Coronary Artery Disease: Atherosclerosis Flashcards
Coronary defenition:
Relating to the arteries which surround and supply the heart
Atherosclerosis definition:
Atheroma; fatty plaque deposit
Sclerosis; Hardening
Coronary Atherosclerosis:
Disease in which plaque builds up inside arteries supplying the heart. Plaque harderns over time and the build-up causes the inside of arteries to become narrower, slowing down blood flow and increasing the pressure in the arteries.
What does a decrease in Arteries compliance lead to?
Hypertension, can also lead to Ischaemia
WHat is ischaemia
Lack of Oxygen in distal tissues that can spread through the body.
Consequenses of Atherosclerosis at: The cerebral and carotid arteries
Cerebovascular disease: stroke, vascular dementia, ischaemic transient heart attack
Consequenses of Atherosclerosis at: The renal arteries
Renovascular disease
Consequenses of Atherosclerosis at: The Aeorta
Aortinc aneurusm- swelling and rupture of aneurusm almost always fatal
Consequenses of Atherosclerosis at: Legs and Arms
Claudation (amputation if severe)
Peripheral gangrene - ischaemic tissue damage (amputation)
Endothelium Dysfunction is:
- the target of almost all CVD risk factors
- Involves Vascular and Cardiac
- Is the initiating factor in atherosclerosis
- indicated before any strucutral damage to vasculature is seen
- Associated with the progression of almost all aquired CVD
What is the endothelium structure?
It is the innermost layer in the arteries: a single cell layer, and elongated in direction of flow.
What is the dysfunction in the endothelium?
A defect in the Nitrogen Oxide production causes impaired endothelim-dependant vasodilation which signals dysfunction, causing increased endothelin (ET-1) and reactive Oxygen species production
What is Atherosclerosis in response to injury also known as?
Atheroma.
Describe the formation of fatty streaks in the arteries (atherosclerosis):
If an intact endothelium is damaged due to injury, there is an increased permeability through the spacing of the endothelial cells.
This causes accumulation of oxidised LDL in the sub-endothelial space causing inflammation and thus promoting atherosclerosis.
There is also leukocyte adhesion across the endothelium intitiating inflammation.
Monocytes stick to the loosening endothelial cell junctons and differentiate into macrophages.
The macrophages engulf LDL by phagocytosis forming FOAM CELLS (fatty streaks).
This stage is early and reversible
What happens if the fatty streaks progress?
There is more plaque growth by further LDL deposition in the intima (second inner-most layer after the endothelium)
This causes arterial re-modelling to try to compensate the plaque build-up and maintain the lumen size and blood flow.
Once the external adventita (outer layer of the endothelium) cannot expand any more, the artery cannot compensate for plaque build up and the plaque growth protrudes the lumen forming a fibrous cap.
If the plaque ruptures, it can cause a thrombus clot and is a medical emergancy.
What do we know aout healed plaques?
They have higher fibrotic content, will still protrude but are more stable and less likely to rupture.
What does the time it takes for Atheroma to develop depend on?
It normally takes years, depending on the intensity of exposure to risk factors.
What is the primary risk of atheroma?
Endothelial Dysfunction causing disruption to the autocrine, endocrine and paracrine function.
WHat are the other risks of Atheroma?
- Diabetes
- Hypertension
- Hyperlipidameia/ high cholesterol
- Metabolic syndrome (increased abdominal fat)
- Smoking (infection of the endothelium)
What do all the risk factors cause?
An increase in cytokines, cellular proliferation, lipid accumulation, inflammation adn calcification (build up of calcium, hardenin vessels). These all lead to the development of Athroma and Coronary Artery Disease.
WHat is Coronary Atheroma disease?
Atheroma anywhere in the major epicardial (layer of the heart wall) coronary arteries
Where does the Athroma often build up?
In the tortuosity and bifurcations (twists and bends) where there is turbulent flow and endothelial shear stress. It is asymptomatic (no symptoms)
What is Collateral vessel formation?
Only happens in some individuals where accessory side branches form if there is partial or full blockage of the original vessel.
How is Collateral vessel formation stimulated?
It is stimulated by various growth factors and is upregulated in response to chronic or repetitive ischaemia.
What is good about Collateral vessel formation?
It is a benefit in bypassing the blockage in the main artery and supply enough oxygenated blood to enable the cardiac tissue to survive and recover.
It is only a superficial solution and will supply 25% of required blood.
