MODELLING OF HEMODYNAMIC STRESS EFFECTS ON RUPTURE MECHANICS AND FIBROUS CAP COLLAGEN ARCHITECTURE OF ATHEROSCLEROTIC PLAQUES

摘要

Cardiovascular plaque rupture in atherosclerosis has been associated extensively with Acute Myocardial Infarctions, a leading cause of death. The mechanics and progression of plaque rupture are not yet fully understood. A protective fibrous cap made of collagen fibers and smooth muscle cells covers the plaque's necrotic core. These fibers provide strength and elasticity to the cap tissue as they realign over time to the prevalent tensile stress orientations as an efficient method to optimize strength without increasing weight and metabolic costs [1]. Fluid structure interaction simulations of normal hemodynamic conditions in a stenosed artery were performed to evaluate stress distribution and orientation within the plaque's main constituents, and to predict the cap's collagen fiber architecture and subsequently its vulnerability. The results show that the principal stress orientations gradually shift from circumferential at the non-stenosed sections of the artery to longitudinal at the peak of the stenosis. This gradual shift can be seen in the collagen architecture of actual histopathological studies of diseased vessels. The higher magnitude stress zones also indicate where plaque disruption may initiate and how fissure propagation can occur. Based on these results we could hypothesize that the rupture mechanics can be treated as a biocomposite matrix failure as fissuring seems to run parallel to the collagen fibers.