Atheroma and Infarction
The old view of atheroma was that when you’re young and healthy you have nice clear
unobstructed blood vessels. But then at some point you get fat stored in your artery
walls, eventually this fat explodes and causes thrombosis.
The modern view of atherosclerosis is that it is a complex inflammatory process. We
now agree that low density lipoprotein is an inflammatory mediator (it “annoys the
endothelium as well as activating various inflammatory cells).
Angiotensin II (a vasoconstrictor) is also an inflammatory mediator, endothelial cells
do not like large amounts of it.
An ongoing systemic inflammatory diseases makes atheroma’s more likely to occur
e.g. rheumatoid arthritis.
The arteries that tend to be affected are branch points in larger arteries like: Carotid
arteries (cause stroke if break off) and circle of Willis, Coronary arteries, iliac arteries
and aorta.
How an Atheroma Develops
Initiation—
Substances like oxidised LDLs, angiotensin as well as inflammation will irritate the
endothelium. As a result the endothelium will become activated and release cytokines
– inflammatory mediators that tell nearby cells to be inflamed and adhesion molecules
– molecules endothelial cells express that allow other cells to stick to endothelial cells
(particularly immune cells).
The result of this activated endothelium is that circulating WBCs (such as monocytes)
will stick to these endothelial cells by the adhesion molecules and enter the artery wall
(diapedesis) and become a tissue macrophage. Monocytes do this all around the body,
in skin, lung etc. but they DO NOT belong in the intima of arteries and this is the start
of an atheroma.
Note the size of the intima in the cartoon below is exaggerated
, Inititation
Plaque Formation—
The tissue macrophage starts to take up circulating fat (LDLs) and become a foam cell.
At the same time it is also releasing lots of inflammatory mediators and growth factors
etc. This encourages nearby smooth muscle cells in media to migrate into the intima
(where they don’t belong).
In the process of moving into the intima and division, the smooth muscle cells start to
synthesise and release collagen and elastin which are structural proteins.
Plaqu
e formation
The old view of atheroma was that when you’re young and healthy you have nice clear
unobstructed blood vessels. But then at some point you get fat stored in your artery
walls, eventually this fat explodes and causes thrombosis.
The modern view of atherosclerosis is that it is a complex inflammatory process. We
now agree that low density lipoprotein is an inflammatory mediator (it “annoys the
endothelium as well as activating various inflammatory cells).
Angiotensin II (a vasoconstrictor) is also an inflammatory mediator, endothelial cells
do not like large amounts of it.
An ongoing systemic inflammatory diseases makes atheroma’s more likely to occur
e.g. rheumatoid arthritis.
The arteries that tend to be affected are branch points in larger arteries like: Carotid
arteries (cause stroke if break off) and circle of Willis, Coronary arteries, iliac arteries
and aorta.
How an Atheroma Develops
Initiation—
Substances like oxidised LDLs, angiotensin as well as inflammation will irritate the
endothelium. As a result the endothelium will become activated and release cytokines
– inflammatory mediators that tell nearby cells to be inflamed and adhesion molecules
– molecules endothelial cells express that allow other cells to stick to endothelial cells
(particularly immune cells).
The result of this activated endothelium is that circulating WBCs (such as monocytes)
will stick to these endothelial cells by the adhesion molecules and enter the artery wall
(diapedesis) and become a tissue macrophage. Monocytes do this all around the body,
in skin, lung etc. but they DO NOT belong in the intima of arteries and this is the start
of an atheroma.
Note the size of the intima in the cartoon below is exaggerated
, Inititation
Plaque Formation—
The tissue macrophage starts to take up circulating fat (LDLs) and become a foam cell.
At the same time it is also releasing lots of inflammatory mediators and growth factors
etc. This encourages nearby smooth muscle cells in media to migrate into the intima
(where they don’t belong).
In the process of moving into the intima and division, the smooth muscle cells start to
synthesise and release collagen and elastin which are structural proteins.
Plaqu
e formation
