Multi-scale simulation of thrombus formation at LVAD inlet cannula connection: Importance of Virchow's triad

TL;DR

This study uses multi-scale simulations incorporating biochemical factors to better understand thrombus formation at LVAD inlet cannula, highlighting the roles of endothelial injury and hypercoagulability in thrombosis risk.

Contribution

It introduces a multi-scale thrombosis model that includes platelet activity and coagulation, emphasizing biochemical factors often overlooked in CFD studies.

Findings

Thrombin formation occurs in stagnation regions near the cannula wall.

High shear activates platelets at the cannula tip, matching clinical thrombus patterns.

Biochemical factors significantly influence thrombosis development at the ventricular-cannula interface.

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|< 0.002 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.