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| Atherosclerosis is an inflammatory disease of major arteries due to fatty lesions forming in arterial walls, causing stenosis (constricting blood flow) or thrombosis (blood clots, blockage). Certain lesions, called vulnerable plaques, are responsible for most deaths from atherosclerosis. The growth and degradation of these plaques is dynamic, involving complex biochemical, hemodynamic, and mechanical interactions. Present experimental means for studying arterial plaque development is limited, calling for augmenting such studies by mathematical modeling, analysis, and simulation. I will outline a strategy for model development, starting with an ODE model of principle chemical processes, and progressing to more complicated, more mechanistic PDE models. This is an early stage investigation, so the talk is a possible roadmap for approaching a variety of questions. |
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