Abstract 2091: A Theory And Computational Framework For Fracture Of Blood Clots

• Published in: Arteriosclerosis, thrombosis, and vascular biology Vol. 44; no. Suppl_1; p. A2091
• Main Authors: Liu, Dongxu, Nguyen, Nhung, Pocivavsek, Luka
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD Lippincott Williams & Wilkins 01.05.2024
• Subjects: Blood coagulation; Thrombosis
• ISSN: 1079-5642; 1524-4636
• DOI: 10.1161/atvb.44.suppl_1.2091

Introduction and Research Questions: The fracture resistance of blood clots is crucial for physiological hemostasis and pathological thrombosis. However, the mechanism of blood clot fracture is still not well understood. Quantifying the fracturemechanisms is essential for diagnosing and treating bleeding disorders and thrombotic diseases. Goals and Methods: This work aims to formulate a thermodynamically consistent, multi-physics theoretical framework fordescribing the time-dependent deformation and fracture of blood clots. This theory concurrentlyincorporates fluid transport through porous fibrin networks, non-linear visco-hyperelastic deformationof the solid skeleton, solid/fluid interactions, mechanical degradation of tissues, gradient enhancementof energy, and protein unfolding of fibrin molecules. The constitutive relations of tissue constituents andthe governing equation of fluid transport are derived within the framework of porous media theory byextending non-linear continuum thermodynamics at large strains. A physics-based, compressiblenetwork model is developed to describe the mechanical response of the fibrin network of blood clots.The kinetic equations of the internal variables are formulated according to the principles ofthermodynamics by incorporating the corresponding energy terms into the total free energy densityfunction. An energy-based damage model is developed to predict the damage and fracture of bloodclots. Results: The proposed model is experimentally validated, which shows that this model can accurately capturethe experimentally measured deformation and fracture. The fracture of blood clots subjected tomultiple loading conditions is simulated, and the results demonstrate that the tissue subject to a higherloading rate is stiffer. The damage at the crack tip initiates earlier and propagates faster when theloading time approaches the characteristic time of viscoelasticity and fluid transport. Conclusions: This work proposes a physics-based theory and computational framework to describe the fracturebehavior of blood clots. The proposed model is validated by comparing the computational results withexperimental data. The mechanisms of blood clots fracture are analyzed systematically.