Agglomeration and capture define a lag distance in SIPA with different dependences on sVWF and iVWF. (A) The computed rolling velocity of a single platelet on a VWF-A1–coated surface under 2 shear rates. (B) The averaged rolling velocity (n = 10) compares favorably with existing in vitro measurements. (C) The capture of platelet agglomerates occurs after a lag distance of around 150 $μ$m in our thrombosis-on-a-chip device. The plot shows the API (n = 40) vs the distance from the entrance of the stenotic section, where the peak API denotes the location that most of the aggregates appear. The snapshots show representative occluded channels; the bright color denotes the captured platelet agglomerates. Flow is from left to right. (D) The lag distance of platelet agglomerates calculated from our in silico model compared against those observed in our and Ruggeri’s in vitro settings. The initial WSR of our in vitro setting is 6500 s⁻¹, which would increase as the channel occludes.³  The WSR of the experiment setting by Ruggeri et al.¹³  is ∼20 000 s⁻¹. Three WSRs, 6500, 10 000, and 20 000 s⁻¹, were simulated, where the VWF/platelet conditions are the same as the experiment. Each in silico data (mean and SD) is based 6 runs with different VWF lengths (changing from 1.6 to 6.4 $μ$m). The lag distance (mean and SD) from Ruggeri et al is estimated from the dispersed number of platelet aggregates shown in Figure 2A taken after 7 s of whole blood perfusion. API of 175 and above is used to quantify the thrombus location. (E) The agglomeration level plotted against time. Agglomeration depends on sVWF but is insensitive to the presence of iVWF. (F) The superficial velocity (normalized by volume-averaged fluid velocity of ∼1.2 cm/s) plotted against time. The capture of the agglomerate requires the presence of iVWF, although excessive iVWF level does not shorten the lag distance. For panels E and F, a 6× normal sVWF concentration was used to obtain a faster capture event.