Stable Angina Flashcards

1
Q

Define the term; Angina

A

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

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2
Q

Name the most common cause of angina and the two rare causes of angina

A
  1. Most common- reduction in coronary artery blood flow to the myocardium (atheroma, spasm or abnormal coronary flow)

RARE=

  1. Reduced O2 transport caused by anaemia
  2. Pathologically increased myocardial O2 demand (caused by left ventricular hypertrophy, aortic stenosis, hypertrophic cardiomyopathy and thyrotoxicosis)
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3
Q

How might stable angina present?

A

Chest pain in the left side and down the left arm

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4
Q

What causes the onset of stable angina?

A

Excess myocardial oxygen demand e.g. exertion, cold weather, emotional stress, following heavy meal.

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5
Q

What % of the vessel lumen must be occluded before angina occurs?

A

> 70%

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6
Q

What differentiates stable angina from unstable angina?

A

Stable= goes away with rest

Unstable= comes on at any time

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7
Q

Describe the SOCRA (first part of SOCRATES) presentation you would expect in a patient presenting with angina

A
  • Site of pain (watch for patient gestures): retrosternal heaviness/tightness is a common presentation
  • Character of pain: often a tight band/pressure/heaviness rather than a traditional “pain”.
  • Radiation sites: neck and/or into jaw, down arms.
  • Aggravated with exertion & emotional stress. Relieving factors such as rapid improvement with GTN or physical rest.
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8
Q

Can myocardial ischaemia be silent?

A

Yes- this often happens with diabetic patients due to reduced pain sensation

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9
Q

List some of the differentials for stable angina

A
  1. Cardiovascular (aortic dissection or pericarditis)
  2. Resp (pneumonia, pleurisy, peripheral pulmonary emboli (pleuritic))
  3. Musculoskeletal (Cervical disease, costochondritis, muscle spasm or strain)
  4. GI (Gastro-oesphageal reflux, oesophageal spasm, peptic ulceration, biliary colic, cholecystitis, pancreatitis)
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10
Q

Name the classification system used to class the severity of angina

A

Canadian classification of angina severity

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11
Q

Explain each classification bracket of the canadian classification of angina severity system

A

I- Ordinary physical activity does not cause angina, symptoms only on significant exertion.

II- Slight limitation of ordinary activity, symptoms on walking 2 blocks or > 1 flight of stairs.

III- Marked limitation, symptoms on walking only 1-2 blocks or 1 flight of stairs.

IV- Symptoms on any activity, getting washed/dressed causes symptoms.

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12
Q

List the 5 non-modifiable risk factors associated with coronary artery disease

A
  1. Age
  2. gender
  3. Creed
  4. Family history
  5. genetics
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13
Q

List the 5 modifiable risk factors associated with coronary artery disease

A
  1. Smoking
  2. Lifestyle- exercise & diet
  3. Diabetes mellitus
  4. Hypertension
  5. Hyperlipidaemia
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14
Q

List the clinical investigations could be conducted when stable angina is suspected?

A
  1. Bloods
  2. ECG
  3. CXR
  4. Exercise tolerance test
  5. Myocardial perfusion imaging
  6. CT coronary ngiography
  7. Echo stress ultrasound
  8. invasive angiography
  9. cardiac catheterisation/coronary angiography
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15
Q

In patients with a confirmed diagnosis of angina, the ECG will be normal in over 50% of cases. What ECG findings might you mind that would indicate a prior MI or left ventricular hypertrophy?

A

MI= Pathological Q waves

Evidence of left ventricular hypertrophy =high voltages, lateral ST-segment depression or “strain pattern

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16
Q

What is the function of an echo stress ultrasound?

A

This technique allows clinicians to take a closer look at the cardiac structures under resting states and stressed states (either physical stress or pharmacological stress)

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17
Q

When would an invasive angiography be appropriate in stable angina patients

A
  • If the patient has an early or strongly positive exercise tolerance test (suggests multi-vessel disease).
  • Symptoms of angina persist despite medication.
  • The diagnosis is still not clear after non-invasive tests.
  • The patient is young and has suffered coronary disease due to work/life effects.
  • The patient’s occupation or lifestyle is associated with risk e.g. drivers etc.
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18
Q

In myocardial perfusion imgaing, what is the pathology if;

A) The tracer is seen at rest but not after stress

B) The tracer is seen neither rest, or after stress

A

A) Tracer seen at rest but not after stress = ischaemia

B) Tracer seen neither rest, or after stress = infarction

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19
Q

What are the general treatment measures used in stable angina?

A

Address risk factors: blood pressure, DM, Cholesterol, physical activity & smoking.

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20
Q

Which three types of drug can be given to influence the progression of disease in acute angina?

A

Statins
ACE inhibitors
Aspirin

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21
Q

What impact do statins have on stable angina?

A
  • Statins reduce low density lipoprotein-cholesterol deposition in atheroma and also stabilises atheroma by reducing plaque rupture and acute coronary syndromes
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22
Q

What would the total cholesterol level have to be in a stable angina patient in order to consider the use of a statin?

A

> 3.5mmol/L

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23
Q

What impact do ACE inhibitors have on stable angina?

A

stabilise the endothelium and also reduce plaque rupture.

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24
Q

What impact does aspirin have on stable angina?

A

protect the endothelium and reduce platelet activation/aggregation.

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25
Q

Which drugs can be used to relieve symptoms in stable angina/

A
  1. Beta blockers
  2. Ca2+ channel blockers
  3. IK channel blockers
  4. Nitrates
  5. K+ Channel blockers
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26
Q

How to beta blockers relieve the symptoms of stable angina?

A

Beta blockers reduce myocardial work. They also have anti-arrhythmic effects and aim to achieve a resting heart rate <60BPM.

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27
Q

How do Ca2+ channel blockers relieve the symptoms of stable angina?

A

Centrally, they achieve a resting heart rate <60BPM

Peripherally, they cause vasodilation

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28
Q

How do IK channel blockers relieve the symptoms of stable angina?

A

They achieve a resting heart rate <60BPM.

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29
Q

Ivabradine is a newer kind of IK channel blocker medication. Explain how it works

A

reduces sinus node rate

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30
Q

How do nitrates relieve the symptoms of stable angina?

A

They cause venous vasodilation reducing the venous return and subsequently reducing the cardiac work

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31
Q

If patients still experience lifestyle limiting symptoms following pharmacological and non-pharmacological intervention what should they be offered?

A

Percutaneous coronary intervention

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32
Q

Name the percutaneous coronary intervention now carried out in 95% of stable angina cases (that are eligible for PCI!)

A

Percutaneous transluminal coronary angioplasty (PTCA) and stenting

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33
Q

Explain what happens during percutaneous transluminal coronary angioplasty (PTCA) and stenting

A

This procedure has similar beginnings to coronary angiography but guidewire is passed across a stenotic lesion. The guidewire is then used to squash the atheromatous plaque into the arterial walls with a balloon and a stent.

34
Q

Does PCI improve prognosis?

A

No- it just improves symptom management

35
Q

What does CABG stand for?

A

Coronary artery bypass grafts

36
Q

In stable angina patients, when would CABG be offered instead of PCI?

A

In diffuse multi-vessel disease

37
Q

Approximately how long to CABG vein grafts last?

A

10 years

38
Q

Describe the three stable angina patient subgroups which are most likely to benefit prognostically from CABG

A

those with >70% stenosis of left main stem artery

Those with significant proximal three-vessel coronary artery disease

Those with two vessel coronary artery disease that includes significant stenosis of proximal left anterior descending coronary artery and who have an ejection fraction < 50%.

39
Q

What % of patients are symptom free 5 years after CABG?

A

80%

40
Q

In patients who have undergone stenting PCI, which drugs must be taken afterwords and why/

A

Aspirin and Clopidogrel should be taken together whilst the endothelium covers the stent struts until the time where the stent will no longer be seen as a foreign body with an associated risk of thrombosis.

41
Q

What are the aims of pharmacological drug treatment in angina patients?

A
  1. Halt the disease process
  2. Regression of the disease process
  3. Prevent myocardial infarction
  4. Prevent death
42
Q

What 3 main effects do beta blockers have on the heart?

A
  1. slows the heart rate
  2. Reduces contractility
  3. Reduces systolic wall tension
43
Q

What impact do beta blockers have upon the exercise threshold of angina

A

Beta blockers increase the exercise threshold at which angina occurs

44
Q

List the 5 contraindications of beta blockers

A
  1. Asthma
  2. Peripheral vascular disease
  3. Raynauds syndrome
  4. Heart failure
  5. existing bradycardia/heart block

(remember that some beta blocking drugs also affect the beta 2 receptors in the lungs and blood vessels hence the above contraindications)

45
Q

What are three important adverse reactions to beta blockers?

A

Tiredness/lethargy/fatigue

Bradycardia

Bronchospasm

46
Q

If a patient is stopping beta blocker medications, why should they be tapered off over the course of a week or two?

A

because sudden cessation of beta blockers can cause an MI

47
Q

what side effect can occur when a beta blocker is used in conjunction with other hypotensive agents?

A

hypotension

48
Q

what side effect can occur when a beta blocker is used in conjunction with rate limiting drugs such as verapamil or diltiazem?

A

bradycardia

49
Q

what side effect can occur when a beta blocker is used in conjunction with negatively inotrophic agents?

A

Cardiac failure

50
Q

What impact can beta blockers have upon insulin or oral hypoglycaemics?

A

Exaggerate or mask

51
Q

Briefly explain how calcium channel blockers work

A

Calcium channel blockers prevent calcium influx into the myocytes and the smooth muscle lining arteries and arterioles by blocking the L-Type calcium channel

52
Q

Name 2 rate limiting calcium channel blockers

A

diltiazem and verapamil

53
Q

What impact do rate limiting calcium channel blockers such as diltiazem and verapamil have upon the heart?

A

reduce heart rate and force of contraction

54
Q

Name a vasodilating calcium channel blocker

A

Amlodipine

55
Q

What impact does a vasodilating calcium channel blocker such as amlodipine have upon the heart?

A

reduce blood pressure and afterload

56
Q

Which calcium channel blocker should NEVER be given to a patient with stable angina and why?

A

NEVER USE NIFEDIPINE IMMEDIATE RELEASE AS IT MAY PRECIPITATE AN ACUTE MI OR STROKE

57
Q

Post myocardial infaction, calcium channel blockers may increase _______ and _______ in patients with impaired LV function

A

Post myocardial infaction, calcium channel blockers may increase morbidity and mortality in patients with impaired LV function

58
Q

List the 4 most common adverse calcium channel blocker reactions

A
  1. Ankle oedema
  2. Headaches
  3. Flushing
  4. Palpatations
59
Q

What % of patients taking calcium channel blockers will develop ankle oedema?

A

15-20%

60
Q

Will ankle oedema caused by calcium channel blockers respond to diuretics?

A

no

61
Q

Name the three most commonly prescribed nitrates

A
  1. Glyceryl trinitrate
  2. Isosorbide mononitrate
  3. Isosorbide dinitrate
62
Q

Explain the administration route for each of the three nitrate medications

A

Glyceryl trinitrate (GTN spray)= Sublingual, buccal, transdermal

Isosorbide mononitrate
& Isosorbide dinitrate= Sustained release formulation, tablets

63
Q

Briefly explain the mechanism of action of nitrates

A

The nitro-vasodilators relax almost all smooth muscle by releasing nitrous oxide which then stimulates the production of cGMP which produces smooth muscle relaxation.

64
Q

Explain how nitrates relieve the symptoms of angina

A

Nitrates relieve angina by:

  1. Causing arteriolar dilatation and so reducing cardiac afterload and thus myocardial work and oxygen demand
  2. Causing peripheral venodilatation and so reduce venous return, cardiac preload and thus myocardial workload
  3. Relieving coronary vasospasm
65
Q

Is there evidence that nitrates reduce mortality?

A

No

66
Q

How can tolerance to nitrates be avoided?

A
  • Giving asymmetric doses of nitrate at 8am and 2pm

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

67
Q

What are the two adverse drug reactions associated with nitrates?

A

Headaches and hypotension

68
Q

How can headaches be avoided when using nitrates/

A

Increase the dose slowly

69
Q

name the three second line therapies used in the treatment of stable angina

A
  • Nicodamids (Cause potassium channel activation)
  • Ivabradine (Causes sinus node inhibition)
  • Ranolazine (Causes late Na+ current inhibition)
70
Q

Explain how nicorandil has a negative ionotropic effect

A

Nicorandil activates ATP sensitive potassium channels allowing entry of potassium into cardiac myocytes and inhibiting calcium influx and so has a negative inotropic action.

71
Q

What impact does nicorandil have on vasculature?

A

Nicorandil Induces relaxation of vascular smooth muscle and has coronary vasodilator properties.

72
Q

briefly explain the mechanism of action of Ivabradine

A

Ivabradine is a selective sinus node If channel inhibitor. It inhibits the If pacemaker current in the sinoatrial node and reduces heart rate.

73
Q

Which patients would qualify for ivabradine?

A

Ivabradine is used for the symptomatic treatment of chronic stable angina in adults with normal sinus rhythm and heart rate ≥ 70 bpm either instead of or alongside beta blockers

74
Q

What 2 things has ivabradine been shown to reduce?

A

fatal and non fatal MI

75
Q

If a patient’s symptoms were still not well controlled on a beta blocker, which medication might you consider adding to the beta blocker?

A

Ivabradine

76
Q

Briefly explain the mechanism of action of Ranolazine

A

Ranolazine inhibits persistent or late inward sodium current (INa) in heart muscle which leads to a reduction in intracellular calcium levels.

77
Q

What is the main effect of ranolazine?

A

Ranolazine inhibits persistent or late inward sodium current (INa) in heart muscle which leads to a reduction in intracellular calcium levels.

78
Q

Is ranolazine a pro-drug?

A

Yes

79
Q

name the liver enzyme that metabolises ranolazine and the liver enzyme that is inhibited by ranolazine

A

Ranolazine is metabolized by CYP3A4

& inhibits CYP2D6

80
Q

Which drugs should you not prescribe with ranolazine?

A

clarithromycin, ketoconazole etc

81
Q

Briefly explain how anti-platelet therapy works

A

Antiplatelet therapy prevents the formation of platelet aggregates which are important in the pathogenesis of angina, unstable angina and acute MI

82
Q

Name two statin?

A

Atorvastatin & simvastatin