Histological investigation along with finite element analysis of arterial wall/atherosclerotic plaque geometries indicates the paradoxical result that ruptures often occur at sites with predicted stresses of half the plaque cap strength. Recent experiments have revealed calcified cells within the cap suggesting that these inclusions, situated close to the cap/luminal blood surface, precipitate rupture at low nominal loads by concentrating stress. In this paper, we investigate the proposition that rupture at low nominal loads occurs by (possibly brittle) decohesion of the calcification/cap interface followed by tearing of cap tissue. A novel boundary value problem is analyzed consisting of a remotely loaded linear elastic layer (extracellular matrix cap) containing a rigid spherical inclusion (calcified cell) that interacts with it through a nonlinear structural interface which models the binding of the calcified cell to the extracellular matrix via integrin receptor proteins. Equilibrium solutions are obtained from equations derived from the Boussinesq potentials for spherical domains. Results indicate a brittle character to the rupture process with the size of the domains between the inclusion center and the matrix surfaces determining the concentration of stress. For an inclusion close to a surface the abrupt unloading of the interface during brittle decohesion produces a sharp spike in circumferential stress. We conjecture that when this dynamic stress exceeds the cap strength, tearing occurs followed by thrombus formation and possibly infarction.
- Inclusion problem
- Interfacial debonding and decohesion
- Plaque rupture
ASJC Scopus subject areas
- Orthopedics and Sports Medicine
- Biomedical Engineering