the three main arteries of the heart which are affected by atherosclerosis
- right coronary artery
- LAD artery
- left circumflex
Risk factors for atherosclerosis
- age (strongest predictor)
- tobacco smoking
- high serum cholesterol
- obesity (increased lipid content of plaques -> increased inflammation)
- diabetes (hyper and hypoglycaemia affect endothelial function)
- hypertension- increased BP can damage endothelium
- family history of coronary artery disease
What is atherosclerosis? what are the main problems which can occur as a result of it?
atherosclerosis= condition where plaque builds up in arteries.
- Plaque may occlude vessel lumen
- Plaque can rupture, leading to thrombus formation, which disrupts blood flow to myocardium by blocking the artery and can possibly cause death
where are atherosclerotic plaques most likely to be found?
in peripheral and coronary arteries
- structure of atherosclerotic plaques
- relevance of the thickness of the cap
fibrous cap covering a mixture of connective tissue and lipids, with a necrotic core of dead cells
- the thicker the fibrous cap, the more stable the plaque; thin plaques are more vulnerable to rupture
Describe process of atherosclerotic plaque formation (7)
1- irritant (smoking/hypertension/hyperlipidemia) -> endothelial dysfunction
2- Increased LDL deposits in the tunica intima leads to the activation of endothelial cells. Endothelial cells express adhesion molecules for white blood cells
3- White blood cells adhere to activated endothelial cells -> allows monocytes and T helper cells to move into the tunica intima layer of blood vessels
4-Monocytes and T helper cells become macrophages which take up oxidised LDLs and become foam cells
5-Foam Cells promote migration of smooth muscle cells from tunica media to intima & smooth muscle proliferation
6- increased smc proliferation -> increased collagen production -> hardening of plaque
7- foam cell dies, unleashing lipid content -> drives growth of plaque (apoptosis)
what does an intermediate atherosclerotic (stage 2) lesion contain?
- lipid-laden macrophages (foam cells)
- vascular smooth muscle cells
- T-lymphocytes
- Adhesion and aggregation of platelets to vessel wall
- isolated pools of extracellular lipid
What is an advanced atherosclerotic plaque (stage 3) and what is it composed of?
Advanced atherosclerotic plaque= fibrous plaque.
- Covered by dense fibrous cap made of extracellular matrix proteins including collagen and elastin- caps may become calcified.
- Inside of plaque contains smooth muscle cells, macrophages, foam cells and T lymphocytes
Treatment options for coronary artery plaque
1- PCI- e.g. insertion of a stent. Normally rug eluting stents e.g. taxol or sirolimus
2- Drugs;
- aspirin
- clopidogrel & ticagreolor (inhibit receptor on platelets)
- Statins- inhibit rate-limiting enzyme (HMG CoA reductase) of cholesterol production pathway, thus decreasing cholesterol synthesis
Four stages of atherosclerosis progression
1- Fatty streaks
2- Intermediate lesion
3- Advanced Lesion/ Fibrous plaque
4- Plaque rupture
fatty streaks (stage 1) consist of
lipid laden macrophages and T lymphocytes within the tunica intima
What happens during plaque rupture (stage 4)?
- fibrous cap has to be resorbed and redeposited in order to be maintained -> if balance shifts in favour of inflammatory conditions (increased enzyme activity), cap becomes weak and plaque ruptures;
- Basement membrane, collagen and necrotic tissue exposure as well as haemorrhage of vessels
- thrombus (clot) formation and vessel occlusion
main 5 risk factors for acute coronary syndromes
- smoking
- hypertension
- diabetes
- hypercholesterolaemia
- positive family history
other risk factors for acute coronary syndromes
- chronic kidney disease
- peripheral arterial disease
- inflammatory conditions e.g. rheumatoid arthritis
- ethnicity
- stress
3 clinical features of unstable angina
- cardiac chest pain at rest
- cardiac chest pain in a crescendo pattern (pain gets worse over time)
- new onset angina (patient develops angina quickly without warning)
difference between STEMI and NSTEMI
- STEMI= ST elevation MI; complete and sustained occlusion- the resulting ischaemia results in loss of a whole territory of heart muscle (and thus significant myocardial necrosis)
- NSTEMI= temporary occlusion which has clear, or a stenosis but not complete occlusion
STEMI diagnosed using
ECG- characteristic features on ECG
Define angina.
Angina is chest pain symptomatic of O2 supply/demand mismatch to the heart experienced on exertion.
What is the most common cause of angina?
Narrowing of the coronary arteries due to atherosclerosis.
Give 5 possible causes of angina.
- Narrowed coronary artery = impairment of blood flow e.g. atherosclerosis.
- Increased distal resistance = LV hypertrophy.
- Reduced O2 carrying capacity e.g. anaemia.
- Coronary artery spasm.
- Thrombosis.
Give 5 modifiable risk factors for angina.
- Narrowed coronary artery = impairment of blood flow e.g. atherosclerosis.
- Increased distal resistance = LV hypertrophy.
- Reduced O2 carrying capacity e.g. anaemia.
- Coronary artery spasm.
- Thrombosis.
Give 5 modifiable risk factors for angina.
- Smoking.
- Diabetes.
- High cholesterol (LDL).
- Obesity/sedentary lifestyle.
- Hypertension.
Briefly describe the pathophysiology of angina that results from atherosclerosis.
On exertion there is increased O2 demand. Coronary blood flow is obstructed by an atherosclerotic plaque -> myocardial ischaemia -> angina.
Briefly describe the pathophysiology of angina that results from anaemia.
On exertion there is increased O2 demand. In someone with anaemia there is reduced O2 transport -> myocardial ischaemia -> angina.
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