Cardiovascular System Flashcards
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.
How do blood vessels try and compensate for increased myocardial demand during exercise.
When myocardial demand increases e.g. during exercise, microvascular resistance drops and flow increases!
Why are blood vessels unable to compensate for increased myocardial demand in someone with CV disease?
In CV disease, epicardial resistance is high meaning microvascular resistance has to fall at rest to supply myocardial demand at rest. When this person exercises, the microvascular resistance can’t drop anymore and flow can’t increase to meet metabolic demand = angina!
How would you describe the chest pain in angina?
Crushing central chest pain. Heavy and tight. The patient will often make a fist shape to describe the pain.
What investigations might you do in someone you suspect to have angina?
- ECG - usually normal, there are no markers of angina.
- Echocardiography.
- CT angiography - has a high NPV and is good at excluding the disease.
- Exercise tolerance test - induces ischaemia.
- Invasive angiogram - tells you FFR (pressure gradient across stenosis).
A young, healthy, female patient presents to you with what appears to be the signs and symptoms of angina. Would it be good to do CT angiography on this patient?
Yes. CT angiography has a high NPV and so is ideal for excluding CAD in
younger, low risk individuals.
Describe the primary prevention of angina.
- Risk factor modification.
2. Low dose aspirin.
Describe the secondary prevention of angina.
- Risk factor modification.
- Pharmacological therapies for symptom relief and to reduce the risk of CV events.
- Interventional therapies e.g. PCI.
Name 3 symptom relieving pharmacological therapies that might be used in someone with angina.
- Beta blockers.
- Nitrates e.g. GTN spray.
- Calcium channel blockers.
Describe the action of beta blockers.
Beta blockers are beta 1 specific. They antagonise sympathetic activation and so are negatively chronotropic and inotropic. Myocardial work is reduced and so is myocardial demand = symptom relief.
Give 3 side effects of beta blockers.
- Bradycardia.
- Tiredness.
- Erectile dysfunction.
- Cold peripheries.
When might beta blockers be contraindicated?
They might be contraindicated in someone with asthma or in someone who is bradycardic.
Describe the action of nitrates.
Nitrates e.g. GTN spray are venodilators. Venodilators -> reduced venous return -> reduced pre-load -> reduced myocardial work and myocardial demand.
Describe the action of Ca2+ channel blockers.
Ca2+ blockers are arterodilators -> reduced BP -> reduced afterload -> reduced myocardial demand.
Name 2 drugs that might be used in someone with angina or in someone at risk of angina to improve prognosis.
- Aspirin.
2. Statins.
How does aspirin work?
Aspirin irreversibly inhibits COX. You get reduced TXA2 synthesis and so platelet aggregation is reduced.
Caution: Gastric ulcers!
What are statins used for?
They reduce the amount of LDL in the blood.
What is revascularisation?
Revascularisation might be used in someone with angina. It restores the patent coronary artery and increases blood flow.
Name 2 types of revascularisation.
- PCI.
2. CABG.
Give 2 advantages and 1 disadvantage of PCI.
- Less invasive.
- Convenient and acceptable.
- High risk of restenosis.
Give 1 advantage and 2 disadvantages of CABG.
- Good prognosis after surgery.
- Very invasive.
- Long recovery time.
What are acute coronary syndromes (ACS)?
ACS encompasses a spectrum of acute cardiac conditions including unstable angina, NSTEMI and STEMI.
What is the common cause of ACS?
Rupture of an atherosclerotic plaque and subsequent arterial thrombosis.
What are uncommon causes of ACS?
- Coronary vasospasm.
- Drug abuse.
- Coronary artery dissection.
Briefly describe the pathophysiology of ACS due to atherosclerotic plaque rupture?
Atherosclerosis -> plaque rupture -> platelet aggregation -> thrombosis formation -> ischaemia and infarction -> necrosis of cells -> permanent heart muscle damage and ACS.
Why do you see increased serum troponin in NSTEMI and STEMI?
Troponin is a sensitive marker for cardiac muscle injury and so is significantly raised in reflection to this.
Give 6 signs/symptoms of MI.
- Unremitting and usually severe central cardiac chest pain.
- Pain occurs at rest.
- Sweating
- Breathlessness.
- Nausea/vomiting.
- 1/3 occur in bed at night.
Give 5 potential complications of MI.
- Heart failure.
- Rupture of infarcted ventricle.
- Rupture of interventricular septum.
- Mitral regurgitation.
- Arrhythmias.
- Heart block.
- Pericarditis.
What investigations would you do on someone you suspect to have ACS?
- ECG.
- Blood tests; look at serum troponin.
- Coronary angiography.
- Cardiac monitoring for arrhythmias.
What might the ECG of someone with NSTEMI show?
The ECG from someone with NSTEMI may be normal or might show T wave inversion and ST depression. There also might be R wave regression, ST elevation and biphasic T wave in lead V3.
What might the ECG of someone with STEMI show?
The ECG from someone with STEMI will show ST elevation in the anterolateral leads. After a few hours, T waves invert and deep, broad, pathological Q waves develop.
What would the serum troponin level be like in someone with NSTEMI/STEMI?
Significantly raised.
