SEATTLE University of Washington (UW) researchers have gathered evidence that dangerous plaques in blood vessels can rupture by overproducing protein-digesting enzymes. Plaques are fat-laden rough spots in the otherwise smooth walls of arteries. When a plaque ruptures, blood accumulates inside of it, a process known as plaque hemorrhage. The plaque enlarges and artery-blocking clots can form. If the flow of oxygen-rich blood is restricted, a heart attack, stroke, or damage to other organs can occur.
Most adults have some degree of plaque in their arteries. The condition, known as atherosclerosis or "hardening of the arteries," generally progresses with age. Not all plaques have a tendency to break open.
"Why plaques become unstable in certain people, and why some plaques become unstable but others plaques in the same person remain stable have been the objects of much conjecture," said Dr. David A. Dichek, the senior researcher on the study, "Some scientists have suspected that an excessive production of protein-digesting enzymes might be linked to 'vulnerable plaque' blood vessel lesions prone to rupture. The findings of our study offer the best cause and effect evidence to date that this is likely the case."
The study is published today, March 29, in Circulation, a scientific journal of the American Heart Association.
Dichek holds the UW Medicine John Locke, Jr. Family Endowed Chair in Cardiovascular Research and Treatment and is a professor of medicine in the Division of Cardiology. He practices general cardiology at the UW Medicine Regional Heart Center.
People start life with clean arteries. Plaques appear when white blood cells burrow into the lining of arteries and engulf harmful cholesterol and lipids. Plaques begin as fatty streaks. Fatty streaks can attract several kinds of cells, including clean-up cells called macrophages. The plaques can enlarge until their cores are filled with dead cells,
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University of Washington