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
What drug is often used for anti-platelet therapy for. stable angina?
Low dose aspirin
26
For which patients with stable angina. should ACE inhibitors be prescribed?
Those with hypertension, diabetes mellitus, left ventricular ejection fraction <40% or CKD
27
What drug is used for lipid management in stable angina?
High intensity statins
28
Describe the pathophysiology of coronary steal syndrome?
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
29
What changes will be seen on ECG for coronary steal syndrome?
ST depression
30
What is the pathophysiology of variant angina?
It is caused by vasospasm, a narrowing of the coronary armies caused by contracting of the smooth muscle tissue in the vessel wall
31
In variant angina, what are the possible triggers for vasospasm?
Smoking Cocaine Alcohol Triptans
32
How is variant angina managed?
Calcium channel blocker GTN Cessation / avoidance of trigger
33
Give examples of causes of acute coronary syndrome other than coronary artery disease?
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
When is angina considered to be unstable?
``` Prolonged - lasting >20 minutes Occurs at rest New-onset severe angina Crescendo angina Post-MI ```
35
Give examples of atypical presentations of acute coronary syndrome?
``` Epigastric pain Recent-onset indigestion Stabbing chest pain Pleuritic chest pain Isolated dyspnoea ```
36
Explain how to differentiate between STEMI, NSTEMI and unstable angina based on ECG and laboratory findings?
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
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?
creatinine kinase - MB
38
CK-MB is an additional cardiac biomarker to troponin. What is the drawback of using ck-mb?
It is not as specific as troponin
39
What is the initial management of unstable angina?
``` Oxygen Aspirin + ticagrelor / clopidogrel Morphine GTN Beta blockers ```
40
If a patient with unstable angina cannot be prescribed a beta blocker, what drug can be used instead?
Calcium channel blocker
41
In NSTEMI, where is the site of the infarct?
Sub-endothelial
42
What is the long-term management of NSTEMI?
``` Aspirin (indefinitely) Clopidogrel / ticagrelor for 12 months Oral beta blockers High intensity statin therapy ACE inhibitors Cardiac rehabilitation Lifestyle modification ```
43
If ST-elevation is present in leads V1 and V2, how is this MI classified and which artery is likely invovled?
Anteroseptal MI | Left anterior descending artery
44
If ST-elevation is present in leads V3 and V4, how is this MI classified and which artery is likely invovled?
Anteroapical MI | Left anterior descending artery
45
If ST-elevation is present in leads V5 and V6, how is this MI classified and which artery is likely invovled?
Anterolateral MI | Left anterior descending artery or left circumflex artery
46
If ST-elevation is present in leads I and aVL, how is this MI classified and which artery is likely invovled?
Lateral MI involving the left circumflex artery
47
If ST-elevation is present in leads II, III and aVF, how is this MI classified and which artery is likely invovled?
Inferior MI involving the right coronary artery
48
What ECG changes may be seen in a posterior MI?
ST depression with tall R waves in V1-3
49
What drugs should all patients with STEMI initially be prescribed?
``` 5-10mg morphine by slow IV injection 10mg IV metroclopramide 300mg soluble oral aspirin STAT 180mg oral ticagrelor 500 units IV heparin ```
50
What is the definitive management of STEMI?
Primary percutaneous coronary intervention | Or if this is not possible, thrombolysis via tenecteplase
51
If a patient with STEMI is not suitable for PPCI, what drug is used for thrombolysis?
Tenecteplase
52
What is the long-term management of STEMI?
``` Oral beta blocker ACE inhibitor or ARB High intensity statin therapy Aspirin (indefinitely) Ticagrelor for 12 months Cardiac rehabilitation +/- aldosterone antagonist ```
53
What type of. arrhythmias most commonly occur post-MI?
Premature ventricular arrhythmias
54
What complications fo STEMI can occur within 24 hours?
Arrythmias Heart failure Cardiogenic shock
55
Interventricular septum rupture can occur post-MI. How many days post-MI does this typically present?
3-5 days
56
Ventricular free wall rupture can occur post-MI. How many days post-MI does this typically present?
5-14 days
57
In what type of STEMI does ventricular free wall rupture most commonly occur?
Anterior STEMI
58
How soon post-Mi can rupture of the papillary muscles occur?
2-7 days
59
Describe the histopathological changes that occur in the heart post-MI
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
What are the ECG criteria for STEMI?
ST elevation >2mm in the chest leads (V1-6) ST elevation >1mm in the limb leads New left bundle branch block
61
What is the management of a patient with STEMI who is not suitable for reperusion therapy with PCI or fibrinolysis?
Medical management with ticagrelolr +/- aspirin, clopidogrel
62
What scoring system is used to guide the management of NSTEMI / unstable angina?
GRACE score
63
What is the management of low risk NSTEMI / unstable angina?
Conservative management with ticagrelor +/- aspirin, without angiography (although angiography may need to be considered later)
64
What is the initial management of intermediate or high risk NSTEMI / unstable angina?
Angiography - immediate if unstable, otherwise within 72 hours Ticagrelor +/- aspirin
65
What is the definitive diagnostic test for stable angina?
CT angiogram
66
Outline the diagnostic process of stable angina?
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
Give examples of non-invasive functional tests for stable angina?
MR with SPECT Stress ECHO MR perfusion
68
Outline the management of stable angina?
``` 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
How can recurrent anginal symptoms be addressed pharmacologically in stable angina?
Beta blocker Calcium channel blocker Combination BB and CCB Long acting nitrate
70
What surgical options are available for refractory stable angina?
PCI | CABG