New treatment offers hope for heart attack sufferers

Unlike many other parts of the body, the heart cannot repair itself after it is damaged.

When someone has a heart attack, a part of the organ dies and is replaced with scar tissue, leaving the remainder often struggling to maintain adequate blood flow around the body.

If the damaged portion of the heart is big enough, it can fail.

Heart failure is a miserable, often terminal, condition. And according to the British Heart Foundation (BHF) someone in the UK suffers from a heart attack every three minutes.

BHF figures also show there are:

Today, researchers led by Paul Riley at Oxford University and Linda Klotz at the Institute of Child Health, opened the door to a potential treatment for those people, a way that their damaged hearts might be coaxed into re-growing and repairing after an attack.

The researchers were studying the lymphatic system around the heart - this is part of a network of vessels in the body that transport fluids and white blood cells.

Experiments on mice showed that lymphatic vessels sprouted around the heart after it became damaged in an attack, an attempt by the body to try to limit the damage.

This made the researchers wonder if artificially stimulating more lymphatic vessels to grow might further limit the damage.

They used a protein called VEGF-C to stimulate the lymphatic vessels and found that the treated mice did indeed end up with less damage in their hearts.

Compared with untreated mice, those which had been given VEGF-C had a 30% improvement in their heart’s ability to pump blood - a significant improvement.

The research is described today in the journal Nature.

Crucially, the new technique stimulates cells that already exist in the heart.

Other approaches to repairing the heart after an attack involve making heart cells from stem cells.

Some of these techniques have even made it into early-stage clinical trials in people, but without huge success.

These techniques also have many problems, including immune rejection by the patient.

A potential treatment based on the latest work would be administered as a drug as soon as a heart attack had occurred, stimulating the lymphatic cells around the heart and thereby limiting the damage.

Hopefully, the vessels might even help re-grow some of the damaged heart.

Lead researcher Professor Paul Riley said: "There was a time when the heart wasn't thought to be repairable.

“We had no real concept of the cell types we wanted to target.

"Now, we're able to identify key cell types that play a role in development of the heart during pregnancy, and are maintained in the adult heart, and can be stimulated to lead to heart repair.

"It might be a cocktail of events to target cells that could give rise to new muscle, new coronary vessels and change the inflammatory environment of the heart.

"All of those things put together give us a lot of hope to moving towards heart repair and regeneration."

There are plenty of hurdles to overcome before Riley’s approach can work in people.

First, scientists need to confirm that the same lymphatic cells exist around the human heart and respond in the same way as those in the mice.

They then have to confirm that VEGF-C can stimulate those cells to do the repair work that they clearly aren't able to do without help or boosting.

A slight advantage here is that VEGF-C has already been tested in animals as a potential treatment for a type of cancer of the lymphatic system, known as lymphoma.

Whereas a basic scientific result like this might have taken decades before it was tested in people, Prof Riley’s work might end up in clinics far faster.

Professor Peter Weissberg, medical director of the British Heart Foundation, says that he is optimistic about the new research, but a solution for patients is still some way off.

"It looks as if the cells may be there [to repair the heart], they're just not waking up and doing the job we're asking them to do,” he said..

The work was funded by the British Heart Foundation, as part of their Mending Broken Hearts appeal.