Abstract

Atherosclerotic plaque rupture remains the leading cause of acute coronary syndrome (ACS), myocardial infarction and stroke (Lloyd-Jones et al. 2010). Atherosclerotic lesions develop inside the arterial wall. Vulnerable plaque (VP), which is characterised by a relatively large extracellular necrotic core and a thin fibrous cap infiltrated by macrophages, is prone to rupture (Virmani et al. 2000). The rupture of the thin-cap fibroatheroma may lead to the formation of a thrombus, causing the acute syndrome and possibly death (Virmani et al. 2006). The disease remains asymptomatic for a long time, but early detection of vulnerable atherosclerotic lesions is a crucial step in preventing risk of rupture and managing ACS and strokes.

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