In individuals without symptoms who have thickened walls of the carotid arteries, two major arteries located on each side of the neck that provide blood and oxygen to the brain, the total blood levels of cholesterol are strongly associated with the presence a lipid, or fat-based,” core within plaque, which have a vulnerability to rupture, researchers report.

“We know that a lipid core, made up of fatty dead tissue deposits, within an atherosclerotic plaque puts the plaque at risk for causing an adverse clinical event, such as a stroke if the plaque is in the carotid artery or a heart attack if the plaque is in the coronary artery,” lead investigator Dr. Bruce A. Wasserman told Reuters Health.

To identify factors associated with a lipid core, Wasserman of Johns Hopkins School of Medicine, Baltimore, and colleagues examined subjects taking part in a study of atherosclerosis, also referred to as hardening of the arteries. All of the subjects were free of cardiovascular disease and were among participants with the thickest carotid artery walls, as determined by ultrasound.

The researchers used MRI and analysis software to assess the composition of 214 plaques with a thickness of at least 1.5 millimeter and found a lipid core in 151 (71 percent) of these plaques, according to the report, published in the medical journal Stroke.

Compared with patients with the lowest levels of total blood cholesterol, those with medium levels had a 2.8-fold increased risk of having a lipid core, after factoring in the possible effects of age, sex, high blood pressure and diabetes. Study participants with the highest cholesterol levels had a 4.6-fold increased risk of having a plaque with a lipid core.

None of the cardiovascular risk factors other than high serum cholesterol was associated with having a lipid core.

“Our study suggests that a person’s cholesterol level is the most important risk factor for developing this dangerous feature of plaque,” concluded Wasserman. “This supports the notion that lowering one’s cholesterol prevents its formation and might reduce one’s risk for such a clinical event.”

SOURCE: Stroke, February 2008.