Available at: http://digitalcommons.calpoly.edu/theses/385
Date of Award
MS in Engineering
Biomedical and General Engineering
Atherosclerosis causes hundreds of thousands of deaths in the US alone every year. Fibrous cap rupture is one of the leading causes of these fatalities. Thin cap atheromas are commonly regarded as vulnerable plaque, however the effect of calcium upon a thin fibrous cap with lipid pool is poorly understood. Some studies have shown that calcium adds to stability of the lesion, while others have proven otherwise. An article by Li et al. 2007 suggests location is the key factor. By varying the percentage of calcium and lipid within a defined region, the stress on the cap was estimated using an idealized finite element arterial model. Also the thickness of the fibrous cap was varied to determine whether the stress was solely a function of lipid percentage or a combination. Plaque, arterial wall, lipid, and calcium were modeled using linear elastic, isotropic, and incompressible material properties. The first test varied the thin cap thickness from 65 to 500 microns and tested the calcified lipid model at varying lipid/calcium percentages. The lipid/Calcium pool increased/decreased 10% each test. As the cap thickness becomes thinner than 100 microns, the stress level increases rapidly. The second test compared a model with lipid pool and calcium behind the lipid with a thin cap of 65 microns to a model with lipid pool of the same size and thin cap of 65 microns but only fibrous tissue surrounding (no calcium). The lipid pool increased from 10 to 90% lipid. The result of this test found that at higher lipid percentages, the calcium increased the stress on the cap. By understanding the material properties of plaque and the structure of the lesion, future developments may be able to evaluate rupture risk. This idealized study illustrates the ability of computation models to provide insight into clinical situations.