Computational modeling reveals the relationship between intrinsic failure properties and uniaxial biomechanical behavior of arterial tissue
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Biomechanical failure of the artery wall can lead to rupture, a catastrophic event with a high rate of mortality. Thus, there is a pressing need to understand failure behavior of the arterial wall. Uniaxial testing remains the most common experimental technique to assess tissue failure properties. However, the relationship between intrinsic failure parameters of the tissue and measured uniaxial failure properties is not fully established. Furthermore, the effect of the experimental variables, such as specimen shape and boundary conditions, on the measured failure properties is not well understood. We developed a finite element model capable of recapitulating pre-failure and post-failure uniaxial biomechanical response of the arterial tissue specimen. Intrinsic stiffness, strength and fracture toughness of the vessel wall tissue were used as the input material parameters to the model. Two uniaxial testing protocols were considered: a conventional setup with a rectangular specimen held at the grips by cardboard inserts, and the other used a dogbone specimen with soft foam inserts at the grips. Our computational study indicated negligible differences in the peak stress and post-peak mechanical behavior between these two testing protocols. It was also found that the tissue experienced only modest localized failure until higher levels of applied stretch beyond the peak stress. A robust cohesive model was capable of modeling the post-peak biomechanical response, which was primarily governed by tissue fracture toughness. Our results suggest that the post-peak region, in conjunction with the peak stress, must be considered to evaluate the complete biomechanical failure behavior of the soft tissue.
KeywordsUniaxial testing Arterial tissue failure properties Intrinsic strength Fracture toughness Post-peak behavior Cohesive-volumetric finite-element method
Research reported in this work was supported by the National Institutes of Health under Award Number 1R01- NS097457-01 and 5T32HL076124-12. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. Human basilar arteries were provided from the Alzheimer Disease Research Center (ADRC) (Grant No. NIA P50 AG005133). The authors would also like to thank Chelsea Stowell and Dr. Y. Wang for providing the sheep carotid arteries used for this study.
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Conflict of interest
The authors declare they have no conflict of interest.
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