Atherosclerosis and IHD Flashcards
Ischaemia
Reduced tissue blood flow
Hypoxia
Oxygen deprivation which causes cell injury by reducing aerobic oxidative respiration.
Infarction
Localized area of ischaemic tissue necrosis - usually coagulative necrosis
Coagulative necrosis
A form of necrosis in which tissue architecture is preserved for at least some time
Define ischaemic heart disease.
Insufficient blood supply relative to myocardial demand.
What are most cases of IHD due to?
Atherosclerosis of coronary arteries (one or more)
Remember IHD = CAD!
xx
List major non-modifiable risk factors for atherosclerosis.
Genetics (e.g. Familial Hypercholesterolemia)
Family history
Increasing Age
Male Gender
List modifiable risk factors for atherosclerosis.
Hyperlipidemia (hypercholesterolemia) HTN Cigarette smoking Diabetes Inflammation (CRP)
What is the pathogenesis behind atherosclerosis?
Arterial response to endothelial injury
Chronic inflammatory and healing response of arterial wall to endothelial injury
Due to endothelial injury or dysfunction
Name the major arteries affected by atherosclerosis.
Elastic arteries e.g. aorta, carotids, iliacs and large medium sized muscular arteries e.g. coronaries
Why do veins and smaller arterioles do not get atherosclerosis?
Not enough pressure
Describe the process of pathogenesis of atherosclerosis.
- Endothelial injury/dysfunction = increased vascular permeability and leukocyte/platelet adhesion
- Increased vascular permeability: LDL and its oxidized form seep into vessel wall
- Monocytes transform into macrophages which engulf lipids to become foam cells
- Smooth muscle cells proliferate and deposit ECM. Also engulf lipids to become foam cells.
- T cells recruited
- Atherosclerotic plaque forms within the intima, encroaches on vascular lumen.
What is another name for the atherosclerotic plaque?
Atheroma
Describe the features of an atheroma.
Fibrous cap –> smooth muscle cells, macrophages, foam cells, lymphocytes, collagen
Necrotic centre –> cell debris, cholesterol crystals, foam cells, calcium
List the complications of atherosclerosis.
- Mechanical obstruction of vessel wall leading to ischaemia. (critical stenosis is about 70% occlusion)
- Increases diffusion distance from lumen to media = degeneration and weakening due to loss of elastic fibres. Leads to aneurysm formation.
- Aneurysms can be saccular or fusiform and commonly contain a mural thrombus
- Aneurysms can rupture
- Haemorrhage into plaque (from new vessels) leading to plaque expansion or rupture
- Plaque ulceration, erosion or rupture leading to thrombosis and partial/complete occlusion of vessel.
Where do aneurysms commonly form?
Abdominal aorta or common iliac arteries
What contributes to acute plaque change?
Haemorrhage into the plaque
Plaque ulceration, erosion or rupture leading to thrombosis
What is the difference between stable and vulnerable plaques in atherosclerosis?
Vulnerable plaque = thick lipid core with fibrous cap
Stable plaque = unlikely to rupture, thrombosis unlikely to form
What are the clinical consequences of atherosclerosis in the arteries of the heart, arteries of the brain, LL arteries and the aorta.
Arteries of the heart –> ischaemic heart disease
Arteries of the brain –> stroke
LL arteries –> peripheral vascular disease
Aorta –> AAA
What causes IHD?
Chronic vascular occlusion by atherosclerosis
Acute plaque change
An element of coronary vasospasm (vasoconstriction)
Name examples of acute plaque change.
Intra-plaque haemorrhage, erosion, rupture
Superimposed thrombosis and possible complete vascular occlusion
What is the clinical presentation of IHD?
One or more of the following:
- Angina Pectoris (Chest Pain)
- MI
- Sudden cardiac death
- Chronic IHD with heart failure
What causes MI?
Ischaemia causing myocardial necrosis
