Cyclic strain in human carotid bifurcation and its potential correlation to atherogenesis: Idealized and anatomically-realistic models

Various mechanical phenomena are thought to contribute to the pathogenesis of atherosclerosis. Most finite-element analyses of arterial-wall mechanics to date have focused on the quantification of mechanical wall stresses, despite an abundance of experimental evidence suggesting that endothelial and smooth muscle cells readily respond to cyclic strain. In this study, we calculate the physiologic cyclic strains in the carotid bifurcation, a common site of disease. Several geometries are constructed in this study, namely (i) a 3-D, but idealized geometry of the human carotid bifurcation, (ii) 3-D subject-specific geometries based on in vivo images of healthy volunteers' carotid bifurcations, and (iii) 2-D models based on histology-derived patient-specific anatomy and intra-plaque components. Results in both types of 3-D model show that the highest variations in cyclic strain are found at the adjoining wall of the external-common carotid and at the carotid apex, both frequent sites of early inflammation, as well as immediately distal to the carotid bulb, a site of late-stage disease, suggesting that cyclic strain may play a role in inflammation in that region as well. The 2-D models of diseased arteries show generally muted cyclic strain, but also regions such as in the shoulder regions of a fibrous cap adjacent to a lipid pool where cyclic strains are considerably elevated.