Repairing Heart Attack Damage

Heart failure affects more than 23 million people around the globe, the condition often follows a heart attack and happens when the heart is damaged and can no longer pump blood properly. People who have had a heart attack are left with patches of scarring which last for life and can lead to heart failure and ultimately death; now scientists may have found a way to restore or remove this dead tissue to get the heart working normally again.

Restarting a growth process which ends during infancy may force the heart to rebuild itself and become healthy again by restoring tissue that was damaged during a heart attack, based in findings from pig studies; when the human gene microRNA-199a was injected into the animal’s hearts their heart function went back to normal within a month of heart attack.

“It is a very exciting moment for the field,”  said Professor Mauro Giacca. “After so many unsuccessful attempts at regenerating the heart using stem cells, which all have failed so far, for the first time we see real cardiac repair in a large animal.”

The gene was found to stimulate the heart to repair itself by restarting production of specialised cardiomyocyte heart cells which develop while a person is still a foetus with some growing further after birth, and they last for the rest of their lives.

Within weeks of the gene being injected into the large animal hearts their heart function was observed to return to normal. However redevelopment was not able to be stopped, which proved to be fatal as the hearts created so many new cells most of the pigs died.

“A treatment that helps the heart repair itself after a heart attack is the holy grail for cardiologists,” said Ajay Shah, chair of the British Heart Foundation.

“This study convincingly demonstrates for the first time that this might actually be feasible and not just a pipe dream. It will take some time before we can proceed to clinical trials. We still need to learn how to administer the RNA as a synthetic molecule in large animals and then in patients, but we already know this works well in mice,”  according to Giacca.

The researchers now hope to try a new version of the gene which will switch off after two weeks. While more testing and further development are required Giacca is confident that a human treatment could be available within 10 years.