Ruptured plaques can be deadly
Scientists have identified a genetic mechanism which appears to determine which fatty deposits in the arteries have the potential to kill us.
Most of these plaques pose no risk to health, but a minority burst, forming blood clots, which can cause heart attacks or strokes.
A Columbia University team pinpointed a gene which seems to make plaques more vulnerable to rupture.
The American study appears in the journal Cell Metabolism.
Fatty deposits begin to form in the arteries of most people in their teens, but the vast majority are harmless.
However, it is thought that around 2% of plaques have the potential to burst.
This can lead to the development of a clot, which can restrict blood supply to the heart or brain, with potentially grave consequences.
Scientists believe one of the key factors determining whether a plaque will burst is the make up of its inner core.
The inner core of plaques vulnerable to rupture often contains a lot of dead cells.
These cells release substances that can weaken the surface cap of the plaque, making rupture more likely.
The Columbia team identified a gene thought to play a key role in the build up of these dead cells.
The researchers bred mice prone to develop plaques, and fed them a high-fat diet for 10 weeks.
The animals which lacked the key gene tended to produce smaller plaques, and to show markedly lower levels of cell death and plaque degradation.
The gene in question produces a protein which plays a central role in a mechanism used by the body to kill off cells that are damaged and unhealthy.
This mechanism key to ensuring our tissues remain in good working order.
But there is some evidence to suggest that the process may sometimes become too aggressive, and may lead to problems such as neurodegenerative diseases and diabetes.
And the latest study suggests it may also turn benign plaques potentially deadly.
Lead researcher Dr Ira Tabas said that previous research had suggested that this mechanism might be involved in plaque rupture, but the magnitude of the effect uncovered in the latest study was a surprise.
He said: "The fact that we were able to isolate one gene encoding one protein with such a profound effect on plaque necrosis (death) was a big surprise."
Dr Tabas said the finding raised hopes of new drugs which could act on the key gene, or the associated mechanism, to cut the risk of dangerous plaques.
"Just about everybody in our society has atherosclerosis (thickening of the arteries) by the time we reach 20," he said.
"So the wave of the future in treating atherosclerosis will be in preventing harmless lesions in young people from becoming dangerous ones, or soothing dangerous plaques so they don't rupture as we age."
Alasdair Little, a cardiac nurse at the British Heart Foundation, said: "This is a very interesting biological study to identify why some plaques that cause coronary artery disease may lead to a heart attack and others do not.
"However, many more years of investigation and study will be needed before it informs clinical practice for the treatment of heart disease."