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Flashcards in Acute Coronary Syndrome Deck (21):

Spectrum of ACS

- Unstable angina
- Non-ST elevation myocardial infarction (NSTEMI)
- ST-elevation myocardial infarction (STEMI)
- Sudden cardiac death


What causes ACS?

Common pathogenesis
- atherosclerotic plaque rupture or erosion
- superimposed platelet aggregation and thrombosis
- vasospasm, and vasoconstriction
- subtotal or transient total occlusion of vessel


What is the goal of pharmacotherapy?

Increase myocardial oxygen supply
- through coronary vasodilation

Decrease myocardial oxygen demand
- Decrease in heart rate
- Decrease in blood pressure
- Decrease preload or myocardial contractility


Features of ACS with STEMI

- 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


How does STEMI usually occur in ACS

- 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.


What are thrombolytic agents and how do they work?

- Thrombolytic agents available today are serine proteases.
- They work by converting plasminogen to the natural fibrinolytic agent plasmin.


How does plasmin break down clots?

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


What are the types of thrombolytic agents?

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

Non-fibrin specific agents:
- Streptokinase


What is the action of fibrin-specific agents?

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


What is the action of non-fibrin specific agents?

They catalyse systemic fibrinolysis


Contraindications to thrombolysis

- 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


Benefits of thrombolysis

Timely thrombolysis is associated with:
- A 23% reduction in mortality
- A 39% reduction when used with aspirin


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

ACS medical treatment protocol


What treatment is involved in ACS medical treatment protocol?

- Aspirin
- Tigagrelor/Clopidogrel
- Fondaparinux/LMW heparin
- Intravenous nitrate
- Analgesia
- Beta blockers
- Statins


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

- Aspirin
- Clopidogrel, prasugrel, ticagrelor, ticlopidine or cilostazol
- Heparin (LMWH)
- Fondaparinux
- GIIb/IIIa receptor blockers
- Statins
- Beta blockers


Antiplatelet Agents: aspirin

- Low dose aspirin (75-150mg)
- Aspirin is a potent inhibitor of platelet thromboxane A2 production


What does thromboxane do?

It stimulates platelet aggregation and vasoconstriction


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

- Reduce mortality by 23%
- In combination with thrombolysis reduce mortality by 42% and reinfarction by 52%


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

- Reduce MI and death by 50%


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

- Reduce reinfarction by 32% and combined vascular events by 25%.


What is Clopidogrel and what does it do?

- 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