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CVS Pathology > Stable Ischaemic Heart Disease and Angina > Flashcards

Stable Ischaemic Heart Disease and Angina Flashcards

1
Q

Definition of angina pectoris

A

A discomfort in the chest and/or adjacent areas associated with myocardial ischaemia but without myocardial necrosis

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2
Q

Definition of myocardial ischaemia

A

A mismatch between supply of O2 and metabolites to myocardium and the myocardial demand for them, resulting in angina symptoms

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3
Q

Most common cause of myocardial ischaemia

A

Reduction in coronary blood flow to the myocardium

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4
Q

Causes of reduction in coronary blood flow to the myocardium

A

Obstructive coronary atheroma (very common)
Coronary artery spasm (rare)
Coronary inflammation / arteritis (very rare)
Uncommon
- reduced O2 transport due to anaemia
- pathologically increased myocardial 02 demand (LVH, thyrotoxicosis)

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5
Q

Most common cause of angina

A

Coronary atheroma

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6
Q

When would myocardial oxygen demands increase?

A

Situations where HR and BP rise

  • exercise
  • anxiety/emotional stress
  • large meal
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7
Q

Risk factors for coronary artery disease

A 
Male
Age 
FH 
Smoking
Lifestyle 
DM
HTN
Hyperlipidaemia
Post menopausal females
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8
Q

Precipitants of stable angina

A

Exertion
Cold weather
Emotional stress
Following heavy meal

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9
Q

Where is the typical distribution of pain / discomfort in stable angina?

A

Left chest

Along left arm

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10
Q

What is used to classify angina?

A

Canadian classification of angina severity (CCS)

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11
Q

CCS stages

A
  1. Ordinary physical activity does not cause angina, symptoms only significant on exertion
  2. Slight limitation of ordinary activity, symptoms on walking 2 blocks of > 1 flight of stairs
  3. Marked limitation, symptoms on walking only 1 - 2 blocks or 1 flight of stairs
  4. Symptoms on any activity, getting washed / dressed causes symptoms
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12
Q

Investigations for stable angina

A 
Bloods 
CXR 
ECG
ETT
Myocardial perfusion imaging 
CT Coronary angiography 
Invasive angiography 
Cardiac catheterisation
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13
Q

What does ETT stand for?

A

Exercise tolerance test

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14
Q

What does ETT rely on?

A

Ability to walk for long enough to produce sufficient CV stress

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15
Q

What makes up a +ve test in ETT for stable angina?

A

Typical symptoms

ST segment depression

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16
Q

How does myocardial perfusion imaging work?

A

Exercise or pharmacological stress (adenosine, dipyramidamole, dobutamine)
Injected in with a radionuclide tracer which follows the blood flow
Injected at peak stress (IV), images obtained
Injected at rest on another and images obtained
Comparison between the images

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17
Q

On myocardial perfusion imaging, if the tracer Is seen at rest but not after stress, what does this indicate?

A

Ischaemia

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18
Q

On myocardial perfusion imaging, if the tracer is seen neither at rest or after stress, what does this indicate?

A

Infarction

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19
Q

When would you do invasive angiography?

A

Early or strong positive ETT
Angina refractory to medical therapy
Diagnosis not clear after non invasive tests
Young cardiac patients due to life work effects
Occupations or lifestyle with risk eg. drivers

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20
Q

How does cardiac catheterisation or coronary angiography work?

A

Local anaesthetic
Arterial cannula inserted into femoral or radial artery
Coronary catheters passed to aortic root and introduced into the ostium of coronary arteries
Radio-opaque contrast injection down coronary arteries and visualised on the xray

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21
Q

Presentation of stable angina

A

Retrosternal pain
Tight band / heaviness / pressure
Radiates to neck / jaw / down arms
Aggravated by exertion, emotional stress

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22
Q

What are the relieving factors for stable angina?

A

GTN

Physical rest

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23
Q

Presentation of MI with no chest pain. Give an example of when this would be the case

A

SOB on exertion
Excessive fatigue on exertion for activity undertaken
Near syncope on exertion

Would be the case in

  • elderly
  • DM (reduced pain sensation)
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24
Q

Differential diagnosis for chest pain

A 
Aortic dissection 
Pericarditis
Pneumonia
Pleurisy 
Peripheral pulmonary emboli (pleuritic) 
Cervical disease 
Costochondritis 
Muscle spasm or strain 
GORD
Oesophageal spasm 
Peptic ulceration 
Biliary coli 
Cholecystitis
Pancreatitis
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25
Q

Signs of stable angina

A 
Tar staining
Obesity
Xanthalasma 
Corneal arcus 
HTN
AAA
Diabetic retinopathy, hypertensive retinopathy 
Noticeable symptoms for angina
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26
Q

General measures to treat stable angina

A

BP
DM
Cholesterol
Lifestyle

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27
Q

What drugs would influence disease progression in stable angina?

A

Statins
ACEis
Aspirin

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28
Q

What drugs would be relieve symptoms in stable angina?

A 
B blockers
CCBs
Ik channel blockers
Nitrates 
K+ channel blockers
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29
Q

What can be used to perform revascularisation?

A

PCI

CABG

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30
Q

What does PCI stand for?

A

Percutaneous coronary intervention

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31
Q

What does CABG stand for?

A

Coronary artery bypass grafting

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32
Q

How does PCI work?

A

Cross stenotic lesion with guidewire and squash atheromatous plaque into walls with balloon and stent
If stent used aspirin and clopidogrel taken together whilst endothelium covers the stent struts and it is no long seen as a foreign body with risk of thrombosis

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33
Q

Complications of PCI

A

MI
Death
Emergency CABG

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34
Q

What is usually the best revascularisation option for stable angina?

A

CABG

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35
Q

Which of CABG and PCI have higher risks?

A

CABG

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36
Q

Who are the patients who derive prognostic benefit from CABG?

A

> 70% stenosis of left main stem artery
Significant proximal three vessel coronary artery disease
Two vessel coronary artery disease that includes significant stenosis of proximal left anterior descending coronary artery who have an ejection fraction < 50%

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37
Q

Example of a vein that can be used in CABG

A

Long saphenous vein

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38
Q

What investigation should higher risk patients have with stable angina?

A

Coronary angiography

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39
Q

What are the acute coronary syndromes?

A

MI

Unstable angina pectoris

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40
Q

What are the types of MI?

A

STEMI

NSTEMI

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41
Q

What does MI stand for?

A

Myocardial infarction

42
Q

What are the chronic / stable ischaemias?

A

Angina pectoris

Silent ischaemia

43
Q

Pathology of hyperlipidaemia causing stable angina

A

Atherosclerosis at the start
Disease of the muscular arteries (not veins) - coronary and cerebral arteries
Progressive deposition of cholesterol esters
Lesions start as fatty acid streaks
Subaccumulation of foam cells (derived from macrophages plus SM cells) filled with lipid
Fibrous plaque - more advanced cause of disease. Develop from fatty streaks and projects into the arterial lumen resulting in reduced blood flow

44
Q

Where do most of the changes from hyperlipidaemia occur?

A

Intimal layer

45
Q

Determinants of demand

A

HR
Systolic BP
Myocardial wall stress
Myocardial contractility

46
Q

What is demand ischaemia?

A

Ischaemia during stress (physical / emotional)

47
Q

What is supply ischaemia?

A

Ischaemia at rest

48
Q

Determinants of supply

A

Coronary artery diameter and tone
Collateral blood flow
Perfusion pressure
HR (duration of diastole)

49
Q

Purpose of drug treatment in stable angina

A 
Relieve symptoms
Halt disease process 
Regression of disease progress
Prevent MI
Prevent death
50
Q

How can drugs decrease myocardial oxygen demand by reducing cardiac workload?

A

Reduce

  • HR
  • myocardial contractility
  • afterload
51
Q

Examples of rate limiting drugs

A

Beta adrenoreceptor antagonists
Ivabradine
CCBs

52
Q

Examples of vasodilator drugs

A

CCBs

Nitrates

53
Q

Examples of beta blockers

A

Bisprolol
Propanolol
Atenolol

54
Q

What are beta blockers?

A

Reversible antagonists of B1 and B2 receptors

55
Q

How do beta blockers work?

A

Block physiological responses to adrenaline and noradrenaline i.e. the sympathetic system - so decrease the 3 major determinants of myocardial oxygen demand
Also improve perfusion of subendocardium by increasing diastolic perfusion time

56
Q

What are the 3 major determinants of myocardial oxygen demand?

A

HR
Contractility
Systolic wall tension

57
Q

Results of beta blockers

A

Decreases

  • HR
  • Force of myocardial contraction
  • CO
  • Velocity of contraction
  • BP
  • protect cardiomyocytes from oxygen free radicals formed during ischaemic episodes
58
Q

What may the sudden cessation of beta blocker therapy may precipitate?

A

MI

59
Q

Contraindications to beta blockers

A 
Asthma
Peripheral vascular disease
Raynauds 
HF 
Bradycardia / heart block
60
Q

Why do patients with HF have a contraindication to BBs?

A

These patients are dependent on sympathetic drive

61
Q

S/Es of Beta blockers

A 
Tiredness / fatigue
Lethargy 
Impotence 
Bradycardia
Bronchospasm
62
Q

What do NSAIDs do to BBs?

A

Antagonist antihypertensive actions

63
Q

Examples of CCBs

A

Diltiazem
Verapamil
Amlodipine

64
Q

How do CCBs work?

A

Prevent calcium influx into myocytes and smooth muscle lining arteries and arterioles by blocking the L-type calcium channel
Rate limiting CCBs like dilitiazem or verapamil also reduce HR and force of contraction
Reduce vascular tone and produce vasodilation and reduce afterload. This reduces myocardial work load

65
Q

Examples of vasodilating CCBs

A

Nifedipine

Amlodipine

66
Q

What may vasodilating CCBs produce?

A

Reflex tachycardia

67
Q

What do rate limiting CCBs do?

A

Reduce the HR and force of myocardial contractility and this reduces the myocardial oxygen requirements

68
Q

Contraindications of CCBs

A

Rapid acting vasodilating CCBs may cause acute MI or stroke
Never use nifedipine immediate release
Post MI
Unstable angina

69
Q

S/Es of CCBs

A

Ankle oedema (15 - 20%) and does not respond to diuretics
Headache
Flushing
Palpitations

70
Q

Examples of nitro-vasodilators

A

Glyceryl trinitrate (GTN)
isosorbide mononitrate
Isosorbide dinitrate

71
Q

When is GTN taken?

A

When pain is coming on or before the patient does something they know will precipitate symptoms

72
Q

How is GTN taken?

A

Sublingual
Buccal
Transdermal

73
Q

What is GTN syncope?

A

When the patient uses GTN and this causes an acute and very rapid reduction in blood pressure and cardiac return, resulting in venule and arterial dilation and they collapse

74
Q

How do nitro-vasodilators work?

A

Relax all smooth muscle by releasing NO which then stimulates release of cGMP which produces smooth muscle relaxation
Reduces preload and afterload so reduces myocardial oxygen consumption

75
Q

How to nitrates relieve angina?

A

Arteriolar dilation and so reducing Cardiac afterload and thus myocardial work and oxygen demand
Peripheral venodilatation and so reducing venous return, cardiac preload and thus myocardial workload
Relieving coronary vasospasm
Redistributing myocardial blood flow to ischaemic areas of the myocardium

76
Q

Do nitrates reduce mortality?

A

No - purely symptomatic

77
Q

When are IV nitrates used?

A

Mainstay in the treatment of unstable angina where they are used in combination with heparin

78
Q

How can one avoid tolerance of nitrate therapy?

A

Giving asymmetric doses of nitrate 8am and 2pm

Using a sustained release preparation which incorporates a “free nitrate period”

79
Q

S/E of nitrates

A

Headache (increase dose slowly)

Hypotension - GTN syncope

80
Q

Examples of potassium channel openers

A

Nicorandil

Ivabradine

81
Q

How does nicorandil work?

A

Activate “silent” potassium channels

The entry of potassium channels into cardiac myocytes inhibits the calcium influx and so negative inotropic action

82
Q

S/E of nicorandil

A

Bowel ulceratiton

83
Q

How does ivabradine work?

A

Selective sinus node If channel inhibitor
Slows down the diastolic depolarisation slope of the SA node
Results in reduction in HR and therefore myocardial oxygen demand

84
Q

S/Es of ivabradine

A

Crohns like symptoms and lesions are microscopically like crohns

85
Q

What are the antiplatelets?

A

Aspirin

Clopidogrel

86
Q

What dose is low dose aspirin?

A

75 - 150 mg

87
Q

How does aspirin work?

A

Potent inhibitor of platelet thromboxane production (thromboxane stimulates platelet aggregation and vasoconstriction)

88
Q

Indications for aspirin

A

Adults unable to tolerate or with a contraindication to use of BBs
In combination with BBs in patients inadequately controlled with an optimal beta blocker dose

89
Q

What is aspirin the most common cause for admission with?

A

GI bleed

90
Q

How does clopidogrel work?

A

Inhibits ADP receptor activates antiplatelet aggregation

Prevention of atherosclerotic events in PVD

91
Q

Examples of cholesterol lowering agents

A

Simvastatin
Pravastatin
Atorvastatin

92
Q

How do cholesterol lowering agents work?

A

HMG CoA reductase inhibitors

Stabilises the atheromatous plaque - reduces the likelihood of split / fissure of atheroma releasing its contents

93
Q

Everyone who has coronary artery disease and angina should be on what?

A

Beta blocker

94
Q

Secondary prevention drug treatment for CV disease

A

Aspirin 75mg daily
ACEI (stable angina and DM)
Statins
BP Tx

95
Q

NICE guidelines for Tx of stable angina

A

1st line - beta blockers
2nd line - CCB added
3rd line - switch to another option or use combination

96
Q

Criteria for stable angina

A
  1. Described as constricting pain
  2. Precipitated by physical exertion
  3. Relieved by GTN spray or rest within 5 mins
97
Q

What is atypical chest pain?

A

2/3 criteria for stable angina

98
Q

What should statins be avoided in?

A

Pregnancy

99
Q

1st line investigation for coronary artery disease

A

Contrast enhanced CT angiogram

100
Q

Treatment of stable angina

A

All patients should receive aspirin and statin
Sublingual GTN for attacks
BB or CCB first line
- if CCB in monotherapy - verapamil or diltiazem
Can be increased to max dose
If still symptomatic with BB add a CCB and vise versa
If on monotherapy and cannot tolerate the addition of CCB/BB, add either
- long acting nitrate
- ivabradine
- nicorandil
- ranolazine
If the patient is already taking CCB + BB, only add third drug IF awaiting assessment for PCI or CABG

CVS Pathology (19 decks)

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