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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
Signs of stable angina
``` Tar staining Obesity Xanthalasma Corneal arcus HTN AAA Diabetic retinopathy, hypertensive retinopathy Noticeable symptoms for angina ```
26
General measures to treat stable angina
BP DM Cholesterol Lifestyle
27
What drugs would influence disease progression in stable angina?
Statins ACEis Aspirin
28
What drugs would be relieve symptoms in stable angina?
``` B blockers CCBs Ik channel blockers Nitrates K+ channel blockers ```
29
What can be used to perform revascularisation?
PCI | CABG
30
What does PCI stand for?
Percutaneous coronary intervention
31
What does CABG stand for?
Coronary artery bypass grafting
32
How does PCI work?
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
33
Complications of PCI
MI Death Emergency CABG
34
What is usually the best revascularisation option for stable angina?
CABG
35
Which of CABG and PCI have higher risks?
CABG
36
Who are the patients who derive prognostic benefit from CABG?
>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%
37
Example of a vein that can be used in CABG
Long saphenous vein
38
What investigation should higher risk patients have with stable angina?
Coronary angiography
39
What are the acute coronary syndromes?
MI | Unstable angina pectoris
40
What are the types of MI?
STEMI | NSTEMI
41
What does MI stand for?
Myocardial infarction
42
What are the chronic / stable ischaemias?
Angina pectoris | Silent ischaemia
43
Pathology of hyperlipidaemia causing stable angina
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
Where do most of the changes from hyperlipidaemia occur?
Intimal layer
45
Determinants of demand
HR Systolic BP Myocardial wall stress Myocardial contractility
46
What is demand ischaemia?
Ischaemia during stress (physical / emotional)
47
What is supply ischaemia?
Ischaemia at rest
48
Determinants of supply
Coronary artery diameter and tone Collateral blood flow Perfusion pressure HR (duration of diastole)
49
Purpose of drug treatment in stable angina
``` Relieve symptoms Halt disease process Regression of disease progress Prevent MI Prevent death ```
50
How can drugs decrease myocardial oxygen demand by reducing cardiac workload?
Reduce - HR - myocardial contractility - afterload
51
Examples of rate limiting drugs
Beta adrenoreceptor antagonists Ivabradine CCBs
52
Examples of vasodilator drugs
CCBs | Nitrates
53
Examples of beta blockers
Bisprolol Propanolol Atenolol
54
What are beta blockers?
Reversible antagonists of B1 and B2 receptors
55
How do beta blockers work?
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
What are the 3 major determinants of myocardial oxygen demand?
HR Contractility Systolic wall tension
57
Results of beta blockers
Decreases - HR - Force of myocardial contraction - CO - Velocity of contraction - BP - protect cardiomyocytes from oxygen free radicals formed during ischaemic episodes
58
What may the sudden cessation of beta blocker therapy may precipitate?
MI
59
Contraindications to beta blockers
``` Asthma Peripheral vascular disease Raynauds HF Bradycardia / heart block ```
60
Why do patients with HF have a contraindication to BBs?
These patients are dependent on sympathetic drive
61
S/Es of Beta blockers
``` Tiredness / fatigue Lethargy Impotence Bradycardia Bronchospasm ```
62
What do NSAIDs do to BBs?
Antagonist antihypertensive actions
63
Examples of CCBs
Diltiazem Verapamil Amlodipine
64
How do CCBs work?
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
Examples of vasodilating CCBs
Nifedipine | Amlodipine
66
What may vasodilating CCBs produce?
Reflex tachycardia
67
What do rate limiting CCBs do?
Reduce the HR and force of myocardial contractility and this reduces the myocardial oxygen requirements
68
Contraindications of CCBs
Rapid acting vasodilating CCBs may cause acute MI or stroke Never use nifedipine immediate release Post MI Unstable angina
69
S/Es of CCBs
Ankle oedema (15 - 20%) and does not respond to diuretics Headache Flushing Palpitations
70
Examples of nitro-vasodilators
Glyceryl trinitrate (GTN) isosorbide mononitrate Isosorbide dinitrate
71
When is GTN taken?
When pain is coming on or before the patient does something they know will precipitate symptoms
72
How is GTN taken?
Sublingual Buccal Transdermal
73
What is GTN syncope?
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
How do nitro-vasodilators work?
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
How to nitrates relieve angina?
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
Do nitrates reduce mortality?
No - purely symptomatic
77
When are IV nitrates used?
Mainstay in the treatment of unstable angina where they are used in combination with heparin
78
How can one avoid tolerance of nitrate therapy?
Giving asymmetric doses of nitrate 8am and 2pm | Using a sustained release preparation which incorporates a "free nitrate period"
79
S/E of nitrates
Headache (increase dose slowly) | Hypotension - GTN syncope
80
Examples of potassium channel openers
Nicorandil | Ivabradine
81
How does nicorandil work?
Activate "silent" potassium channels | The entry of potassium channels into cardiac myocytes inhibits the calcium influx and so negative inotropic action
82
S/E of nicorandil
Bowel ulceratiton
83
How does ivabradine work?
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
S/Es of ivabradine
Crohns like symptoms and lesions are microscopically like crohns
85
What are the antiplatelets?
Aspirin | Clopidogrel
86
What dose is low dose aspirin?
75 - 150 mg
87
How does aspirin work?
Potent inhibitor of platelet thromboxane production (thromboxane stimulates platelet aggregation and vasoconstriction)
88
Indications for aspirin
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
What is aspirin the most common cause for admission with?
GI bleed
90
How does clopidogrel work?
Inhibits ADP receptor activates antiplatelet aggregation | Prevention of atherosclerotic events in PVD
91
Examples of cholesterol lowering agents
Simvastatin Pravastatin Atorvastatin
92
How do cholesterol lowering agents work?
HMG CoA reductase inhibitors | Stabilises the atheromatous plaque - reduces the likelihood of split / fissure of atheroma releasing its contents
93
Everyone who has coronary artery disease and angina should be on what?
Beta blocker
94
Secondary prevention drug treatment for CV disease
Aspirin 75mg daily ACEI (stable angina and DM) Statins BP Tx
95
NICE guidelines for Tx of stable angina
1st line - beta blockers 2nd line - CCB added 3rd line - switch to another option or use combination
96
Criteria for stable angina
1. Described as constricting pain 2. Precipitated by physical exertion 3. Relieved by GTN spray or rest within 5 mins
97
What is atypical chest pain?
2/3 criteria for stable angina
98
What should statins be avoided in?
Pregnancy
99
1st line investigation for coronary artery disease
Contrast enhanced CT angiogram
100
Treatment of stable angina
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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