Numerical modeling of stress in stenotic arteries with microcalcifications: a micromechanical approximation.
Most finite element models of atherosclerotic arteries do not account for the heterogeneity of the plaque constituents at the microscale. Failure of plaque lesions has been shown to be a local event, linked to stress concentrations caused by cap thinning, inflammation, macroscopic heterogeneity, and recently, the presence of microcalcifications. There is growing evidence that microcalcifications exist in the fibrous cap of plaque lesions. However, their role is not yet fully understood. The goal of the present work is to investigate the effects of localized regions of microcalcifications on the stress field of atherosclerotic plaque caps in a section of carotid artery. This is achieved by performing finite element simulations of three-dimensional fluid-structure interaction models. The material response in the region of microcalcification is modeled using a combination of finite elements, homogenization theory, and a stress concentration function that approximates the average local stresses in the fibrous tissue and microcalcification phases. The results indicate that the circumferential stress in the fibrous tissue phase increases as the volume fraction of microcalcifications is increased, and that the stress exceeds a critical threshold when the fibrous cap thickness is decreased. Furthermore, the presence of the microcalcifications significantly influences the distribution of stress by shifting the maximum circumferential stress away from the cap shoulders, where failure is most common when the effective region of microcalcification is located at the center of the cap. This is a possible explanation of why 40% of plaque ruptures occur away from the shoulder region of the cap.
Wenk
Jonathan F
JF
Department of Mechanical Engineering, University of California-Berkeley, CA 94720-1740, USA. jwenk1@me.berkeley.edu
Papadopoulos
Panayiotis
P
Zohdi
Tarek I
TI
D001158:Arteries / Q000473:pathology / Q000503:physiopathology*; D050197:Atherosclerosis / Q000473:pathology / Q000503:physiopathology; D002114:Calcinosis / Q000473:pathology* / Q000503:physiopathology; D002339:Carotid Arteries / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D008954:Models, Biological; D013314:Stress, Mechanical; D014652:Vascular Diseases / Q000473:pathology* / Q000503:physiopathology*