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CARD - 1 > Acute Coronary Syndrome - Treatment > Flashcards

Acute Coronary Syndrome - Treatment Flashcards

1
Q

What is ACS?

A

Umbrella term covering a number of acute presentations of ischaemic heart disease -
STEMI, NSTEMI, unstable angina

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2
Q

What causes acute coronary syndromes?

A

Atherosclerotic plaque rupture or erosion,
superimposed platelet aggregation and thrombosis, vasospasm and vasoconstriction,
subtotal or transient total occlusion of a vessel.

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3
Q

What does STEMI normally occur as a result of?

A

Coronary artery occlusion due to formation of a thrombus overlying an atheromatous plaque.

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4
Q

What is thrombolysis?

A

Dissolution of the clot via IV injection

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5
Q

How do modern thrombolytic agents work?

A

They are serine proteases that work by converting plasminogen to the natural fibrinolytic agent plasmin. Plasmin lyses clot by breaking down the fibrinogen and fibrin in the clot.

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6
Q

What are the two different types of fibrinolytics?

A

Fibrin specific agents such as alteplase, repeals, tenecteplase - all catalyse conversion of plasminogen to plasmin in the absence of fibrin.

Non-fibrin-specific agents such as streptokinase catalyse systemic fibrinolysis.

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7
Q

What is the problem with streptokinase?

A

Extracted from a mycobacterium and commonly causes anaphylaxis if used a second time.

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8
Q

In which situations is the use of fibrinolytic agents contraindicated?

A

Prior intracranial haemorrhage (ICH)
Known structural cerebral vascular lesion
Known malignant intracranial neoplasm
Ischaemic stroke within 3 months
Suspected aortic dissection
Active bleeding or bleeding diathesis (excluding menses)
Significant closed-head trauma or facial trauma within 3 months

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9
Q

What benefits are associated with thrombolysis?

A

If timely:
23% reduction in mortality
39% when used with aspirin

Remember you still have the atheromatous plaque but you break down the clot to reestablish blood flow to the heart.

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10
Q

How does aspirin improve ACSs?

A

The formation of platelet aggregates are important in the pathogenesis of angina, unstable angina and acute MI - aspirin is a potent inhibitor of platelet thromboxane A2 production and thromboxane stimulates platelet aggregation and vasoconstriction.

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11
Q

How should aspirin be given in ACS?

A

Loading dose (300mg) then low dose thereafter (e.g. 75mg)

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12
Q

What is clopidogrel and what does it do?

A

It’s a prodrug that inhibits ADP receptor activated platelet aggregation - specifically and irreversibly inhibits the P2Y12 ADP receptor which is important in aggregation of platelets and cross-linking by fibrin.

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13
Q

What is the issue with clopidogrel?

A

14% of the population show some level of resistance as they have variable CYP 2C19 activity which controls break down of clopidogrel and us they experience no effect.

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14
Q

What is clopidogrel always used in combination with? and why?

A

Aspirin, relative risk reduction of 21% when used together with aspirin. Much more effective when used in combination.
Claimed lower incidence of GI bleed (but bleed very common).

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15
Q

How would someone be resistant to clopidogrel?

A

Clopidogrel activated by CYP 2C19

14% of the population has low CYP 2C19 levels and demonstrate resistance.

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16
Q

What drug, similar to clopidogrel shows lower resistance?

A

Ticagrelor

Ticagrelor and aspirin are more effective than clopidogrel and aspirin

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17
Q

What is prasugrel?

A 
A member of the thienopyridine class of ADP receptor inhibitors, like clopidogrel. 
Compared to cloidogrel prasugrel inhibits ADP-induced platelet aggregation more rapidly, more consistently.
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18
Q

What is the major benefit of prasugrel over clopidogrel?

A

Less incidence of death, MI, stroke and major bleed with prasugrel use.

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19
Q

What are the four low molecular weight herapins? What is the one we use in Scotland?

A

Enoxaparin, Dalteparin, Tinzeparin, Fondaparinux.

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20
Q

What is fondaparinux?

A

A selective inhibitor of factor Xa.
It is a synthetic pentasaccaride (single chemical entity).
It is high selective for antithrombin
(advs - once daily administration, no need for platelet monitoring)

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21
Q

What are the benefits of using enoxaparin in comparison with fondaparinux?

A

Reduction in bleeding risk, death, MI…

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22
Q

What is glycoprotein IIb/IIIa?

A

An integral complex found on platelets. Its receptor for fibrinogen aids in platelet aggregation. Platelet activation by ADP (blocked by clopidogrel) leads to conformational changes in platelet GPIIb/IIIa receptor that induces binding to fibrinogen.

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23
Q

Give 2 examples of GPIIb/IIIa receptor inhibitor drugs.

A

abciximab, tirofiban

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24
Q

How do IV GPIIb/IIIa inhibitors work?

A

They block platelet aggregation by inhibiting fibrinogen binding to a conformationally activated form of the GPIIb/IIIa receptor on two adjacent platelets.

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25
Q

What are the major adverse effects of GPIIb/IIIa receptor inhibitors?

A

Major bleed occurs in 1.4% patients and minor bleeding in 10.5%.
Blood transfusion req to terminate bleeding and to improve bleeding related anaemia in 4% of all patients. Thrombocytopenia was more often with tirofiban and heparin than with heparin alone.

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26
Q

When are beta blockers used in relation to MIs?

A

In the treatment of acute MI

For secondary prevention in the survivors of MIs

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27
Q

Which two drugs can be used to reduce mortality following an acute MI?

A

IV atenolol or metoprolol

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28
Q

What are the effects of oral beta blockers?

A

Whether started weeks or months post MI reduce cardiac death by 22% and second MI by 26%.

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29
Q

How do the beta blockers work to improve mortality post MI?

A

Beta blockers competitively inhibit the myocardial effects of circulating catecholamines and reduce myocardial oxygen consumption by lowering heart rate, blood pressure and myocardial contractility.

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30
Q

What patients would be at increased risk of cardiogenic shock when given beta blockers?

A

Patients who’s:
age > 70 yrs
heart rate > 100 beats/min
systolic BP <120mmHg

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31
Q

In what other patients would you avoid the use of beta blockers?

A

Those with symptoms of vasospasms and cocaine users.

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32
Q

Who does ACS generally develop in?

A

Those who have had IHD

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33
Q

What is IHD also known as?

A

Coronary heart disease and coronary artery disease

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34
Q

What does IHD generally describe?

A

The gradual build up of fatty plaques within the walls of coronary arteries –>
1. gradual narrow –> less blood + O2 reaching myocardium at times of stress –> exertional chest pain

  1. Risk of sudden plaque rupture –> sudden occlusion of artery –> no blood/O2 reaches myocardium (MI)
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35
Q

What are non-modifiable RFs for ischaemic heart disease?

A

Increased age
Male
FH

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36
Q

What are modifiable risk factors for IHD?

A 
Smoking
DM
HTN
Hypercholesterolaemia
Obesity
37
Q

What is the pathophysiology of IHD?

A
  1. Endothelial dysfunction (triggered by smoking, hyperglycaemia, hypertension..)
  2. Po-inflammatory, pro-oxidant, pro-proliferative changes to endothelium with reduced ntiric oxide bioavailability
  3. Fatty infiltration of subendothelial space by LDL particles
  4. Monocytes migrate from blood + differentiate into macrophages which phagocytose oxidised LDL slowly turning into foam cells (these macrophages then die + further propagate the inflammatory process)
  5. Smooth muscle proliferation + migration from the tunica media into the intima –> fibrous capsule covering fatty plaque
38
Q

What is the classic and most common features of ACS?

A

Chest pain

39
Q

Describe the pain experienced in ACS?

A

Central/left sided
May radiate to jaw/L arm
Heavy/constricting

40
Q

What patients are prone to not experience any chest pain during an ACS?

A

Diabetics, elderly

41
Q

Apart from chest pain, what are other possible features an ACS may present with?

A

SoB
Sweating
NV

42
Q

What are some physical signs someone with an ACS may present with?

A

Pulse, BP, temp, O2 sats often normal or only mildly altered

Patient may appear pale and clammy

43
Q

What are the two most important investigations when assessing a patient with chest pain?

A

ECG

Cardiac markers, e.g. troponin

44
Q

What artery is affected in an ‘anterior MI’?

A

Left anterior descending

45
Q

Where are the ECG changes in an anterior MI?

A

V1-4

46
Q

What artery is affected in an ‘inferior’ MI?

A

Right coronary

47
Q

Where are the ECG changes in an inferior MI?

A

II, III, aVF

48
Q

What artery is affected in a lateral MI?

A

Left circumflex

49
Q

Where are the ECG changes in a lateral MI?

A

I, V5-6

50
Q

What are the aims of treating ACS?

A

Prevent worsening of presentation, i.e. further occlusion
Revascularise (unblock) the vessel
Treat pain

51
Q

What mnemonic is useful in the treatment of ACS?

A 
MONA
Morphine
Oxygen (NB not all pts req)
Nitrates
Aspirin
52
Q

When should oxygen therapy be given in ACS?

A

Only if O2 sats are <94% aiming for sats of 94-98%

Those at risk of hypercapnic failure target SpO2 88-92%

53
Q

In addition to MONA what other drugs/therapy should be given to someone who has had a STEMI?

A

2nd antiplatelet: clopidogrel, prasugrel, ticagrelor

PCI

54
Q

What is PCI?

A

Percutaneous coronary intervention: blocked arteries are opened up using a balloon (angioplasty) and then a stent is inserted

Done by inserting a catheter into the radial/femoral artery

55
Q

How should a NSTEMI be managed (apart from MONA)?

A

Risk stratification (e.g. using GRACE) to decide on mx
If high risk/clinically unstable –> coronary angiography
Lower risk –> coronary angiography at later date

56
Q

What is standard secondary prevention for ACS?

A 
Aspirin
2nd antiplatelet if appropriate, e.g. clopidogrel
Beta blocker
ACE inhibitor
Statin
57
Q

What is the first line method of revascularisation in STEMI?

A

PCI

58
Q

When might patients be given fibrinolysis for management of a PCI?

A

If they cannot get primary PCI within 120 minutes

NB PCI can be given up to 12h after onset of symptoms, so if 90 minutes after giving fibrinolysis, the patients ECG doesn’t show resolution of the MI –> require PCI

59
Q

What drugs are given in STEMI to relieve symptoms?

A

Sublingual glyceryl nitrate
IV morphine
Metoclompramide

60
Q

What drug should be given to ALL STEMI patients?

A

Aspirin 300mg

61
Q

How do ticagrelor, prasurgel and clopidogrel work?

A

Antagonists of P2Y12 adenoside disphosphate receptor

62
Q

What are other treatments that may be given in STEMI?

A

Bivalirudin (usually given alongside aspirin + clopidogrel)

Heparin (LMWH/UFH)

63
Q

What is bivalirudin?

A

A direct thrombin inhibitor

64
Q

What should all patients with NSTEMI recieve?

A

Aspirin 300mg

Nitrates/morphine to relieve chest pain if req

65
Q

What other things are involved in the management of NSTEMI?

A

Antithrombin treatment (fondaparinux or UFH if high creatinine/having angiography in next 24h)

Ticagrelor/prasugrel (prasugrel preferred if going for PCI) - given for 12 months usually

IV glycoprotein IIb/IIIa receptor antagonists

Coronary angiography

66
Q

Give e.g.s of glycoprotein IIb/IIIa receptor antagonists

A

Eptifibatide, tirofiban

67
Q

Which NSTEMI patients should be given glycoprotein IIb/IIIa receptor antagonists?

A

Those with an intermediate/high risk of adverse cardiovascular events (predicted 6 month mortality above 3%) and are scheduled to undergo angiography w.i 96h of hospital admission

68
Q

When should coronary angiography be considered in NSTEMI?

A

Consider in first 96h of admission if 6 month mortality >3% OR ASAP in those who are clinically unstable

69
Q

What is the mechanism of action of aspirin?

A

Antiplatelet - inhibits production of thromboxane A2

70
Q

What is the mechanism of action of clopidogrel?

A

Antiplatelet - inhibits ADP binding to its platelet receptor

71
Q

What is the mechanism of action of enoxaparin?

A

Activates antithrombin III, which inhibits Xa

72
Q

What is the mechanism of action of fondaparinux?

A

Activates antithrombin III, which inhibits Xa

73
Q

What drug is usually given to those who are going to have PCI for STEMI?

A

UFH (alt: LMWH)

74
Q

What drugs ca be used for thrombolysis in STEMI?

A

tPA

Tenecteplase

75
Q

How should you monitor progress post-thrombolysis in STEMI?

A

ECG performed after 90 minutes, if not greater than 50% resolution in ST elevation –> rescue PCI

76
Q

What is the recommended glycaemic control for those with DM in MI?

A

Dose-adjusted insulin infusion with regular BG monitoring to keep levels below 11mmol/l

77
Q

When can sexual activity resume after a non-complicated MI?

A

4 weeks after

78
Q

When can sildenafil be used after an MI?

A

6 months (BUT avoid if on nitrates/nicroandil)

79
Q

What 2nd antiplatelets are more widely used in 2ndary prevention of MI?

A

Ticagrelor and prasugrel

80
Q

How are ticagrelor and prasugrel used as secondary prevention for different situations?

A

Post-ACS medically managed - add ticagrelor to aspirin, stop after 12m
Post-PCI - prasugrel/ticagrelor + aspirin, stop 2nd antiplatelet after 12 months

81
Q

Which patients should get an aldosterone antagonist after an MI?

A

Those with symptoms of heart failure/LV systolic dysfunction

Start within 3-14 days after MI, preferably after ACE inhibitor therapy

82
Q

What aldosterone antagonist is licensed for post-MI treatment?

A

Eplerenone

83
Q

What is the NICE recommendations for patients presenting with chest pain re. referral to hospital?

A

Current chest pain/pain in last 12h + abnormal ECG –> emergency admission

Chest pain 12-72h ago –> same day referral

Chest pain >72h ago –> perform full ECG and troponin measurement first

84
Q

How do NICE define angina?

A
  1. constricting discomfort of front of the chest, or in the neck, shoulders, jaw or arms
  2. precipitated by physical exertion
  3. relieved by rest/GTN in about 5 minutes

3 features = typical angina
2 = atypical angina
1/0 = non-anginal chest pain

85
Q

If stable angina cannot be excluded by clinical assessment alone, what investigations do NICE recommend?

A

1st line: CT coronary angiography
2nd line: non-invasive functional imaging (looking for reversible myocardial ischaemia)
3rd line: invasive coronary angiography

86
Q

Give e.g.s of non-invasive functional imaging

A

Myocardial perfusion scintigraphy with single photon emission computed tomography (MPS with SPeCT) or
Stress echocardiography or
First pass contrast enhanced magnetic resonance perfusion or
MR imaging for stress induced wall motion abnormalities

87
Q

If a patient has an indication for anticoagulation (e.g. AF) post-MI how should they be managed?

A

Anticoagulant monotherapy (NO antiplatelets)

88
Q

What are poor prognostic factors for ACS?

A 
Age
Development/hx heart failure
PVD
Reduced systolic BP
Kilip class
Initial serum Cr conc
Elevated initial cardiac markers
Cardiac arrest on admission 
ST deviation
89
Q

What is kilip class?

A

System used to stratify risk post-MI

CARD - 1 (28 decks)

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