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1

Week 206 - Myocardial Infarction: What ECG changes would you expect minutes after an MI?

• Elevated ST segments, Tall pointed T waves, in the leads facing the affected area.

2

Week 206 - Myocardial Infarction: What ECG changes would you expect hours after an MI?

• Pathological Q Waves, T-waves invert.

3

Week 206 - Myocardial Infarction: What effect does partial thickness ischaemia have on an ECG?

• ST depression in leads facing the ischaemia.

4

Week 206 - Myocardial Infarction: What effect does full thickness ischaemia have on an ECG?

• ST elevation in leads facing the affected area.

5

Week 206 - Myocardial Infarction: When myocardium dies after iscahemia what effect does the have on an ECG?

• The dead tissue becomes 'silent', forming a window through the heart so leads opposite the injured area begin to see pathological q waves and inverted t-waves.

6

Week 206 - Myocardial Infarction: What is the GRACE scoring system?

Using a series of parameters it is able to predict the likely hood of an individual suffering from Death or MI either in hospital or within 6 months.

7

Week 206 - Myocardial Infarction: Which ECG leads look at the inferior part of the heart?

II, III, aVF.

8

Week 206 - Myocardial Infarction: Which ECG leads look at the lateral aspects of the heart?

I, aVL (Left side)
V5,V6 (Right side)

9

Week 206 - Myocardial Infarction: Which ECG leads look at the anterior aspects of the heart?

V3, V4

10

Week 206 - Myocardial Infarction: Which ECG leads look at the septal part of the heart?

V1, V2

11

Week 206 - Myocardial Infarction: What is the blood concentration of blood lipids dependant on?

• Intake or excretion from the intestine.
• Uptake and secretion from cells.

12

Week 206 - Myocardial Infarction: What is the pathway for the poductions of LDLs?

• The liver converts unused food metabolites into very-low density lipoproteins (VLDL) and secretes them into plasma.
• In the plasma they are converted into intermediate density lipoproteins (IDLs) then into LDLs.

13

Week 206 - Myocardial Infarction: Which particles carry fats from the intestine to the liver?

Chylomicrons.

14

Week 206 - Myocardial Infarction: What is the role of HDLs?

• 'Good Cholesterol'
• Transport cholesterol back to the liver for excretion.

15

Week 206 - Myocardial Infarction: What is the classification of primary lipid disorders called?

Frederickson.

16

Week 206 - Myocardial Infarction: An increase in chylomicrons or VLDLs, would lead to elevated serum levels of what particle?

Triglyceride

17

Week 206 - Myocardial Infarction: An increase in LDLs or IDLs, would lead to elevated levels of what particle?

Cholesterol

18

Week 206 - Myocardial Infarction: What is familial hypercholesterolaemia? What is the pathology behind it?

• Autosomal dominant disorder, defined as a type IIa hyperlipidaemia.
• It occurs due to a mutation with the LDL receptors which prevents efficient uptake of LDLs, there are various types of mutation.

19

Week 206 - Myocardial Infarction: Which clinical sign is virtually diagnostic for familial hypercholesterolaemia?

Tendon xanthomata.
(Corneal arcs and xanthelasma are also common findings but are less specific.)

20

Week 206 - Myocardial Infarction: What is the diagnostic criteria for definite familial hypercholesterolaemia?

• Total cholesterol above 7.5mmol/L or LDL cholesterol above 4.9mmol/L
AND
• Tendon xanthomata in patient or 1/2nd degree relative.

21

Week 206 - Myocardial Infarction: How should familial hypercholesterolaemia be treated relative to sporadic hypercholesterolaemia?

More aggressively, since there is a much greater risk of coronary heart disease.

22

Week 206 - Myocardial Infarction: What is the medical treatment of familial hypercholesterolaemia?

Statins (high dose)

23

Week 206 - Myocardial Infarction: What is the mechanism of action of statins?

• Inhibition of HMG CoA in the liver, this is a rate limiting step of endogenous cholesterol production.
• Reduction in plasma cholesterol and LDL.
• Increase in LDL receptors
• Small decrease in plasma triglyceride and VLDLs.
• Modest increase in HDL.

24

Week 206 - Myocardial Infarction: What layer of the arterial wall do atheromas form?

Intima

25

Week 206 - Myocardial Infarction: What are the two basic components of an atheromatous plaque?

• Connective tissue cap
• Core - Extracellular lipid with surrounding macrophages.

26

Week 206 - Myocardial Infarction: What is the basic mechanism behind the formation of an atheromatous plaque?

• Endothelial dysfunction leads to platelet and WBC adhesion.
• Passage of inflammatory cells into the subepithileum space.
• Accumulation of lipid-rich cells, smooth muscle and new blood vessel growth.

27

Week 206 - Myocardial Infarction: What is the potential anti-atherogenic role played by NO?

• NO is produced by endothelial cells.
- Inhibits smooth muscle proliferation.
- Inhibits monocyte adhesion and migration through endothelium.
- Anti-platelet effects.
- Promotion of macrophage apoptosis.
- Inhibition of lipid oxidation.

28

Week 206 - Myocardial Infarction: What are foam cells?

These are macrophages that have ingested modified lipids that occupy the sub-epithelial space.

29

Week 206 - Myocardial Infarction: When vascular smooth muscles are in the intima that take on a different phenotype from the contractile phenotype they normally express?

• 'Synthetic phenotype'
• Produces growth factors, proteases, collagen and elastin.

30

Week 206 - Myocardial Infarction: What are the characteristics of an unstable plaque?

• Large lipid cores.
• Unstable cap, in which structure is disorganised.
• High densities of macrophages.
• Low densities of smooth muscle cells.