The metal springs that can give failing hearts a boost

Beat it: Innovative, new design could revive heart function, increasing cardio health

A tiny metal spring that is implanted into the heart could revolutionise treatment of heart failure, a condition that affects almost a million people.

The device pushes against the walls of the left ventricle, the heart’s main pumping chamber, to help it expand and fill with blood.

When the chamber is full and the heart contracts, these springs give way, allowing the left ventricle to fully contract and force out as much oxygen-rich blood as possible to the circulation, so organs, muscles and tissues continue to get a healthy supply.

The device is being tested in a ten-patient trial in Israel.

Every year, about 270,000 people in Britain have a heart attack. Damaged by the lack of oxygen, the heart can undergo what cardiologists call adverse remodelling, where damaged muscle begins to change shape. Within days, areas of firm heart muscle can become soft and thin, dramatically reducing the heart’s performance.

In many cases, this leads to heart failure, where weakened heart muscle is unable to deliver sufficient oxygen to tissues.

In some patients, the heart stops contracting as it should; in others, the heart doesn’t relax enough, so the left ventricle doesn’t expand and fill with blood. 

The new implant is designed for the latter group of patients and helps the left ventricle expand as much as possible as it relaxes.

Heart failure causes symptoms such as severe tiredness, shortness of breath and chest pain. It can also be caused by high blood pressure or heart rhythm problems.

There are medicines that can control the symptoms. However, many people gradually deteriorate, and up to 40 per cent die within a year of diagnosis.

National health scare: Every year,  270,000 people in Britain have a sudden heart attack

National health scare: Every year, 270,000 people in Britain have a sudden heart attack

The new implant, called CORolla, is placed inside the heart’s left ventricle under general anaesthetic. Doctors can insert it via two routes: either through an incision in the groin and through the blood vessels to reach the heart; or through the chest wall.

The device is pushed through on the end of a tube, called a catheter, and fed into the left ventricle. Once in situ, the implant opens and the three wire prongs, connected to each other with tiny wire springs, open up and attach to the bottom corner of the left ventricle. The implant pushes hard up against the walls of the chamber to help it open wider and fill with more blood.

When the heart contracts, the springs — a bit like those you would find on a clothes peg — allow the three prongs to collapse, or give way, so the left ventricle can fully contract. The springs then instantly return the prongs back to their original position, forcing the walls of the ventricle to fully expand again.

The trial at Rambam Medical Center in Haifa, Israel, will assess the spring implant’s effectiveness in improving cardiac function and easing heart failure symptoms. Patients will be monitored for two years. The first results are due next year but it is hoped that the relatively simple technology could help thousands in the years to come.

Commenting on the implant, Martin Cowie, a professor of cardiology at Royal Brompton Hospital in London, said: ‘This idea seems interesting and makes sense from the scientific point of view. But it is at a very early development stage.’

Julian Halcox, a professor of cardiology at Swansea University, added: ‘In principle, this strategy looks very promising, but we need to see what the real benefit is in terms of symptoms.’

MEANWHILE, Canadian researchers have found a human protein can help heart muscle grow normally after heart failure.

The team from Ottawa Hospital and the University of Ottawa injected a protein called cardiotrophin 1, which is also found in human muscle, into mice and rats with heart failure for two weeks.

Heart scans showed it made the heart grow bigger and healthier, in a similar way to changes induced by exercise, they report in the journal Cell Research. It could lead to a new drug for heart failure and researchers hope to test it in humans within three years.