U12C3 MI

Question 1

What is angina?

Answer 1

• Pain in the chest of cardiac origin due to inadequate blood and O₂ supply to myocardium from occlusion of coronary arteries
• Atheroma = very common, mostly asymptomatic
• Atheromatous deposits → plaques → atherosclerosis
• Stable → unstable angina → thrombosis/MI
• Vasospasm of coronary arteries - rare (Prinzmetal’s)

Question 2

What is atherosclerosis?

Answer 2

• Disease of arterial vessels
• Progressive and cumulative

Question 3

What are lipids and the different types?

Answer 3

Fatty acids:

• SFA = saturated fatty acid (0 double bonds)
• MUFA = mono-unsaturated fatty acid (1 double bond)
• PUFA = poly-unsaturated fatty acid (>1 double bond)

Cholesterol

Triglycerides

Lipoproteins (= lipids + proteins):

• Chylomicrons
• VLDL = very low density lipoprotein
• IDL = intermediate-density lipoprotein
• LDL = low-density lipoprotein (1 copy of ApoB-100)
• HDL = high-density lipoprotein

Question 4

What is the LDL receptor and how can it be mutated?

Answer 4

• Single-pass type I membrane protein (839 amino acids)
• Widely distributed
• Binds LDL, the major cholesterol-carrying lipoprotein, and transports it into cells by endocytosis
• Familial hypercholesterolaemias →↑ serum LDL

Type I = mutation in LDL-R

• Autosomal dominant (many known mutations) →
• ↓ expression levels; ↓ affinity for LDL; ↓ uptake of LDL;

Type II = mutation in ApoB

• Autosomal dominant
• Defective ApoB-100
• Prevents binding to LDL-R

Question 5

How is lipid/cholesterol transported?

Answer 5

From gut via lymph to body/liver = exogenous pathway

• “fat absorption”
• Chylomicrons
• TGs → FAs + glycerol – absorbed into cells
• Cholesterol esters → liver → endogenous pathway or bile acids

From liver to body = endogenous pathway

• “cholesterol transport” to body
• Liver → VLDL → IDL → LDL (LP density ↓ as they deliver lipids to cells)
• Deliver TGs (FAs & glycerol) and cholesterol to cells (via LDL-R)

From body to liver

• “reverse cholesterol transport”
• Non-liver cells → HDL using ApoA and ABCA1 containing cholesteryl esters
• HDL binds to Scavenger Receptor B1 (SCARB1) on liver

From liver to gut and back again…

• “enterohepatic circulation”
• Bile acid synthesis requires a large amount of cholesterol
• Synthesised de novo, re-cycled via EHC or from blood (LDL)

Question 6

How is cholesterol recycled?

Answer 6

Question 7

How is choleseterol synthesised?

Answer 7

Question 8

What is the physiology of angina?

Answer 8

Question 9

Stable vs unstable angina pathophysiology

Answer 9

Stable angina occurs when there’s a temporary imbalance between the heart’s demand for oxygen and its supply due to narrowed coronary arteries, often caused by atherosclerosis. Unstable angina involves more unpredictable and severe symptoms, typically due to a partially blocked artery or a blood clot forming on a ruptured plaque, leading to decreased blood flow to the heart. This can progress to a heart attack.

Question 10

What is the pathophysiology of an MI?

Answer 10

Question 11

What is the pathogenesis of atherosclerosis?

Answer 11

Question 12

What is the progression of a plaque?

Answer 12

Question 13

What are the risk factors for coronary artery disease?

Answer 13

Obesity – total blood volume and cardiac output are increased with cardiac workload normally higher leading to hypertension as well as associated with dyslipidaemia, insulin resistance and inflammation which can lead to atherosclerosis
Smoking – oxidant compounds of cigarette smoke cause endothelium dysfunction which leads to the atherosclerotic process as well as the plaques of smokers having a high vulnerability of rupture due to a higher lipid content
Hypertension - in picture
Physical activity – decreases vascular inflammation, improves endothelial function and coronary circulation preventing myocardial ischaemia
Hypocholesterolaemia – leads to the formation of more plaques within the coronary arteries leading to atherosclerosis and increase MI risk
Diabetes mellitus – higher risk of insulin resistance, hyperinsulinemia and vascular calcification which not only promote the occurrence of atherosclerosis but also accelerate the progression of stable plaques to unstable plaques or plaque rupture leading to thrombosis
Men - historically, men had higher rates of unhealthy habits such as smoking and stress as well as naturally occurring hormones in women playing a protective role as heart disease risk increases after menopause
Advancing age – potentially to do with oxidative stress caused by excess production of ROS leading to inflammation (IL-6, TNF-α) which then leads to cardiac remodeling of ECM caused by impaired ECM turnover causing fibrosis that can lead to AF… also are more likely to develop hypertension, diabetes and atherosclerosis which also contributes
Socioeconomic status – limited access to healthcare services, higher stress level (crime and unemployment), poorer dietary habits, higher smoking and alcohol levels, higher rates of depression as well as higher education and income are associated with higher acceptance and compliance with CVD
Geographic location – fewer visits to doctors, less lipid screening, poorer blood pressure control and less use of stains in older adults with diabetes

Question 14

What is QRISK3?

Answer 14

• Adults aged 40-74 who attend NHS health checks have their cardiovascular disease risk score calculated using the QRISK calculator
• QRISK is an algorithm that calculate an individual’s 10 year risk of having a heart attack or stroke… it is in review and updated every year… for example, NICE recommended adding severe mental illness
• It is not to be used opportunistically in unselected people – rather use systemic strategy
• It can be used for people aged 25 to 84 years old
• Don’t use in people who already have CVD

Question 15

What are the different types of angina?

Answer 15

1. Atypical angina:
   is described by NICE as chest pain with two out of three of the features classical angina.
   
   2. Non-angina chest pain:
      is described by NICE as chest pain with one out of three of the features above.
   3. Variant (Prinzmetal’s) angina:
      caused by coronary artery spasm and results in angina that occurs without provocation, usually at rest. Characteristically, there is ST segment elevation on the ECG during the pain.
   4. Unstable angina:
      increases rapidly in severity, occurs at rest, or is of recent onset (less than 24 hours) (acute coronary syndrome)
   5. Refractory angina:
      refers to patients with severe coronary disease in whom revascularization is not possible and angina is not controlled by medical therapy.
   6. Microvascular angina:
      symptoms of angina, a positive exercise test and normal coronary arteries on angiogram. It is thought to result from functional abnormalities of the coronary microcirculation. While it has a good prognosis, it is often highly symptomatic and can be difficult to treat.

Question 16

What are the symptoms of angina? Stable vs unstable

Answer 16

• ‘Heavy’, ‘tight’ or ‘gripping’ central or retrosternal pain which may radiate to the jaw and/or arms.
• Pain which occurs with exercise or emotional stress.
• Pain which eases rapidly with rest or with GTN (glyceryl trinitrate)

Question 17

What are the symptoms of a MI?

Answer 17

Question 18

What is the Canadian Cardiovascular Society functional classification of Stable angina?

Answer 18

Question 19

Which is the most commonly blocked coronary artery?

Answer 19

LAD as it supplies a large area of the heart and has a longer an more tortuous course

Question 20

What does each coronary artery supply?

Answer 20

Question 21

How is MI diagnosed?

Answer 21

ECG- NSTEMI (ST depression), STEMI (ST elevation)
Angiography- narrowing of arteries
Troponins- high levels of

Question 22

NSTEMI vs STEMI

Answer 22

Question 23

What are the features of a 1st, 2nd and 3rd degree heart block on an ECG?

Answer 23

Question 24

What are the manifestations of MI?

Answer 24

Question 25

How does a coronary angiogram work?

Answer 25

Question 26

What would the cardiac bio markers show?

Answer 26

Question 27

What is the flow diagram of treatment for stable angina?

Answer 27

Question 28

What is a primary coronary angioplasty?

Answer 28

Question 29

What are the differential diagnoses of ST elevation?

Answer 29

- **E**lectrolyte (Hyperkalemia) - **L**eft bundle branch block - **E**arly repolarization - **V**entricular hypertrophy - **A**neurysmal Left ventricular - **T**hrombotic occlusion (MI) - **I**nflammation (Pericarditis) - **O**sborn (Hypothermia) - **N**eurogenic - **S**udden death (Brugada)

Question 30

What are the types of infarcts?

Answer 30

Question 31

What is the pathophysiology of cardiogenic shock?

Answer 31

- Cardiac output falls - Rt atrial pressure rises - Baroreceptor and other responses activated by fall in BP and cardiac damage - Sympathetic system activation – vasoconstriction, increased venous return and stimulation of heart - Reduced renal blood flow, reduced urine output, fluid retention - Danger of reduced BP causing poor myocardial perfusion esp through diseased coronary circulation, and cycle of further myocardial damage

Question 32

What are the complications of an MI?

Answer 32

Question 33

What could cause ST elevation other than MI?

Answer 33

1. Pericarditis 2. Myocarditis 3. Pericardial effusion 4. LV hypertrophy 5. Right Bundle Branch Block (BBB)

Question 34

What is cardiac rehab?

Answer 34