LONDON (Reuters) – A US research team said yesterday it had found evidence why some plaque build-ups in arteries may lead to heart attacks and stroke while others do not.

A gene had been found in mice that makes artery-clogging plaques more likely to break apart and cause stroke or heart attacks, Ira Tabas of Columbia University in New York and colleagues reported.

The findings could lead to new drugs to prevent heart disease, one of the world's biggest killers, they added in the journal Cell Metabolism.

"The billion dollar question is why 98 percent (of plaques) cause no problem and two percent do," Tabas said in a statement.

"So the wave in treating atherosclerosis will be in preventing harmless lesions in young people from becoming dangerous ones, or soothing dangerous plagues so they don't rupture as we age."

Heart disease usually develops slowly, as "plaque" builds up in arteries, reducing blood flow and causing unstable clumps that can break off and cause strokes or heart attacks.

Tabas and colleagues studied two groups of mice engineered to develop plaque build-ups, one with and one without a gene called CHOP that plays an important role in cell death.

They found that dangerous plaques were much smaller in mice without the gene, providing a potential drug target to treat heart disease, the researchers said.

The study also suggests that such new drugs could protect people not on statins – the world's top-selling drugs – to cut heart attack and stroke risk, though a healthy lifestyle remains the best strategy, the researchers added.

"Our understanding of atherosclerosis may be changing, but the old standbys, diet, exercise, and keeping your risk factors like cholesterol and blood pressure in check remain the best option," Tabas said.