Abstract
Acute coronary syndrome (ACS) is caused when myocardial blood supply is acutely compromised, which results in prolonged chest pain. The common underlying mechanisms of ACS include erosion or sudden rupture of an atherosclerotic plaque within the wall of a coronary artery. The disrupted plaque consequently stimulates both thrombosis and coagulation through different mechanisms, which end with thrombus formation. The thrombus itself further obstructs the blood flow within the affected coronary artery, with its effect on the myocardium e.g. irreversible necrosis if reperfusion is not re-established.1
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