Mapping Computational Thrombosis Modelling to Shear Regimes: An Application to Post-Stenotic Platelet Aggregation

Thrombosis is governed by the interplay between local haemodynamics, blood haemostatic potential, and vessel-wall thrombogenicity. These factors regulate the transport of cellular and soluble blood constituents, coagulation kinetics, and platelet adhesive and activation dynamics, such that different mechanisms dominate across venous, arterial, and pathological shear conditions. We introduce a shear-dependent mechanistic map that relates these haemodynamic settings to the minimum set of transport, biochemical, and mechanochemical processes required in a continuum model. In low-shear venous flow, this includes coagulation-factor transport, thrombin generation, and fibrin polymerisation; at low arterial shear, platelet activation, agonist amplification, and integrin-dependent aggregation become necessary; at high arterial shear, platelet recruitment requires von Willebrand factor (VWF)-mediated glycoprotein Ibα (GPIbα) capture, tethering, translocation, and stabilisation. At pathological shear, bulk-phase VWF self-association and activation-independent platelet agglomeration require an additional closure. Applied to the high-shear arterial regime, we develop a three-population finite-element flow–transport–growth model that resolves free-flowing, rolling, and stabilised platelets, and evaluate it in a high-expansion-ratio double-stenosis microfluidic benchmark. At a fixed inlet wall shear rate of 5000s−1, aggregate growth is governed primarily by post-stenotic flow topology rather than by peak shear at the stenosis apex. Increasing the expansion angle β from 30∘ to 150∘ increases both the peak rolling-platelet concentration and the axial extent of the near-wall rolling-platelet corridor by approximately 2.5-fold. Model predictions agree closely with in vitro measurements, particularly at high expansion angles, and show that explicit representation of rolling platelets is required to reproduce the observed aggregate morphologies. The present mechanistic map provides a basis for selecting the continuum model components required to represent thrombosis in both the vasculature and blood-contacting devices.