Atherosclerotic disease remains a leading cause of mortality and morbidity worldwide despite significant advances in its management (1). Atherosclerosis, characterized by plaque consisting a lipid-rich necrotic core encapsulated in a fibrous cap, may result in plaque rupture and subsequently cause acute ischaemic events such as myocardial infarction and stroke. Under physiological conditions, plaque is subjected to mechanical loading due to blood pressure and flow and rupture possibly occurs if these extra loadings exceed the material strength of the fibrous cap (2–4). This hypothesis has been indirectly validated by the combination of histological examination and finite element simulations that the rupture site often bears a high stress concentration either in carotid (3, 5, 6) or coronary (2) plaques. It has been noted that most rupture sites are located at the shoulder region (2), where the curvature is locally large (4) leading to a high stress level (7). However, the rupture site does not always coincide with the site where high stress concentrations appear and about thirty to forty percent of ruptures occur in the middle region where the calculated stress is relatively low (2, 8). This demonstrates the limitations of current approaches.

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