Atherosclerotic plaques may rupture without warning and cause subsequential acute syndromes such as myocardial infarction and cerebral stroke. Plaque disruption tends to occur at points where the plaque surface is weakest i.e. at points where biomechanical stresses caused by the pulsatile blood flow are concentrated. Therefore, both plaque vulnerability (intrinsic disease) and rupture triggers (extrinsic forces) are important for plaque disruption [1]. The former predisposes the plaque to rupture while the latter may precipitate it.

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