Inflammation serves a purpose, after all

Scientists have discovered that, as far as arteries are concerned, inflammation can be both good
and bad. In its well-known bad role, it can aid atherosclerosis, the plaque-forming process that
clogs up arteries and raises the risk of heart attacks and strokes.
New research, however, has also revealed that during the advanced stages of atherosclerosis,
inflammation helps to keep the plaques stable, which reduces the risk of heart attacks and
The study was done at the University of Virginia (UVA) at Charlottesville and now features in
the journal Nature Medicine.
These findings have important implications for drugs that treat advanced atherosclerosis by
reducing inflammation.
The investigators draw attention to the "high-profile drug" canakinumab, which is undergoing
trials for the treatment of advanced atherosclerosis.
Based on their results, they suggest that, should it receive federal approval, the drug should only
be given to "a select group of patients."
"What our data suggest," says senior study author Gary K. Owens, a professor of cardiovascular
research at UVA, "is that you need to be extremely cautious in starting to give this drug more
broadly to lower-risk patients."
"If you give it to the wrong person, it could do the opposite of what you intended," he warns.
The Centers for Disease Control and Prevention (CDC) estimate that each year in the United
States, around 795,000 people have a stroke and 790,000 have a heart attack.
Most strokes and heart attacks are the result of the complex process of atherosclerosis.
The process builds up plaques in the inside walls of arteries, or blood vessels that supply the
heart and other organs and tissues with oxygen and nutrients. The plaques are made of calcium,
fats, cholesterol, and other blood borne substances.
As atherosclerosis progresses, these plaques harden and cause the affected arteries to narrow and
impede blood flow.
This increases the risk of heart attack if the artery nurtures heart muscle, or stroke if it is one that
feeds the brain.
The traditional view is that the body deposits potentially harmful substances in the plaques and
after this they do not change much and enter a dormant state. The "fibrous caps" that seal the
plaques are thought to be inert, serving like patches on tires.

By working with cell cultures and mice, however, Prof. Owens and his colleagues revealed that
the caps are far from inert and can change rapidly and dramatically over time; they are constantly
They noticed that treatment with a drug that blocked an inflammation promoter weakened the
cap structure, causing the plaque to rupture more readily.
The scientists suggest that reducing inflammation at the wrong time sends a signal that the job of
sealing the plaque is done.
"This study," reports first author Ricky Baylis, who is a student in Prof. Owens's laboratory,
"seems to indicate that the fibrous cap, as a structure, is actually much more plastic than
previously thought."
Though at first this might appear to be a problem, Baylis says that it may actually present "a
much greater opportunity to strengthen the caps to prevent heart attacks and strokes."
Prof. Owens reckons that studies similar to theirs should lead to better design of drugs that target
the "bad parts of inflammation" while preserving and even promoting the "good parts" so as to
"increase the stability of atherosclerotic lesions."
"[W]e believe our data suggest that if you suppress inflammatory response without first
removing or reducing the cause of the inflammation […] that this could become dangerous and
have unintended consequences” says Owens.


No comments.

Leave a Reply

Your email address will not be published. Required fields are marked *