Abstract
Mechanical interactions between flowing and coagulated blood (thrombus) are crucial in dictating the deformation and remodeling of a thrombus after its formation in hemostasis. We propose a fully-Eulerian, three-dimensional, phase-field model of thrombus that is calibrated with existing in vitro experimental data. This phase-field model considers spatial variations in permeability and material properties within a single unified mathematical framework derived from an energy perspective, thereby allowing us to study effects of thrombus microstructure and properties on its deformation and possible release of emboli under different hemodynamic conditions. Moreover, we combine this proposed thrombus model with a particle-based model which simulates the initiation of the thrombus. The volume fraction of a thrombus obtained from the particle simulation is mapped to an input variable in the proposed phase-field thrombus model. The present work is thus the first computational study to integrate the initiation of a thrombus through platelet aggregation with its subsequent viscoelastic responses to various shear flows. This framework can be informed by clinical data and potentially be used to predict the risk of diverse thromboembolic events under physiological and pathological conditions.
Highlights
Under physiological conditions, blood clots form at sites of vascular injury to prevent blood loss, but they eventually resolve as the vascular wall heals [1, 2]
Thromboembolism is associated with detachment of small thrombus pieces from the bulk in the blood vessel
These detached pieces, known as emboli, travel through the blood flow and may block other vessels downstream, e.g., they may plug the deep veins of the leg, groin or arm, leading to venous thromboembolism (VTE)
Summary
Blood clots form at sites of vascular injury to prevent blood loss, but they eventually resolve as the vascular wall heals [1, 2]. The situation can be very different in pathological cases, in aortic dissection, which represents a severe injury to the vessel wall that manifests as a delamination that propagates through the media [3], a key clinical question is whether the thrombosis in the false lumen will remain biologically active or be resolved or remodeled as part of the healing process Other pathological conditions, such as deep vein thrombosis [4,5,6], pulmonary embolism [7, 8], and atherothrombosis [9, 10], exhibit excessive and undesirable thrombi within the lumen that can result in partial or complete thrombotic vessel occlusion. Fibrin monomers form a network that strengthens the platelet aggregates and facilitates thrombus maturation within minutes to hours
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