Acute Coronary Syndromes
Update Management on ACS
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ACS

Overview

Plaques

Properties
Role of acute changes
Erosion & Disruption
Types
Fissuring & Rupture

MI

Different forms of MI
Q Wave MI
Non-Q MI & Unstable Angina
Treatment of ACS
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Treatment of Acute Coronary Syndromes

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¡@ ¡@ Unstable Angina and Non-Q MI
¡@ ¡@ Medical therapy
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Aspirin, Clopidogrel

Low molecular Heparin (no need to monitor APTT/PT) 
Glycoprotein IIb/IIIa inhibitors: Reopro, Integrilin
Symptomatic relieve: Lasix, Inderal
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Revascularization therapy

(catheter-based revascularization (such as PTCA) or surgical revascularization with coronary artery bypass surgery (CABG))
Coronary angiogram and PTCA
Indicated with failed medical therapy, hemodynamical instability
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¡@ ¡@ ST elevated MI¡@
Medical Therapy

Aspirin

Thrombolytic


Reperfusion Therapy

(In this procedure, a catheter affixed with an inflatable balloon is inserted into the patient's artery and guided to the site of the blockage where the balloon is inflated to effectively force open the clot and restore blood flow to the heart walls before permanent damage occurs.)
Failed thrombolytic
Primary PTCA
Upon positive stress test during rehabilitation

Take Home

- Acute coronary syndromes compose of a spectrum of clinical entities that range from unstable angina, non-Q MI to Q wave MI.

- Plaque fissuring and rupture is the underlying mechanism and its extent determines the resulting coronary event.

Messages
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Plaque after Fibrinolysis. This plaque was related to an infarct and the patient has been treated with fibrinolytic therapy 10 days before death. The plaque has a crater (arrow) in the surface on the floor, of which a layer of residual thrombosis is present. The lumen is paten but narrowed by the upward bulge of the plaque, which is expanded by organizing thrombus within the core.
Plaque after Fibrinolysis. Thrombus has been totally removed from the lumen of this infarct-related artery but a hole is still present in the plaque cap (arrow) and within the core there is residual thrombus. Lysis 5 days before death. It is easy to see why such a lesion has a high risk of recurrent thrombotic occlusion.
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