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New culprit for heart diseases identified

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New culprit for heart diseases identifiedWashington: Researchers have identified a new culprit, in the form of fragmentation of elastic fibers within the arterial wall, that could lead to heart diseases, a finding that may change the scope of cardiovascular disease detection and treatment for millions.

Medical professionals 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, researchers said.

While high blood pressure and artery stiffness are often associated with plaque buildup, new findings from researchers at Washington University in St Louis (WTUSL) in the US shows they are not the direct causes.

They suggest a new culprit – fragmentation of elastic fibers within the arterial wall.

“Our surprising results suggest that treating patients for hypertension and arterial stiffness may have no effect on plaque buildup because we are not treating the underlying defect of elastic fibber fragmentation,” said Jessica Wagenseil from WUTSL.

Researchers used two different groups of mice in the study. Some were genetically predisposed to hypertension and reduced aortic compliance, or increased artery stiffness.

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.

After extensive testing, researchers could detect no significant differences in plaque buildup between the two groups of mice. That led them to explore a third factor not typically associated with plaque accumulation – the structure of elastic fibbers within the arterial wall.

In ageing humans and in previous animal studies, hypertension and increased arterial stiffness are accompanied by fragmentation of the elastic fibbers, researchers said.

In the new study, the mice had reduced amounts of elastic fibbers, which caused hypertension and increased arterial stiffness, but no elastic fibber fragmentation, which may be the critical difference in plaque accumulation, they said.

“We found that hypertension and arterial stiffness alone, without elastic fibber fragmentation, have no effect on plaque buildup,” said Wagenseil.

The idea that increased artery stiffness is a consequence of plaque buildup, as opposed to a cause of it, as suggested by the findings, offers a different approach in the study of heart disease, researchers said.

It also could lead to a re-examination of the relationship between increased plaque and diet, exercise and other lifestyle choices commonly associated with artery health, they said.

The findings were published in the journal Atherosclerosis.

PTI

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