Abstract

The climatic event in atherosclerotic progression is the rupture of the plaque’s fibrous cap, releasing thrombogenic lipid material into the lumen which may result in an occlusion. This mechanism is responsible for about 60% of heart attacks and strokes. Vulnerability to rupture for a particular fibrous cap is a key clinical question, but relatively little is known about the mechanisms of these events. Presumably, the tissue is overloaded, either by increase of the effective stress or decrease of the effective material strength. Previous work in our group has looked at the role of geometric and material property-mismatch in increasing stresses. One limitation of such an approach is that the failure stresses of the fibrous cap in vitro are several times higher than the maximum in vivo stresses predicted by computational models. This suggests a more complicated failure mechanism of the material. The focus for the present work is in understanding the micromechanics basis for the strength of the fibrous cap. It is hypothesised that the strength of the fibrous cap comes from the nature of the fibrous collagen network making up the tissue. Therefore, parameters of the network can be considered and modelled to predict material properties of the tissue as a whole. Preliminary tensile experiments on carotid tissue have been completed, along with SEM images to analyse the fibrous structure of the tissue. It is hoped that understanding the micromechanics of the failure of atherosclerotic plaques will lead to better prediction of plaque vulnerability to rupture and suggest avenues for novel treatments.