  As pump thrombosis is reduced in current-generation ventricular assist
devices (VAD), adverse events such as bleeding or stroke remain at unacceptable
rates. Thrombosis around the VAD inlet cannula (IC) has been highlighted as a
possible source of stroke events. Recent computational fluid dynamics (CFD)
studies have attempted to characterize the thrombosis risk of different
IC-ventricle configurations. However, purely CFD simulations relate thrombosis
risk to ad-hoc criteria based on flow characteristics, with little
consideration of biochemical factors. This study investigates the genesis of IC
thrombosis including two elements of the Virchow's triad: Endothelial injury
and Hypercoagulability. To this end a multi-scale thrombosis simulation that
includes platelet activity and coagulation reactions was performed. Our results
show significant thrombin formation in stagnation regions (|u|< 0.002 m/s)
close to the IC wall. In addition, high shear-mediated platelet activation was
observed over the leading-edge tip of the cannula which mirrors the thrombus
deposition pattern observed clinically. The current study reveals the
importance of biochemical factors to the genesis of thrombosis at the
ventricular-cannula junction which can inform clinical decisions in terms of
anticoagulation/antiplatelet therapy and guide engineers to develop more robust
designs.
