Research shows segments of carotid artery respond differently to atherosclerotic plaque buildup

Jul 14 2009

Different segments of the carotid artery that supply the brain with blood respond in different fashions to the build-up of complex, health-threatening plaque, according to researchers from Wake Forest University Baptist Medical Center and their colleagues.

The research provides important information because blockages in the carotid arteries are a major cause of stroke, said J. Greg Terry, M.S., a research associate in the endocrinology section of internal medicine at Wake Forest Baptist. He presented the findings in June at the International Symposium on Atherosclerosis held in Boston.

The left and right carotid arteries include the common segment, which widens into the bulb segment and then splits into two different arteries -- the internal carotid artery, which supplies the brain, and the external carotid artery, which supplies the face. The health of the carotid arteries is considered to be an index of artery health in the heart as well. Plaque, which is comprised of cholesterol, calcium and fibrous tissue, can build up on the inside of the arteries and compromise blood flow.

The researchers used MRI scans to measure each part of the carotid artery, including the interior (lumen) and wall areas of the common, bulb and internal segments. They analyzed the carotid arteries of 191 men and women who had no symptoms of carotid disease.

The study confirmed the hypothesis that different segments of the carotid artery respond to plaque differently. In people with complex plaques, the common carotid artery expanded outward by 11 percent on average to preserve the lumen or central opening where the blood flows, compared to subjects with no plaque.

Although the common carotid compensated for atherosclerosis or plaque build-up by increasing in size, the bulb and internal segments narrowed with plaque. Within the internal segment of the carotid artery, the area of blood flow was decreased by as much as 16 percent and the wall of the artery was thickened by 14 percent on average. That overall narrowing or stenosis caused by the "remodeling" may lead to reduced blood flow compared to subjects with no plaque.

"This may help explain why so many significant blockages occur in the internal carotid and the bulb area and so few occur in the common segment, which seems to be protected," said Terry.

The study findings could not be explained by known risk factors. This suggests that variation in carotid artery remodeling within an individual are related to differences in arterial anatomy or local blood flow patterns. However, differences in artery remodeling between individuals may be related to genetics or risk factors that have not been identified.

The research presented was based on analysis of baseline data; study participants also received a follow-up MRI two years after the baseline image that will allow the investigators to study changes over time.

The research is part of a study called the Carotid Atherosclerosis MRI Progression Study (CAMPS) funded by the National Institutes of Health and led by John R. Crouse III, M.D., of Wake Forest Baptist and Chun Yuan, PhD, of the University of Washington-Seattle. The research at Wake Forest Baptist was carried out in the General Clinical Research Center and the Center for Biomolecular Imaging (CBI). In addition to Terry, the research team includes Haiying Chen, M.D., Ph.D., Ethel Kouba, Ph.D., Bob Kraft, Ph.D., and Jeff Carr, M.D., of Wake Forest Baptist and Hunter Underhill, M.D., and Tom Hatsukami, M.D., from the University of Washington.