Scientists are developing a pill to stop people suffering heart attacks and strokes. The drug would be taken regularly by middle-aged men and women to prevent their arteries clogging up or developing fatal blockages in later life.

A project led by Professor John Martin of University College, London, is designed to tackle the world's heart disease crisis and stems from a 10-year collaboration between Finnish, German, Italian and British researchers.

'Heart disease is the developed world's number one killer and even in the developing world it kills more people than malaria or Aids,' said Martin. 'We need to take urgent preventative action. Our pill - which will be ready for use in 10 years - will do just that.'

Martin's main collaborator, Professor Seppo Yla-Herttuala of Kuopio University in Finland, agreed. 'Drugs can lower cholesterol levels and prevent heart attacks or strokes in many cases. But in others, this does not work and we don't know why. We simply do not know what causes heart disease in many cases. We therefore need something that tackles the condition at its roots,' he said.

The group - whose work was recently highlighted at the European Commission's Descartes Prize awards in Prague - has concentrated on a substance called vascular endothelial growth factor (VEGF), a natural body chemical that stops arterial cell division.

Sometimes, however, VEGF does not act quickly enough and too many cells are produced. These form mounds inside the artery. Cholesterol floating through arteries sticks to the mounds. White blood cells also get trapped there.

The mound turns into a major blockage, the artery closes, and eventually a stroke or a heart attack is triggered.

'The root of the problem lies with those initial mounds,' said Yla-Herttuala. 'If we stop the mounds in the first place, then cholesterol will have nothing to stick to and no blockages will occur.'

The solution, said Martin, is to persuade the body to make extra VEGF. 'It is a natural substance, but in later life - for as yet unknown reasons - we stop producing enough.'

To get round this problem, Martin's team has taken the gene for VEGF and inserted it into a virus. These genetically modified viruses are then used to infect artery cells, in the process carrying extra VEGF genes into them.

The cells, armed with extra VEGF, produce more growth factor and this triggers a rapid cutback in cell production.

'This has an immediate clinical use,' added Martin. 'During surgery, when two blood vessels are stitched together, excess arterial cells are produced and these can cause serious blockages - a major problem for surgeons and patients.'

Martin - who set up a biotechnology company, the London-based Ark Therapeutics, last year to fund his work - has created a collar which contains modified viruses that surrounds a newly joined artery and stimulates its cells to produce VEGF, curtailing their growth.

Clinical trials of the VEGF collars began last year and are scheduled to continue for another 12 months. 'So far, everything has worked extremely well,' said Martin. 'We are showing that VEGF can greatly reduce the build-up of mounds of cells inside an artery.'

But using genetically modified viruses to deliver VEGF is only useful for medical operations. As a means of delivering a preventative drug to be taken regularly by millions of people, it is extremely impractical.

'We need to devise a version that can be taken orally,' said Yla-Herttuala. 'That is the only practical solution: a pill that can be swallowed once or twice a week.'

Simply giving people capsules of VEGF would not work, however. Acids in the gut would destroy growth factor molecules long before they got into the blood.

'We have to pinpoint the active part of VEGF - the bit that fits into a cell and triggers the release of the chemicals that stop arterial mounds building up,' he said.

This is what the international researchers are now doing. It has found a couple of candidate substances - both relatively small molecules that can survive the rigours of the digestive system - and is preparing to begin tests to see which will switch on VEGF production in the body.

Once swallowed, the drug would simply flow through arteries and help to ensure that the production of wall cells is curtailed as quickly as possible and so ensure that no deadly mounds of cells build up.

'Obviously, we still have a lot of work to do, but we are well on the road now,' said Martin.

'Initially our pills would be used to help people at high risk of heart disease - such as diabetics - but in the end I see this being taken by anyone reaching middle age who wants to stop their arteries clogging and stop a heart attack.'