Key result
Mathematical model of blood flow and inflammation reproduces atherosclerotic plaque emergence in low wall shear stress.
This computational modeling study provides a mathematical framework for understanding the early inflammatory processes and blood flow dynamics involved in atherosclerotic lesion formation.
Offers a platform for testing atherogenesis hypotheses; leaves open prospective validation before clinical translation.
This article is devoted to the construction of a mathematical model describing the early formation of atherosclerotic lesions. The early stage of atherosclerosis is an inflammatory process that starts with the penetration of low density lipoproteins in the intima and with their oxidation. This phenomenon is closely linked to the local blood flow dynamics. Extending a previous work [5] that was mainly restricted to a one-dimensional setting, we couple a simple lesion growth model relying on the biomolecular process that takes place in the intima with blood flow dynamics and mass transfer. We perform numerical simulations on a two-dimensional geometry taken from [6,7] that mimicks a carotid artery deformed by a perivascular cast and we compare the numerical results with experimental data.
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Calvez et al. (2010) studied Atherosclerosis. Mathematical modeling was evaluated. A mathematical model coupling blood flow dynamics, mass transfer, and inflammatory processes successfully reproduced the emergence of atherosclerotic plaques in areas of low wall shear stress.
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