Key result
Atherosclerotic plaque stiffness increases with mineral content, revealing computational models underestimate calcified tissue stiffness.
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Clinical events such as heart attack and stroke can be caused by the rupture of atherosclerotic plaques in artery walls. Computational modeling is often used to better understand atherosclerotic disease progression to identify "vulnerable" plaques (i.e., those likely to rupture) and to tailor treatments according to tissue composition. However, because of the heterogeneity of plaque tissue, there are limited data available on the material properties of individual plaque constituents. The goal of this study was to use nanoindentation to measure the mechanical properties of blood clots, fibrous tissue, partially calcified fibrous tissue, and bulk calcifications from human atherosclerotic plaque tissue. Fourier transform infrared (FTIR) spectroscopy was used to quantify the amount of mineral and lipid in each tissue region tested. The results demonstrate that the stiffness of plaque tissue increases with increasing mineral content. In addition, by providing the first experimental data on atherosclerotic calcifications, these data show that some of the estimated modulus values commonly used in computational models greatly underestimate the stiffness of the fully calcified tissue.
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Ebenstein et al. (2008) studied Atherosclerotic plaques. Nanoindentation and Fourier transform infrared (FTIR) spectroscopy vs. Estimated modulus values commonly used in computational models was evaluated on Mechanical properties (stiffness/modulus) and mineral/lipid content of atherosclerotic plaque constituents. Nanoindentation and FTIR spectroscopy demonstrated that human atherosclerotic plaque stiffness increases with mineral content, showing computational models underestimate fully calcified tissue stiffness.
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