A continuum model for the elongation and orientation of Von Willebrand factor with applications in arterial flow

<p>The blood protein Von Willebrand factor (VWF) is critical in facilitating arterial thrombosis. At pathologically high shear rates, the protein unfolds and binds to the arterial wall, enabling the rapid deposition of platelets from the blood. We present a novel continuum model for VWF dynamics in fow based on a modifed viscoelastic fuid model that incorporates a single constitutive relation to describe the propensity of VWF to unfold as a function of the scalar shear rate. Using experimental data of VWF unfolding in pure shear fow, we fx the parameters for VWF&rsquo;s unfolding propensity and the maximum VWF length, so that the protein is half unfolded at a shear rate of approximately 5000 s&minus;1 . We then use the theoretical model to predict VWF&rsquo;s behaviour in two complex fows where experimental data are challenging to obtain: pure elongational fow and stenotic arterial fow. In pure elongational fow, our model predicts that VWF is 50% unfolded at approximately 2000 s&minus;1 , matching the established hypothesis that VWF unfolds at lower shear rates in elongational fow than in shear fow. We demonstrate the sensitivity of this elongational fow prediction to the value of maximum VWF length used in the model, which varies signifcantly across experimental studies, predicting that VWF can unfold between 2000 and 3200 s&minus;1 depending on the selected value. Finally, we examine VWF dynamics in a range of idealised arterial stenoses, predicting the relative extension of VWF in elongational fow structures in the centre of the artery compared to high shear regions near the arterial walls.</p>