Heart attack trigger found

October 20, 2000

The latest advance in the fight against heart disease comes from Glasgow University researchers involved in a long-term investigation of cholesterol levels.

The team led by Chris Packard of Glasgow's department of pathological biochemistry has discovered that an enzyme carried in blood can identify patients with a high risk of heart disease. The research, funded principally by the British Heart Foundation, draws on the latest analysis of the West of Scotland Coronary Prevention Study, which involved more than 6,500 middle-aged men with moderately high cholesterol levels but no history of heart disease.

Packard said the study showed the beneficial effects of lowering LDL, the carrier of the most damaging cholesterol, with drugs called statins. But some men with high LDL cholesterol do not develop heart disease. Known factors such as high cholesterol, high blood pressure and smoking account for just half the cases of heart disease.

"We know there are other factors out there and set about searching for them," Packard said. "We tested a particular enzyme, LpPLA2, that floats in the body, stuck on to LDL. We discovered that if you have a high level of this enzyme, your risk is increased about twofold, even if you have the same level of LDL."

High levels of LDL get stuck in artery walls, where free radicals oxidise them. The team's findings, published in the latest New England Journal of Medicine , show that the enzyme attacks oxidised LDL, producing inflammation in the blood that causes havoc in the artery wall, killing cells, promoting the rupture of large cholesterol deposits and blood clotting, and potentially precipitating a heart attack.

"What we seem to have hit upon is the enzyme that releases the oxidisation processes," Packard said.

"It's like a molecular trigger. If LDL is the gun, the oxidisation process is the bullet, and this is the trigger."

The findings may also explain why some people with average cholesterol levels get heart attacks: they may have high levels of LpPLA2, which causes damage even if only a small amount of LDL enters the artery wall. The research not only helps better identification of patients who will benefit from existing drugs, but also offers a new target for drug development.

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