This provides a summary of Coronary Artery Disease as a condition including the background, symptoms and signs/clinical presentation, investigations to diagnose the condition and management plan.
§ Imbalance between myocardial oxygen supply and demand, causing ischaemia of the muscle
PATHOPHYSIOLOGY
Arteriosclerosis ® Atherosclerosis
= thickening of the arterial wall, which causes loss of elasticity
§ Focal disease of the large and medium sized arteries
§ Clinical manifestations include: CAD, cerebrovascular disease, peripheral artery disease
§ Due to formation of fatty plaques in arterial walls.
There are 3 stages of atherosclerotic development.
1. Endothelial damage
§ The endothelium of an artery is involve in maintaining vasomotor tone, and does so by vasodilators (NO,
PGI2) and vasoconstrictors (angiotensin II, endothelin).
§ It is also involved in thrombosis and leukocyte interaction, and it does so by expressing cellular adhesion
molecules.
§ Therefore, if this endothelium is damaged, these functions are impaired and it is thus dysfunctional – it
will display inappropriate vasoconstriction and anti-thrombotic properties.
§ Damage can be caused by: shear stress, toxicity, hyperlipidaemia, infection.
2. Formation of foam cells (infiltration of macrophages)
§ Once the endothelium is damaged, oxidised LDLs can pass into it.
o Oxidation is facilitated by ROS from cellular damage
o Glycation can also occur, this is facilitated by high glucose levels. Glycated LDLs are more likely
to be oxidised.
§ Diabetics will therefore have higher glycated LDL numbers.
§ These are taken up by the scavenger receptor.
o Usually, unmodified LDLs are taken up by the LDL receptor, which recognises apolipoprotein
B100. Negative feedback occurs and once the LDLs are internalised, then surface LDL receptors
decrease in order to decrease LDL uptake.
o But modified LDLs aren’t recognised by the LDL receptor.
o There is no negative feedback of the scavenger receptor, so uptake of modified LDLs is
unlimited.
§ The oxidised LDLs in the endothelial wall stimulate expression of inflammatory mediators (including
monocyte adhesion molecules).
§ This attracts monocytes, which can bind to and cross the endothelium, where they become
macrophages.
§ Macrophages can then accumulate the oxidised LDLs to become foam cells (these appear as fatty
streaks).
3. Fibrous cap formation
§ Endothelial cells and macrophages release growth factors (platelet derived growth factor/PDGF).
§ PGDF causes proliferation of smooth muscle cells in the tunica intima of the artery, as well as collagen
production.
§ This proliferation causes atrophy of the internal elastic lamina, and the artery becomes loses elasticity.
§ These smooth muscle cells can also become foam cells as they can also take up modified LDLs.
§ This leads to further plaque formation.
§ Collagen will form the fibrous cap on top of the plaque – this can be fragile and dislodges easily (stable
vs unstable).
This atherosclerosis can occur in the coronary circulation, and narrowing of the arterial lumen due to plaque
reduces blood flow through that artery, and therefore reduces oxygen delivery to the myocardium. This results in
ischaemia.
Ø There are two main outcomes of narrowing – angina and MI.
Ø The type of lesion leads to the clinical manifestation.
o Stenotic/stable lesion ® angina
o Non-stenotic/unstable lesion ® MI
§ This one is susceptible to rupture and thrombus formation.
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