Injecting adult stem cells into the heart could potentially halve the number of deaths from heart failure, a study has suggested.
The study, published in the Lancet, found that patients who received the treatment had a 37 per cent lower rate of death and hospitalisation for heart failure-related problems.
The study involved 126 patients from hospitals across America. Sixty patients were injected with stem cells while 66 were injected with a placebo. The procedure took two hours and most patients were discharged a day after surgery.
In the non-placebo group, stem cells were taken from the patients’ bone marrow, grown in culture, and then injected directly into the patients’ hearts.
In the stem cell therapy group 3.4 per cent of the patients died and 51.7 per cent were hospitalised, compared to 13.7 per cent and 82.4 per cent respectively in the group that received a placebo.
Dr Amit Patel, director of Cardiovascular Regenerative Medicine at the University of Utah, said: ‘For the last 15 years everyone has been talking about cell therapy and what it can do. These results suggest that it really works.’
He said it works either because it ‘slows down or reverses the rate of progression of disease’. Rather than increasing the number of muscle cells or blood vessels in the heart, he said, it likely makes the existing cells work better.
However, the study authors say they found only a small overall improvement in heart function.
The researchers are hoping to start a larger phase 3 clinical trial involving more heart failure patients.
About 900,000 people in Britain live with heart failure, which blocks blood vessels and reduces blood supply to the body.
Damage and or injury to the heart muscle is generally held to be irreversible. Drugs can improve symptoms and slow their progression; but for individuals with severe heart failure, the symptoms (breathlessness, fluid retention; diminished exercise capacity) can be intrusive and limiting. A few patients gain long-term benefit from implantation of mechanical devices that augment pump function and, for a few, heart transplantation holds hope.
The ‘holy grail’ of heart failure treatment is to provide a regenerative capacity that will allow new cells to repopulate damaged tissue and thereby to restore lost function. Last week’s Lancet carried a paper testing such an approach.
Although a relatively large trial in this field, the number of patients studied numbered only 126, with 60 receiving the active treatment. This trial showed positive effects in reducing a combined measure of death and hospitalisation.
Unusually, the total number of events was compared between groups — even if the same patient had more than one event. This double-counting is unusual in medical trials.
Despite the benefit in reducing ‘events’, there was no benefit in measures of actual heart pump function or in how much physical activity a person’s heart could support (judged by walking distance) when compared with placebo.
So, we are left with a trial showing a modest difference between groups as manifest in a very small number of patients, using an unusual endpoint and with no demonstrable benefit in symptoms or physical capability. Couple this with a considerable uncertainty of how the intervention might actually work at a cellular level and one is left with a trial that raises interesting possibilities but remains a preliminary observation.