Despite decades of research, atherosclerosis remains one of the leading killers in the modern world. Consequently, the atherosclerosis-prone mouse is frequently employed to study the pathophysiology of atherogenesis. To date, no investigator has conclusively observed natural plaque rupture in these commonly-studied strains. A likely explanation for the lack of observation of plaque rupture is that mouse plaques are morphologically different than human plaques and that the consequence of this difference is a solid mechanical environment in the mouse that is unlike that of humans. To investigate this possibility, we used finite element modeling based on histology specimens of mouse and human plaques to examine the spatial distribution of stresses within the walls of plaques in each organism.

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