Acute Coronary Syndrome Flashcards

1
Q

Spectrum of ACS

A
  • Unstable angina
  • Non-ST elevation myocardial infarction (NSTEMI)
  • ST-elevation myocardial infarction (STEMI)
  • Sudden cardiac death
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2
Q

What causes ACS?

A

Common pathogenesis

  • atherosclerotic plaque rupture or erosion
  • superimposed platelet aggregation and thrombosis
  • vasospasm, and vasoconstriction
  • subtotal or transient total occlusion of vessel
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3
Q

What is the goal of pharmacotherapy?

A

Increase myocardial oxygen supply
- through coronary vasodilation

Decrease myocardial oxygen demand

  • Decrease in heart rate
  • Decrease in blood pressure
  • Decrease preload or myocardial contractility
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4
Q

Features of ACS with STEMI

A
  • Patients with STEMI have a high likelihood of a coronary thrombus occluding the infarct artery.
  • Angiographic evidence of coronary thrombus formation is seen in more than 90% of patients with STEMI
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5
Q

How does STEMI usually occur in ACS

A
  • STEMI usually occurs as a result of coronary artery occlusion due to formation of thrombus overlying an atheromatous plaque.
  • If no PCI within 2 hours then thrombolysis is indicated.
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6
Q

What are thrombolytic agents and how do they work?

A
  • Thrombolytic agents available today are serine proteases.

- They work by converting plasminogen to the natural fibrinolytic agent plasmin.

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7
Q

How does plasmin break down clots?

A

Plasmin lyses clot by breaking down the fibrinogen and fibrin contained in a clot

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8
Q

What are the types of thrombolytic agents?

A
Fibrinolytics are divided into two categories:
Fibrin-specific agents:
- Alteplase 
- Reteplase 
- Tenecteplase

Non-fibrin specific agents:
- Streptokinase

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9
Q

What is the action of fibrin-specific agents?

A

They catalyse the conversion of plasminogen to plasmin in the absence of fibrin

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10
Q

What is the action of non-fibrin specific agents?

A

They catalyse systemic fibrinolysis

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11
Q

Contraindications to thrombolysis

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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12
Q

Benefits of thrombolysis

A

Timely thrombolysis is associated with:

  • A 23% reduction in mortality
  • A 39% reduction when used with aspirin
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13
Q

If there is no evidence of a STEMI, what treatment is given?

A

ACS medical treatment protocol

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14
Q

What treatment is involved in ACS medical treatment protocol?

A
  • Aspirin
  • Tigagrelor/Clopidogrel
  • Fondaparinux/LMW heparin
  • Intravenous nitrate
  • Analgesia
  • Beta blockers
  • Statins
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15
Q

What is used in the management to reduce risk from NSTEMI?

A
  • PCI or CABG
  • Aspirin
  • Clopidogrel, prasugrel, ticagrelor, ticlopidine or cilostazol
  • Heparin (LMWH)
  • Fondaparinux
  • GIIb/IIIa receptor blockers
  • Statins
  • Beta blockers
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16
Q

Antiplatelet Agents: aspirin

A
  • Low dose aspirin (75-150mg)

- Aspirin is a potent inhibitor of platelet thromboxane A2 production

17
Q

What does thromboxane do?

A

It stimulates platelet aggregation and vasoconstriction

18
Q

What does the regular use of aspirin in acute MI do?

A
  • Reduce mortality by 23%

- In combination with thrombolysis reduce mortality by 42% and reinfarction by 52%

19
Q

What does the regular use of aspirin in unstable angina do?

A
  • Reduce MI and death by 50%
20
Q

What does the regular use of aspirin in secondary prevention do?

A
  • Reduce reinfarction by 32% and combined vascular events by 25%.
21
Q

What is Clopidogrel and what does it do?

A
  • Clopidogrel is a prodrug
  • 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