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Cardiology > Coronary Artery Disease and Myocardial Infarction > Flashcards

Coronary Artery Disease and Myocardial Infarction Flashcards

1
Q

Define ischaemic heart disease disease?

A

An imbalance between myocardial oxygen demand and supply from the coronary arteries

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2
Q

What conditions fall under the bracket of acute coronary syndrome?

A

Unstable angina
NSTEMI
STEMI

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3
Q

Coronary artery syndrome is caused by atherosclerosis. What is the pathophysiology of atherosclerosis?

A

The endothelium becomes injured due to hypertension, tobacco etc. LDL particles are able to leak into the intimal layer of the vessel and become oxidised. Oxidised LDL act as a pro-inflammatory antigen, inducing an immune response. Macrophages enter the arterial walls and phagocytose oxidised LDL particles to create foam cells. The accumulation of foam cells underneath the endothelium creates a fatty streak. Platelet and endothelial cells release PDGF, FGF. and TGF-beta which stimulate smooth muscle proliferation and migration into the tunica intimal. This proliferation stimulates the production of extracellular matrix which results in the formation of a fibrous cap overlying the lipid core. This plaque can obstruct the lumen and may rupture. If the plaque ruptures (due to MMP degradation of the fibrous cap) platelets form a fibrin clot at the site of rupture which further occludes the vessel

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4
Q

What are the non-modifiable risk factors for atherosclerosis?

A

Age
Family history
Black ethnicity

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5
Q

What are the modifiable risk factors for atherosclerosis?

A

Hypertension
Diabetes mellitus
Smoking
Dyslipidaemia

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6
Q

How far obstructed does the lumen of the coronary artery need to be to cause symptoms of angina?

A

70% stenosis

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7
Q

What are the less common causes of ischaemic heart disease despite atherosclerosis?

A

Coronary. artery embolism
Vasculitis
Vasospasm

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8
Q

What are the risk factors for coronary embolism?

A

Atrial fibrillation
Infective endocarditis
Left atrial / ventricular thrombus
Cardiac catheterisation

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9
Q

What is the most likely cause of coronary artery disease in children?

A

Kawasaki disease (this is a type of vasculitis)

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10
Q

How is it possible for an atherosclerotic plaque cause. near-total occlusion of a coronary artery without causing infarction?

A

Because atherosclerosis develops slowly overtime which allows collateral vessels to develop

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11
Q

What are the three key characteristics of classical angina pain?

A

Substernal chest discomfort
Provoked by exercise or stress
Relieved with rest or glyceryl trinitrate

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12
Q

What groups of people are more likely to present with atypical symptoms of coronary artery disease or acute coronary syndrome?

A

Women
Patients with diabetes
Elderly people

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13
Q

What are the possible symptoms of an atypical angina / coronary artery. disease presentation?

A

Nausea
Vomiting
Mid-epigastric discomfort
Sharp chest pain

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14
Q

Where does angina pain typically radiate to?

A

Neck, jaw, epigastrium or arms - typically on the left side

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15
Q

Describe the character of anginal pain?

A

Tightness, pressure, heaviness

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16
Q

What are the associated symptoms of angina?

A 
Dyspnoea
Nausea
Vomiting
Perspiration
Light-headedness
Fatigue
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17
Q

What are the exacerbating factors of. angina?

A 
Exercise
Stress
Sexual activity
Tachycardia of any cause
Metabolic demands of fever / thyrotoxicosis / hypoglycaemia
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18
Q

What examination findings might you expect in coronary artery disease?

A

Physical examination is. often normal
May be signs of associated conditions e.g. heart failure, valvular disease or hypertrophic cardiomyopathy
May be signs of non-coronary atherosclerotic disease e.g. diminished pedal pulses, carotid bruit
Signs of hypercholesterolaemia - xanthelasma
Hypertension

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19
Q

What initial laboratory tests should be conducted in suspected stable angina?

A 
Haemoglobin
Blood. glucose
Lipid Panel
U&Es
TFTs
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20
Q

Besides blood tests, what investigations should be conducted for suspected. stable angina?

A

Resting ECG
Resting echocardiogram
+/- exercise stress testing, SPECT, PET, CCTA, invasive coronary angiography

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21
Q

What drug is used. to terminate acute episodes of angina or for prophylaxis. before activities known to induce angina?

A

Sublingual glyceryl trinitrate

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22
Q

What is the onset of action of sublingual glyceryl trinitrate?

A

Minutes

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23
Q

What is involved in education and lifestyle modification for stable angina?

A

Weight management - increasing exercise, healthy diet
Smoking cessation
Stress and depression recognition and management
Annual influenza vaccine

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24
Q

What is involved in medical management of stable angina?

A 
Antiplatelet therapy
Beta blockers
RAAS antagonists
Lipid management
Blood pressure control
Diabetes management
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25
Q

What drug is often used for anti-platelet therapy for. stable angina?

A

Low dose aspirin

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26
Q

For which patients with stable angina. should ACE inhibitors be prescribed?

A

Those with hypertension, diabetes mellitus, left ventricular ejection fraction <40% or CKD

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27
Q

What drug is used for lipid management in stable angina?

A

High intensity statins

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28
Q

Describe the pathophysiology of coronary steal syndrome?

A

This can occur when a vasodilation medication is given to an individual with stable angina. The vasodilator results in vasodilation of all the coronary arteries, except the ones which are obstructed because these arteries are already maximally dilated beyond the point of obstructed. As a result blood is diverted away from the ischaemic myocardium to non-ischaemic areas, further worsening the ischaemia

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29
Q

What changes will be seen on ECG for coronary steal syndrome?

A

ST depression

30
Q

What is the pathophysiology of variant angina?

A

It is caused by vasospasm, a narrowing of the coronary armies caused by contracting of the smooth muscle tissue in the vessel wall

31
Q

In variant angina, what are the possible triggers for vasospasm?

A

Smoking
Cocaine
Alcohol
Triptans

32
Q

How is variant angina managed?

A

Calcium channel blocker
GTN
Cessation / avoidance of trigger

33
Q

Give examples of causes of acute coronary syndrome other than coronary artery disease?

A

Increase myocardial oxygen requirements such as in fever, tachycardia and thyrotoxicosis
Reduce coronary blood flow e.g. hypotension
Reduced myocardial oxygen delivery e.g. in anaemia or hyperaemia

34
Q

When is angina considered to be unstable?

A 
Prolonged - lasting >20 minutes
Occurs at rest
New-onset severe angina
Crescendo angina
Post-MI
35
Q

Give examples of atypical presentations of acute coronary syndrome?

A 
Epigastric pain
Recent-onset indigestion
Stabbing chest pain
Pleuritic chest pain
Isolated dyspnoea
36
Q

Explain how to differentiate between STEMI, NSTEMI and unstable angina based on ECG and laboratory findings?

A

If there is ST elevation on ECG then this is STEMI
If there are no ECG changes or there is ST depression / T wave inversion then this is NSTEMI or unstable angina
In NSTEMI troponin will be elevated but in unstable angina troponin will be normal

37
Q

Troponin remains elevated for up to 10-14 days after release. Thus, if a patient present with chest discomfort within several days of an MI, troponin measurements cannot be used reliably. What other cardiac biomarker would be used in this case?

A

creatinine kinase - MB

38
Q

CK-MB is an additional cardiac biomarker to troponin. What is the drawback of using ck-mb?

A

It is not as specific as troponin

39
Q

What is the initial management of unstable angina?

A 
Oxygen
Aspirin + ticagrelor / clopidogrel
Morphine
GTN
Beta blockers
40
Q

If a patient with unstable angina cannot be prescribed a beta blocker, what drug can be used instead?

A

Calcium channel blocker

41
Q

In NSTEMI, where is the site of the infarct?

A

Sub-endothelial

42
Q

What is the long-term management of NSTEMI?

A 
Aspirin (indefinitely)
Clopidogrel / ticagrelor for 12 months
Oral beta blockers
High intensity statin therapy
ACE inhibitors
Cardiac rehabilitation
Lifestyle modification
43
Q

If ST-elevation is present in leads V1 and V2, how is this MI classified and which artery is likely invovled?

A

Anteroseptal MI

Left anterior descending artery

44
Q

If ST-elevation is present in leads V3 and V4, how is this MI classified and which artery is likely invovled?

A

Anteroapical MI

Left anterior descending artery

45
Q

If ST-elevation is present in leads V5 and V6, how is this MI classified and which artery is likely invovled?

A

Anterolateral MI

Left anterior descending artery or left circumflex artery

46
Q

If ST-elevation is present in leads I and aVL, how is this MI classified and which artery is likely invovled?

A

Lateral MI involving the left circumflex artery

47
Q

If ST-elevation is present in leads II, III and aVF, how is this MI classified and which artery is likely invovled?

A

Inferior MI involving the right coronary artery

48
Q

What ECG changes may be seen in a posterior MI?

A

ST depression with tall R waves in V1-3

49
Q

What drugs should all patients with STEMI initially be prescribed?

A 
5-10mg morphine by slow IV injection
10mg IV metroclopramide
300mg soluble oral aspirin STAT
180mg oral ticagrelor
500 units IV heparin
50
Q

What is the definitive management of STEMI?

A

Primary percutaneous coronary intervention

Or if this is not possible, thrombolysis via tenecteplase

51
Q

If a patient with STEMI is not suitable for PPCI, what drug is used for thrombolysis?

A

Tenecteplase

52
Q

What is the long-term management of STEMI?

A 
Oral beta blocker
ACE inhibitor or ARB
High intensity statin therapy
Aspirin (indefinitely)
Ticagrelor for 12 months
Cardiac rehabilitation
\+/- aldosterone antagonist
53
Q

What type of. arrhythmias most commonly occur post-MI?

A

Premature ventricular arrhythmias

54
Q

What complications fo STEMI can occur within 24 hours?

A

Arrythmias
Heart failure
Cardiogenic shock

55
Q

Interventricular septum rupture can occur post-MI. How many days post-MI does this typically present?

A

3-5 days

56
Q

Ventricular free wall rupture can occur post-MI. How many days post-MI does this typically present?

A

5-14 days

57
Q

In what type of STEMI does ventricular free wall rupture most commonly occur?

A

Anterior STEMI

58
Q

How soon post-Mi can rupture of the papillary muscles occur?

A

2-7 days

59
Q

Describe the histopathological changes that occur in the heart post-MI

A

After 4hours, coagulative necrosis begins - myocardial cells become hypercontracted
1-3 days post-MI there is extensive coagulative necrosis with neutrophil infiltration
3-14 days post-MI, macrophages phagocytose necrotic tissue and yellow granulation tissue develops
2 weeks - several months post-MI, granulation tissue forms and neovascularisation occurs

60
Q

What are the ECG criteria for STEMI?

A

ST elevation >2mm in the chest leads (V1-6)
ST elevation >1mm in the limb leads
New left bundle branch block

61
Q

What is the management of a patient with STEMI who is not suitable for reperusion therapy with PCI or fibrinolysis?

A

Medical management with ticagrelolr +/- aspirin, clopidogrel

62
Q

What scoring system is used to guide the management of NSTEMI / unstable angina?

A

GRACE score

63
Q

What is the management of low risk NSTEMI / unstable angina?

A

Conservative management with ticagrelor +/- aspirin, without angiography (although angiography may need to be considered later)

64
Q

What is the initial management of intermediate or high risk NSTEMI / unstable angina?

A

Angiography - immediate if unstable, otherwise within 72 hours

Ticagrelor +/- aspirin

65
Q

What is the definitive diagnostic test for stable angina?

A

CT angiogram

66
Q

Outline the diagnostic process of stable angina?

A

Clinical assessment including risk factor assessment
Then, basic bloods (FBC, HbA1c, lipid panel, TFTs (if indicated by history)) and resting ECG

If stable angina cannot be ruled out by clinical assessment, bloods and ECG then order CT angiogram

If CT angiogram is inconclusive then order Non-invasive functional testing

If this is inconclusive then order invasive cardiac angiography

67
Q

Give examples of non-invasive functional tests for stable angina?

A

MR with SPECT
Stress ECHO
MR perfusion

68
Q

Outline the management of stable angina?

A 
Lifestyle modification 
Aspirin (+ consider dual-anti platelet therapy with addition of clopidogrel)
Beta blocker
Short acting GTN for relief
ACEi if hypertensive
Optimal management of diabetes
69
Q

How can recurrent anginal symptoms be addressed pharmacologically in stable angina?

A

Beta blocker
Calcium channel blocker
Combination BB and CCB
Long acting nitrate

70
Q

What surgical options are available for refractory stable angina?

A

PCI

CABG

Cardiology (12 decks)

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