Researchers have long known that the buildup of plaque in arteries can cause them to narrow and harden, potentially leading to a whole host of health problems, including heart attack, heart disease and stroke. While high blood pressure and artery stiffness are often associated with plaque buildup, recent studies have hinted at other causes. Now, a study from researchers at Washington University in St. Louis identifies a new cause of heart disease, namely, fragmentation of elastic fibers within the arterial wall. The team state that their findings could change the scope of heart disease detection and treatment for millions of Americans. The study is published in the journal Atherosclerosis.
Previous studies show that high blood pressure and reduced aortic compliance are associated with increased atherosclerotic plaque accumulation in humans. Animal studies support these associations, however, additional factors, such as fragmented elastic fibers are present in most previous animal studies. The current study shows that increased blood pressure and reduced aortic compliance are not direct causes of increased aortic plaque accumulation, with fragmentation of elastic fibers necessary to alter plaque accumulation.
The current study utilises two different groups of mice, some were genetically predisposed to hypertension, reduced aortic compliance, or increased artery stiffness; whilst the other mice were not genetically predisposed to the heart conditions. All of the mice were fed a Western (high-fat) diet for 16 weeks. Results showed no significant differences in plaque buildup between the two groups of mice. This led the group to explore a third factor not-typically associated with plaque accumulation, namely, the structure of elastic fibers within the arterial wall.
The researchers explain that in aging humans and previous animal studies, hypertension and increased arterial stiffness are accompanied by fragmentation of the elastic fibers. Data findings show that the mice had reduced amounts of elastic fibers, which causes hypertension and increased arterial stiffness, and no elastic fiber fragmentation, which may be the critical difference in plaque accumulation.
The lab note that they were able to separate the effects of elastic fiber fragmentation from hypertension and arterial stiffness in plaque accumulation. Results show that hypertension and arterial stiffness alone, without elastic fiber fragmentation, have no effect on plaque buildup. The group state their findings suggest that increased artery stiffness is a consequence of plaque buildup, as opposed to a cause of it, and offers a different approach in the study of heart disease. They conclude that their findings could lead to a re-examination of the relationship between increased plaque and diet, exercise and other lifestyle choices commonly associated with artery health.
The team surmise that their results suggest treating patients for hypertension and arterial stiffness may have no effect on plaque buildup as the underlying defect of elastic fiber fragmentation is not being treated, with elastic fiber fragmentation likely a key player in plaque buildup. For the future, the researchers state that the next step is to determine how fragmentation affects the movement and activation of molecules and cells that are involved in plaque formation.
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