Mechanics and microstructure of blood plasma clots in shear driven rupture

Intravascular blood clots are subject to hydrodynamic shear and other forces that cause clot deformation and rupture (embolization). A portion of the ruptured clot can block blood flow in downstream vessels. The mechanical stability of blood clots is determined primarily by the 3D polymeric fibrin n...

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Published inSoft matter Vol. 2; no. 21; pp. 4184 - 4196
Main Authors Ramanujam, Ranjini K, Garyfallogiannis, Konstantinos, Litvinov, Rustem I, Bassani, John L, Weisel, John W, Purohit, Prashant K, Tutwiler, Valerie
Format Journal Article
LanguageEnglish
Published England Royal Society of Chemistry 29.05.2024
The Royal Society of Chemistry
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ISSN1744-683X
1744-6848
1744-6848
DOI10.1039/d4sm00042k

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Summary:Intravascular blood clots are subject to hydrodynamic shear and other forces that cause clot deformation and rupture (embolization). A portion of the ruptured clot can block blood flow in downstream vessels. The mechanical stability of blood clots is determined primarily by the 3D polymeric fibrin network that forms a gel. Previous studies have primarily focused on the rupture of blood plasma clots under tensile loading (Mode I), our current study investigates the rupture of fibrin induced by shear loading (Mode II), dominating under physiological conditions induced by blood flow. Using experimental and theoretical approaches, we show that fracture toughness, i.e. the critical energy release rate, is relatively independent of the type of loading and is therefore a fundamental property of the gel. Ultrastructural studies and finite element simulations demonstrate that cracks propagate perpendicular to the direction of maximum stretch at the crack tip. These observations indicate that locally, the mechanism of rupture is predominantly tensile. Knowledge gained from this study will aid in the development of methods for prediction/prevention of thrombotic embolization. Intravascular blood clots are subject to hydrodynamic shear and other forces that cause clot deformation and rupture (embolization).
Bibliography:https://doi.org/10.1039/d4sm00042k
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ISSN:1744-683X
1744-6848
1744-6848
DOI:10.1039/d4sm00042k