Primary hemostasis and dynamics of clot formation after microvascular injury
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arXiv
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| Natura: | Preprint |
| Pubblicazione: |
2026
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| _version_ | 1866911723699568640 |
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| author | Topuz, Alper Gompper, Gerhard Fedosov, Dmitry A. |
| author_facet | Topuz, Alper Gompper, Gerhard Fedosov, Dmitry A. |
| contents | Primary hemostasis is initiated by platelet adhesion and aggregation at a site of vascular injury and is strongly regulated by local hydrodynamic conditions. At elevated shear rates, platelet capture is mediated by von Willebrand factor (vWF), a multimeric protein that undergoes shear-induced unfolding and becomes adhesive. We investigate early-stage clot formation under physiological high-shear-flow conditions by employing particle-based mesoscale hydrodynamics simulations with explicitly resolved red blood cells, platelets, and mechano-sensitive vWF in a microchannel geometry. The model incorporates vWF-mediated adhesion of platelets to a hemostatic surface, together with non-periodic inflow-outflow boundary conditions that allow continuous material supply and transport. We analyze the dynamics of platelet-vWF aggregation, clot growth dynamics, clot geometry and internal stresses, and thrombo-embolization across a range of elevated flow rates. Our results demonstrate that clot formation proceeds through the establishment of platelet-vWF aggregates at the hemostatic site, and that the clot reaches a finite size determined solely by hydrodynamic forces, without invoking biochemical stabilization mechanisms. Beyond a critical size, increased drag from fluid flow leads to recurrent embolization events that limit further growth. These findings highlight the central role of hydrodynamic stresses in regulating primary hemostasis and provide a mechanistic framework for understanding clot stability under physiological flow conditions. |
| format | Preprint |
| id |
arxiv_https___arxiv_org_abs_2605_28096 |
| institution | arXiv |
| publishDate | 2026 |
| record_format | arxiv |
| spellingShingle | Primary hemostasis and dynamics of clot formation after microvascular injury Topuz, Alper Gompper, Gerhard Fedosov, Dmitry A. Biological Physics Soft Condensed Matter Primary hemostasis is initiated by platelet adhesion and aggregation at a site of vascular injury and is strongly regulated by local hydrodynamic conditions. At elevated shear rates, platelet capture is mediated by von Willebrand factor (vWF), a multimeric protein that undergoes shear-induced unfolding and becomes adhesive. We investigate early-stage clot formation under physiological high-shear-flow conditions by employing particle-based mesoscale hydrodynamics simulations with explicitly resolved red blood cells, platelets, and mechano-sensitive vWF in a microchannel geometry. The model incorporates vWF-mediated adhesion of platelets to a hemostatic surface, together with non-periodic inflow-outflow boundary conditions that allow continuous material supply and transport. We analyze the dynamics of platelet-vWF aggregation, clot growth dynamics, clot geometry and internal stresses, and thrombo-embolization across a range of elevated flow rates. Our results demonstrate that clot formation proceeds through the establishment of platelet-vWF aggregates at the hemostatic site, and that the clot reaches a finite size determined solely by hydrodynamic forces, without invoking biochemical stabilization mechanisms. Beyond a critical size, increased drag from fluid flow leads to recurrent embolization events that limit further growth. These findings highlight the central role of hydrodynamic stresses in regulating primary hemostasis and provide a mechanistic framework for understanding clot stability under physiological flow conditions. |
| title | Primary hemostasis and dynamics of clot formation after microvascular injury |
| topic | Biological Physics Soft Condensed Matter |
| url | https://arxiv.org/abs/2605.28096 |