The pill features a protein called cardiotrophin 1 (CT1), which can trick the heart into growing in a healthy manner and pumping more blood, much as the organ does in response to working out or pregnancy, according to a Tuesday report in the journal Cell Research.
CT1 was shown to be effective at repairing heart damage in the team’s studies on mice and rats, and cells the researchers grew in a lab.
“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 senior author Lynn Megeney, a professor at the University of Ottawa.
Heart failure is a growing problem around the world and a leading cause of death in high-income nations. It occurs when the heart cannot sufficiently pump blood throughout the body, often as a result of a heart attack that damaged the organ’s muscle tissue.
“We found that CT1 causes heart muscles to grow in a more healthy way and it also stimulates blood vessel growth in the heart,” Megeney said. “This actually increases the heart’s ability to pump blood, just like what you would see with exercise and pregnancy.”
As part of their research, the scientists compared CT1 to a drug called phenylephrine, which causes unhealthy heart growth. The team found that heart muscle cells treated with CT1 become longer, healthier fibers, while those treated with phenylephrine grew only wider. CT1 also caused blood vessels to grow alongside the new muscle tissue and increased the heart’s ability to pump blood. Phenylephrine did neither.
CT1 greatly improved heart function in two models of heart failure, the first of which is caused by a heart attack, affecting the left side of the heart, The other stems from high blood pressure in the lungs, known as pulmonary hypertension. The latter model affects the right side of the heart.
“This experimental therapy is very exciting, particularly because it shows promise in treating both left and right heart failure,” said co-senior author Duncan Stewart, 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.”
Co-author Patrick Burgon, a scientist at the University of Ottawa Heart Institute, was encouraged by the success of the CT1 treatment in more than one type of animal.
“An intriguing aspect of this research was how human CT1 was able to promote a healthy growth response in multiple animal models,” he said. “This suggests the action of CT1 is universally conserved and puts us much closer to therapy.”
The team said that while exercise could provide the same benefits as CT1, people with heart failure are typically limited in their ability to physically exert themselves.
Megeney and Stewart have patents pending for the CT1 treatment, and hope to establish partnerships to test the protein in patients. If the trials are successful, it will take several years for the treatment to become widely available.
(Photos by Cell Research show how CT1 treatment repaired heart muscle after a heart attack in a rat. The blue areas are scar tissue and red sections are healthy heart muscle.)