Gene therapy could be an effective way to improve survival rates among heart attack patients, new research funded by the British Heart Foundation (BHF) suggests. Academics at the University of Bristol found that boosting levels of a natural growth factor in the heart could help the muscle to recover after a heart attack. The death rate from a heart attack was halved in mice that received the treatment.
Heart attacks occur when a blood clot blocks off the blood supply to part of the heart muscle. Deprived of oxygen, the tissue dies and cannot regenerate. If the person survives, they can be left with a weakened heart that can't pump blood as effectively - causing severe ill health. Each year, around 140,000 people suffer a heart attack in the UK.
Nerve growth factor (NGF) is so called because it promotes the growth of nerve cells, but Dr Costanza Emanueli, a BHF Senior Research Fellow, previously showed that it could also stimulate the growth of new blood vessels.
In a new study published in the journal Circulation Research, Dr Emanueli and her team in Bristol investigated whether NGF could help the heart recover from a heart attack by encouraging new blood vessels to grow into and nourish the injured muscle.
The researchers used a specially engineered virus to deliver extra copies of the gene for NGF into the hearts of mice. Thirty days after having a heart attack, 80 per cent of the mice that received this treatment were still alive, compared with only 60 per cent of mice that did not. The pumping ability of the heart was also significantly improved in mice that received the NGF gene.
In contrast, mice that were given an antibody that neutralised NGF fared significantly worse after they had a heart attack, with higher rates of cell death and more severely impaired heart function.
When the researchers looked at post mortem human hearts that had suffered a heart attack, they found that levels of NGF near the blood-starved part of the heart were higher than normal, suggesting that increasing NGF production is a normal part of the tissue's response to oxygen deprivation.