Large-deformation phase-field modeling of thrombus fracture with fiber reorientation

Abstract

Thrombus fragmentation remains a major challenge in mechanical thrombectomy because it increases the risk of distal embolization. Thrombi are multiscale composites of fibrin networks and blood cells, and their failure depends on finite hyperelastic deformation, anisotropy, composition-dependent properties, and microscopic fiber rearrangement. Because fibrin fibers may reorient under large stretch, the local fiber architecture should be treated as an evolving structural variable rather than a fixed material descriptor. Here, we develop a finite-deformation anisotropic phase-field fracture model that couples composition-dependent constitutive parameters, fiber-induced anisotropy, stretch-driven fiber reorientation, and damage degradation. The preferred fiber direction evolves toward the local maximum principal stretch direction, linking fibrin-network adaptation to anisotropic energy storage and crack-driving forces. After validation against uniaxial fracture experiments, the model is used to study spontaneous crack initiation, branching, and propagation under mixed-mode loading relevant to aspiration thrombectomy. The results show that fiber dispersion and reorientation strongly regulate fragmentation. Increasing the dispersion parameter from 0.12 to 0.25 weakens anisotropy, reduces the critical tensile reaction force by 26.9%, and increases failure displacement by 30%, indicating a transition from tension-shear coupled failure to tensile-dominated rupture. Greater dispersion also suppresses crack branching and promotes localized failure paths. Composition-dependent simulations show that higher fibrin content increases fracture toughness, whereas increased hydration reduces total fracture energy despite increasing initial stiffness. These findings clarify how evolving microstructural anisotropy and biochemical composition govern thrombus fragmentation risk and may guide thrombectomy strategy optimization.