 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. This growth is reversible, similar to that which occurs in response to endurance exercise or pregnancy. The Ottawa researchers, including scientists from The Ottawa Hospital, the University of Ottawa, the University of Ottawa Heart Institute and Carleton University and private industry, have worked to understand the signalling pathways, genes and cellular processes associated with CT-1. 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. "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. 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. “Treatment with CT-1 might get them to that point.” 
 
 In the research with mice and rats, CT-1 was delivered with a mini-pump about the size of a tablet inserted under the skin. 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. 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. They believed the negative effects were compensating for something else. After the baby is born or the athlete stops exercising, the heart returns to its original state, said Megeney, a senior scientist at The Ottawa Hospital and professor at the University of Ottawa. 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. 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. “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.” 
 
 Score one for basic science. 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. 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. Therapy using the protein, which the Ottawa researchers have already proved in animal models, will likely be ready for clinical trials in patients with right heart failure and myocardial infarction — heart attack — in two or three years.
– Scientists in Canada say they've found a way to trick the heart, making it behave as if it were the beneficiary of exercise even if no exercise was able to be done. According to a study in Cell Research, the Ottawa researchers discovered that protein cardiotrophin 1 (CT1) can fuel healthy heart growth, repair heart damage, and cause the heart to pump more blood in cases of left heart failure, as a result of heart attack, and right heart failure, as a result of high blood pressure in the lungs, reports Medical News Today. It's a big deal since medications used to treat left heart failure don't work on right heart failure, which usually requires a heart transplant, per a release. Exercise can be beneficial because it boosts the heart's ability to pump blood, but "people with heart failure usually can't exercise," researcher Lynn Megeney tells the Ottawa Citizen. The heart usually responds by expanding, irreversibly, in an unhealthy way. But that's why CT1 is "very exciting," Megeney says. It "causes heart muscles to grow in a more healthy way and it also stimulates blood vessel growth in the heart," increasing blood flow just like with exercise. And just like with exercise, the heart returns to its original size afterward. Megeney says the discovery could lead to fewer heart transplants, but he says it could be two or three years before researchers begin clinical trials on humans and, assuming they go well, a decade before treatment is available to the public. (To avoid heart issues, avoid beer?)