Elucidating atherosclertic vulnerable plaque rupture by modeling cross substitution of ApoE-/- mouse and human plaque component stiffnesses - Biomechanics and Modeling in Mechanobiology. (in press), 2011 - The structure of mouse atherosclerotic lesions may differ from that of humans, and mouse atherosclerotic plaque do not rupture except in some specific locations such as the brachiocephalic artery. Recently, our group was the first to observe that the amplitudes of in vivo stresses in ApoE-/- mouse aortic atherosclerotic lesions were much lower and differed from those found in a previous work performed on human lesions. In this previous preliminary work, we hypothesized that the plaque mechanical properties (MP) may in turn be responsible for such species differences. However, the limited number of human samples used in our previous comparative study was relevant but not sufficient to broadly validate such hypothesis. Therefore, in this study, we propose an original finite element strategy that reconstructs the in vivo stress/strain (IVS/S) distributions in ApoE-/- artherosclerotic vessel based on cross substitution of ApoE-/- mouse and human plaque components stiffnesses and including residual stress/strain (RS/S). Our results: 1) showed that including RS/S decreases by a factor 2 the amplitude of maximal IVS/S, and more importantly 2) demonstrated that the MP of the ApoE-/- plaque constituents are mainly responsible for the low level - compared to human - of intraplaque stress in ApoE-/- mouse aortic atherosclerotic lesions (8.362.63 kPa versus 182.2555.88 kPa for human). Our study highlights that such differences in the distribution and amplitude of vessel wall stress might be one key feature for explaining for the difference in lesion stability between human coronary and mouse aortic lesions.
Fig. 1: Influence of the mechanical properties (MP) of the atherosclerotic vessel on the in vivo stress distributions. Finite-Element (FE) simulations were performed for 3 atherosclerotic mouse lesions. Column a: Zero-stress configurations of pathological samples # 3, 4 and 2 for mice of 20, 25 and 30 weeks, respectively (yellow: LiRi regions, orange: CeFb regions, red: HyFb regions, white: arterial wall). Column b) In vivo stress distributions computed by considering the mouse MP. Column c) In vivo stress distributions computed by considering the human MP. A pressure of 14.5 kPa was used for these FE simulations. Red arrows indicate regions with higher stresses.
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