More than half of the 500,000 coronary artery disease deaths every year are due to the sudden rupture of vulnerable plaque. Several pathological studies of ruptured plaques have provided morphological descriptions of the high-risk, or vulnerable, coronary plaque that is prone to rupture or erosion as a positively remodeled lesion rich in vasa-vasorum, containing a lipid-rich core with an overlying thin fibrous cap infiltrated by macrophages. Virmani et al. [1] described thin-cap fibroatheroma with a large necrotic core and a fibrous cap < 65 μm as a more specific precursor of plaque rupture due to tissue stress. Despite the above observations, the mechanism of vulnerable plaque rupture has remained a mystery since ruptures often occur in regions where computational finite element (FEM) and fluid structure interaction (FSI) models do not predict maximal stress. Forty percent of ruptures occur in the central part of the cap rather than regions of high curvature at the shoulders of the lipid core where FEM models predict maximum tissue stresses [2]. Similarly, the latest study by Tang et al. [3] predicts that maximal stress often appears at healthy parts of the vessel where the vessel wall is thinner than the wall on the diseased plaque side or where vessel wall curvature is large.

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