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L12 Atherosclerosis
Atherosclerosis is a chronic inflammatory, fibro-proliferate disease of the artery wall
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Primary atherosclerosis: as above take decades to develop symptoms
Transplant atherosclerosis: narrowing of arteries at the point of engraftment of transplant organs
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Months-years to develop symptoms
Atherosclerosis distribution is not systemic
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This is due to haemodynamic:
 Some flow is laminar = fine
 At bifurcations the blood hits the wall = complex patterns of flow (can get back flow and points of stasis at some
points of cardiac cycle)
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These areas have low shear stress
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But where there is pulsating flow the cells
present another phenotype
Atheroma mainly develops in the intima
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Cellular pathology of atherosclerosis
 Lots of immune cells
o Infiltration of T cells and monocytes
o Monocytes differentiate in to macrophages which take up
cholesterol (LDL or oxidised LDL) and become foam cells (full of
cholesterol ester)
o Foam cells Drives the inflammatory response
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Development of Atherosclerotic plaque
1
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a
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Intermediate of Fibrofatty lesion – a connective tissue matrix (collagen fibrils, elastic, fibres, and proteoglycans)
a
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b
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Advanced fibrous plaque
a
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Lots of foam cells and some T cells
c
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Fibrous cap – stops it from degrading from the forces of blood flow
i
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Not many active inflammatory cells, low lipid content
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Vunerable plaque – thinner cap (especially around shoulders)
1
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High lipid and inflammatory cell content
4
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Rupture of plaque expose contents of the plaque to the blood  very thrombogenic  form a
thrombus  may block any residual lumen  ischaemic tissue downstream
b
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Blocks of microcirculation  ischaemia
Disease associated with atheroma distribution
 Peripheral vascular disease (mainly in legs)
o Intermittent claudication
 Femoral arteries blocked where at rest there is enough O2 to supply tissue
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o Ulceration
 If severe blockage can’t supply immune cells and plasma = small wounds can rapidly ulcerate –
difficult to clear up
o Gangrene
 Circulation completely cut off = tissues are starved of O2 and die
 Coronary Heart disease
o Acute angina
 Vessels compromised = when at ‘rest’ enough O2
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o Unstable angina
 Associated with formation of a thrombus from a ruptured plaque
 Unpredictable as to when symptoms will present
 But a good indicator that a myocardial infarction could occur
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 Cerebrovascular disease
o Stroke (due to embolic events)
Cellular elements of the plaque and how they interact to promote atherosclerosis

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