Protein- An effective treatment for heart failure

Ontario, Canada: A research team including members from the Ottawa Hospital and the University of Ottawa in Ontario, Canada found a protein called cardiotrophin 1, which might be an effective treatment for heart failure.

The researchers in the journal “Cell Research” mentions 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.” The study paper also describes how, in animal models of heart failure, cardiotrophin 1 (CT1) promotes heart repair and improves blood flow.

In the cases of “heart failure”, 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 the numbers are rising.

As per the data, in the United States only- where around 5.7 million adults are living with heart failure – around half of patients die within 5 years of being diagnosed.

The new study finds:

The new study represents 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.”

Animals with heart failures were 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.

When treated with CT1, heart muscle cells grow into longer, healthier fibres, 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.

CT1 showed improvement in the heart condition:

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.

The team is excited by these findings because, if they translate to humans, they could vastly improve the prognosis for patients with heart failure.

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.