Abstract
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| < 0.005 m/s) close to the IC wall. In addition, high shear-mediated platelet activation was observed over the leading-edge tip of the cannula. The current study reveals the importance of biochemical factors to the genesis of thrombosis at the ventricular-cannula junction in a perioperative state. This study is a first step toward the long-term objective of including clinically relevant pharmacological kinetics such as heparin or aspirin in simulations of inflow cannula thrombosis.