,” she added. ||||| A protein called cardiotrophin 1 might be an effective treatment for heart failure, according to researchers who found that it tricks the heart into growing in a healthy way. This growth is reversible, similar to that which occurs in response to endurance exercise or pregnancy. 
 
 
 
 Researchers from Canada have shown that it may be possible to trick the heart into growing healthily, without having to exercise. Researchers from Canada have shown that it may be possible to trick the heart into growing healthily, without having to exercise. 
 
 The team, including members from the Ottawa Hospital and the University of Ottawa in Ontario, Canada, reports the finding in the journal Cell Research. 
 
 The study paper also describes how, in animal models of heart failure, cardiotrophin 1 (CT1) promotes heart repair and improves blood flow. 
 
 Heart failure is a serious condition in which the heart cannot pump enough oxygen-rich blood to meet the needs of the body and its organs. The condition commonly results from heart muscle damage following a heart attack, the main cause of which is coronary artery disease. 
 
 There are around 26 million people living with heart failure worldwide, and numbers are rising. 
 
 Step forward in regenerative medicine 
 
 The outlook for patients diagnosed with heart failure are poor; their survival rates are worse than those of patients with breast, prostate, and bowel cancer. 
 
 In the United States - where around 5.7 million adults are living with heart failure - around half of patients die within 5 years of being diagnosed. 
 
 If heart failure is diagnosed and treated early, it is possible to improve survival and quality of life. Treatment usually consists of drug therapy, reducing dietary sodium, and exercising regularly. 
 
 The new study represents a step forward in a regenerative medicine approach to the treatment of heart failure, where the aim is to treat or even cure the disease by regrowing damaged tissue or restoring function. 
 
 Co-senior study author Lynn Megeney, a professor at the University of Ottawa, explains that when part of the heart dies - as it does in heart failure - "the remaining muscles try to adapt by getting bigger, but this happens in a dysfunctional way and it doesn't actually help the heart pump more blood." 
 
 But he says that, in animals with heart failure, they found that CT1 caused the heart muscles to "grow in a more healthy way," and it also stimulated the heart to grow new blood vessels. "This actually increases the heart's ability to pump blood, just like what you would see with exercise and pregnancy," he adds. 
 
 CT1 investigated in several models 
 
 Prof. Megeney and team investigated the effects of CT1 in laboratory-grown heart muscle cells, rats, and mice. They also compared the effects of CT1 with those of phenylephrine (PE), which is a drug that stimulates the "bad kind of heart growth," such as the harmful, irreversible enlargement that occurs in heart failure. 
 
 The researchers found that, when treated with CT1, heart muscle cells grow into longer, healthier fibers, whereas treatment with PE just results in wider growth. Also, with CT1, the new heart muscle tissue formed with new blood vessels alongside, which helps the heart to pump better. PE did not have this effect. 
 
 Furthermore, the heart growth that occurs with CT1 is reversible; when treatment stops, the organ returns to its original size, as it does when exercise stops or after pregnancy. The unhealthy heart growth that results from PE, on the other hand, is irreversible; when treatment stops, the heart remains dysfunctionally enlarged. 
 
 In two animal models of heart failure - one caused by heart attack, which damages the left side of the heart, and the other caused by pulmonary hypertension, or high blood pressure in the lungs, which damages the right side - CT1 treatment led to "dramatic improvements" in heart function. 
 
 Finally, although both CT1 and PE use the "cell suicide," or apotosis, molecular pathway to trigger heart muscle growth, CT1 showed superior ability to control the pathway. 
 
 The team is excited by these findings because, if they translate to humans, they could vastly improve the prognosis for patients with heart failure. 
 
 Promising for both types of heart failure 
 
 Co-senior author Prof. Duncan Stewart - cardiologist, senior scientist, and executive vice president of research at the Ottawa Hospital - explains that, at present, the "only treatment for right heart failure is a transplant." 
 
 "And although we have drugs that can reduce the symptoms of left heart failure," he adds, "we can't fix the problem, and left heart failure often leads to right heart failure over time." 
 
 The researchers are hopeful that CT1 will work in humans with heart failure because it did so in several animal models of the condition. 
 
 They also point out that, while in theory, exercise is an obvious way to reap the benefits that CT1 appears to offer, this route is not open to people with heart failure, who can only exercise in a limited way. 
 
 Profs. Megeney and Stewart already have patents pending for using CT1 to treat heart problems, and they hope to partner with others to test the protein in human patients. 
 
 Nevertheless, they say that it will be several years, even if the tests are successful, before the treatment is ready for widespread clinical use. ||||| Researchers have discovered that a protein called cardiotrophin 1 (CT1) can trick the heart into growing in a healthy way and pumping more blood, just as it does in response to exercise and pregnancy. They show that this good kind of heart growth is very different from the harmful enlargement of the heart that occurs during heart failure. They also show that CT1 can repair heart damage and improve blood flow in animal models of heart failure. The results are published in Cell Research. The research team is from The Ottawa Hospital, the University of Ottawa, the University of Ottawa Heart Institute and Carleton University. 
 
 Heart failure is a leading cause of death and disability in high-income countries and a growing problem around the world. It occurs when the heart can't pump enough blood through the body, often because a heart attack has damaged the heart muscle tissue. 
 
 "When part of the heart dies, the remaining muscles try to adapt by getting bigger, but this happens in a dysfunctional way and it doesn't actually help the heart pump more blood," said Dr. Lynn Megeney, senior author of the study and a senior scientist at The Ottawa Hospital and professor at the University of Ottawa. "We found that CT1 causes heart muscles to grow in a more healthy way and it also stimulates blood vessel growth in the heart. This actually increases the heart's ability to pump blood, just like what you would see with exercise and pregnancy." 
 
 Dr. Megeney and his colleagues conducted a variety of studies in mice, rats and cells growing in the lab. In addition to CT-1, some of the studies involved a drug called phenylephrine (PE), which is known to cause the bad kind of heart growth. They found: 
 
 Heart muscle cells treated with CT-1 become longer, healthier fibres, while those treated with PE just grow wider. 
 
 CT-1 causes blood vessels to grow alongside the new heart muscle tissue and increases the heart's ability to pump blood, while PE does neither. 
 
 When CT-1 treatment stops, the heart goes back to its original condition, just like it does when exercise or pregnancy end. However, the dysfunctional heart growth caused by PE is irreversible. 
 
 CT-1 dramatically improves heart function in two animal models of heart failure - one caused by a heart attack (affecting the left side of the heart) and one caused by high blood pressure in the lungs (pulmonary hypertension, affecting the right side of the heart). 
 
 Both CT-1 and PE stimulate heart muscle growth through a molecular pathway that has traditionally been associated with promoting cell suicide (apoptosis), but CT-1 has a better ability to control this pathway. 
 
 "This experimental therapy is very exciting, particularly because it shows promise in treating both left and right heart failure," said Dr. Duncan Stewart, a cardiologist, senior scientist and co-senior author on the paper who is also Executive Vice-President of Research at The Ottawa Hospital and a professor at the University of Ottawa. "Currently, the only treatment for right heart failure is a transplant. And although we have drugs that can reduce the symptoms of left heart failure, we can't fix the problem, and left heart failure often leads to right heart failure over time." 
 
 "An intriguing aspect of this research was how human CT1 was able to promote a healthy growth response in multiple animal models," said co-author Dr. Patrick Burgon, scientist at the University of Ottawa Heart Institute and assistant professor at the University of Ottawa. "This suggests the action of CT1 is universally conserved and puts us much closer to therapy." 
 
 The researchers also note that while exercise could theoretically have the same benefits as CT-1, people with heart failure are usually limited in their ability to exercise. 
 
 Dr. Megeney and Dr. Stewart have patents pending for the use of CT-1 to treat heart conditions and they hope to develop partnerships to test this protein in patients. If this testing is successful it will take a number of years for the treatment to become widely available. 
 
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 Full reference: Cardiotrophin 1 Stimulates Beneficial Myogenic and Vascular Remodeling of the Heart. Cell Research advance online publication 8 August 2017; doi:10.1038/cr.2017.87 Mohammad Abdul-Ghani, Colin Suen, Baohua Jiang, Yupu Deng, Jonathan J. Weldrick, Charis Putinski, Steve Brunette, Pasan Fernando, Thomas T. Lee, Peter Flynn, Frans H. H. Leenen, Patrick G. Burgon, Duncan J. Stewart, and Lynn A. Megeney http://www. nature. com/ cr/ index. html 
 
 Funding and other acknowledgements: Dr. Megeney and Dr. Stewart are part of The Ottawa Hospital's Regenerative Medicine Program, which includes the Sprott Centre for Stem Cell Research and the Sinclair Centre for Regenerative Medicine. This research was possible because of generous support from the community for Regenerative Medicine Research. This study was also supported by the Canadian Institutes of Health Research, the Ontario Research Fund, the Heart and Stroke Foundation of Canada and Fate Therapeutics. Fate also contributed scientifically to this research. 
 
 Media contact: Amelia Buchanan; ambuchanan@ohri.ca; Office: 613-798-5555 x 73687; Cell: 613-297-8315 
 
 About the partner institutions: The Ottawa Hospital is one of Canada's largest learning and research hospitals with over 1,100 beds, approximately 12,000 staff, over one million patient visits per year and an annual budget of over $1.2 billion. Along with the University of Ottawa Heart Institute, we are proudly affiliated with the University of Ottawa, one of Canada's top 10 research universities. The Hospital and Heart Institute were awarded exemplary status from Accreditation Canada and together with the University, have developed a roadmap for cardiovascular research excellence in the region.
– How do you mend a broken heart? Stem cells. Or at least that's the hope after scientists successfully used lab-created heart muscle cells to partially repair damaged hearts in monkeys, Live Science reports. The healthy stem cells were easily absorbed into the damaged hearts and allowed the organ to pump blood more easily. The procedure could lead to a new way to treat heart attacks and at least partially repair heart damage, the Guardian reports. Heart disease is the leading cause of death for men and women in the US. Scientists are intrigued by the idea of treating damaged hearts by using a patient's own skin cells to create healthy heart cells, which are less likely to be rejected since they don't come from a donor. In the latest study in the journal Nature, the team at Shinshu University induced heart attacks in five macaques and then injected them with heart cells made from the skin of a healthy macaque who was a close genetic match. To avoid rejection, they ensured the donor monkey had a type of protein similar to the recipients' and they gave the sick monkeys anti-rejection drugs. After studying the macaques for three months, researchers found their immune systems tolerated the new cells, which replaced about 16% of the damaged heart tissue. In the end, the monkeys' heart muscles contracted better, pumping blood more efficiently. Human trials are not coming anytime soon, though, after the macaques developed irregular heartbeats. Still, doctors said the findings raise the possibility of treating damage caused by heart attacks. "Currently, the only long term option for these patients is heart transplantation, but there are not enough donors to meet the current demand," heart researcher Sam Boateng told the Guardian. (Monkeys on a strict low-calorie diet lived much longer.)