20 Coronary Heart Disease, Angina, MI, Embolism Flashcards

1
Q

How does coronary artery disease present

A

1) Sudden cardiac death
2) Acute coronary syndrome (acute MI and unstable angina)
3) Stable angina
4) Heart failure
5) Arrhythmia

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2
Q

What are the lifestyle risk factors and how do they increase the risk of coronary artery disease

A
Smoking
Alcohol
Physical inactivity
Unhealthy diet
These contribute to hyperlipidaemia, obesity, diabetes and hypertension which contribute to 80% of CHD
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3
Q

What is the world mortality rate caused by CHD

A

17 million per year

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4
Q

True or false: CHD is the leading cause of death in developing countries but not developed countries

A

False, it is the world leading cause of death in both

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5
Q

What is the incidence of CHD

A

88,000 CHD deaths / year

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6
Q

True or false: The death rate of CHD in the UK is decreasing

A

True, but the UK has higher death rates than the rest of Europe

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7
Q

Is the incidence of angina in the UK increasing or decreasing

A

Increasing

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8
Q

What is the pathophysiology of myocardial ischaemia

A

Mismatch between myocardial oxygen supply and metabolic demand. The heart is unable to increase flow to match increased demand

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9
Q

What are prearteriols and arterioles sensitive to

A

Prearterioles: flow/BP
Arterioles: metabolites

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10
Q

What is the role of coronary arteries and how does the coronary circulation ensure this

A

Maintains flow under a range of perfusion pressure

Epicardial artery and intramyocardial arteries are in concert. If there is coronary stenosis in the epicardial region, intramyocardial arteries will dilate to maintain flow under the control of autonomic nervous system

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11
Q

At what extent of stenosis will the coronary flow be affected and severely reduced

A

50% stenosis will cause a small reduction in flow

70% stenosis will cause a huge disruption in flow

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12
Q

Define coronary flow reserve

A

The ratio between resting coronary flow rate to the flow rate under maximal stress

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13
Q

State the stages of ischaemic cascade

A
Normal function
Perfusion abnormality
Regional diastolic dysfunction
Regional systolic dysfunction
Ischaemic ECG changes
Angina pectoris
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14
Q

What is angina pectoris

A

Caused by exertion or emotional stress
Discomfort in shoulder, chest, jaw, arms and back
Treatment: rest

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15
Q

Why is investigation of angina important

A

To confirm diagnosis
To calculate the risk of future adverse CVD
Choice of test dependent on clinical probability of CHD

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16
Q

What are the investigations for CHD

A

Non-invasive/functional: exercise ECG
Non-invasive/anatomical: CT coronary angiogram
Invasive/functional: CFR
Invasive/anatomical: coronary angiogram

17
Q

What is the management for CHD

A
  1. Prevent progression of atherosclerosis
    - education
    - lifestyle modification
    - statins, aspirin
  2. Reduce myocardial oxygen demand
    - HR: beta blocker, Ca2+ channel antagonist
    - Wall stress: ACE inhibitor (captopril)
  3. Improve blood supply
    - Vasodilators: nitrates
    - Revascularisation (PCI and CABG)
18
Q

What are the mechanisms underlying MI

A
  1. Disrupted blood flow: coronary plaque erosion and rupture, dissection
  2. Myocardial cell death by: apoptosis and oncosis

*plaque rupture more frequently seen

19
Q

Differentiate between two types of thomboses

A
White thrombus:
- Occurs in arteries/higher pressure
- Platelet rich
- Benefit from antiplatelet therapy
Red thrombus:
- Occurs in veins/lower pressure
- Fibrin rich and trapped erythrocytes
- Benefit from anticoagulant
20
Q

What is the universal definition of acute MI

A

Rise or fall of cTn I/T AND one of the below:

  • symptoms suggestive of ischaemia
  • New ST-T changes or LBBB on ECG
  • Development of pathological Q wave
  • Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality
  • Identification of intracoronary thrombus on angiography or at autopsy
21
Q

State two types of acute coronary syndromes and how are they differentiated

A

Acute MI: ST elevation due to complete blockage of coronary artery

Unstable angina: No ST elevation (ST depressoin or T inversion or even normal ECG) due to partial occlusion which embolises distal capillaries

22
Q

How does acute MI develop

A

Necrotic zone initiates from intramyocardium. Particularly, subendocardium is most at risk and is important in heart function

23
Q

Differentiate between transmural endocardial infarction and sub-endocardial infarction

A

Transmural endocardial infarction: entire muscle

Sub-endocardial infarction: only inner muscle wall

24
Q

How much cell death does reperfusion injury account for

A

40%

25
Q

What is the mechanism of left ventricular wall remodelling

A
  1. Infarct thinning, elongation, expansion
  2. LV dilatation
    – Minimise the increase in wall tension
    – Maintains cardiac output
  3. Non-infarcted myocardium
    – LVH + myofilament dysfunction
    – Altered electromechanical coupling
    – Myocardial fibrosis
    – Apoptosis
    – Inflammation
26
Q

What are the consequences of left ventricular remodelling

A
  • Increased wall tension
  • Increased myocardial oxygen demand
  • Reduce myocyte shortening
  • Dysynchronous depolarisation/contraction
  • Reduced subendocardial perfusion
  • Mitral regurgitation
27
Q

What is the management to stabilise plaque

A

Mechanical: stent
Drug: ACE inhibitor (captopril) and statins

28
Q

What is are the drugs for LV remodelling

A

Beta blockers
ACE inhibitors
Angiotensin receptor blockers
Aldosterone receptor antagonists

29
Q

What is the management for thrombolytic burden

A

Thrombectomy
Anti-coagulent (Factor Xa inhibitor)
Anti-platelets

30
Q

What is the management for embolism

A

Thrombectomy
Fibrinolysis
Antiplatelet