Biomechanics and Motion Analysis

Stress Transfer to Coronary Vasa Vasorum After Stenting: A Finite Element Model

Project Coordinator: Mark Zobitz — zobitz.mark@mayo.edu

Figure 63: Coronary vessel with stent expanded

In-stent restenosis is a major health issue in the United States. Although it is characterized by excessive cell proliferation, the underlying mechanisms are not well understood. When vasa vasorum in the outer wall of coronary arteries become damaged, neointimal proliferation and subsequent artery stenosis result. We hypothesized that stents damage vasa during balloon inflation and through sustained compression by the individual stent struts. The aim of this study was to develop a finite element analysis (FEA) model of stented coronary arteries to determine stresses induced in the vessel wall in order to predict vasa compression by the stent, which could initiate the restenotic process.

Figure 64: Principal stress following stent expansion

A 3D FEA model of the coronary artery wall (Figure 63) was developed using ABAQUS finite element software. Vasa vasorum were modeled in the wall at a location 70% of the wall thickness. The vessel wall was modeled as isotropic, linear elastic, and incompressible. An internal pressure of 95mmHg was applied to simulate the mean blood pressure. Two sizes of vasa were modeled; 50 and 150 mm diameter. Two degrees of stent diameter expansion were considered (16% and 34%). The expanded 3D stent geometry was simulated from 3D microscopic-CT images. Stent expansion was simulated by applying radial displacements to the nodes of the vessel wall surface where stent contact would occur.

Figure 64 shows the stress contours through a plane in the midsection of the model. On the luminal stented side, stresses were greater than 1,500mmHg with a maximum of 4,000 and 10,000mmHg for 16% and 34% expansions, respectively. The stress decreased in a non-linear manner with increased distance from the lumen. In the region where vasa are located, stresses exceeded 500 and 1,000mmHg for the two expansions. In comparison, prior to stenting, stresses in the wall induced by the blood pressure were lower (<30mmHg).

This study demonstrates a dramatic increase in stresses within the vessel wall in response to stent implantation including the region where vasa vasorum are located. Therefore, it would be expected that these stresses are sufficient to compress the vasa and impair vessel wall perfusion. The subsequent hypoxia can lead to increased release of growth factors and to cell proliferation and restenosis. This model can be used to predict stresses induced by various stent types and to optimize stent design to minimize impact on vasa vasorum.