Palladium-Based Metallic Glass with High Thrombogenic Resistance for Blood-Contacting Medical Devices

Advancements in the design of mechanical blood circulatory devices have greatly improved patient survival rates, but currently employed metals still provoke a thrombosis response upon contact with blood, with potential life-threatening consequences. While coating strategies have been developed to address this limitation, they possess inherent drawbacks such as susceptibility to crack formation and delamination. Herein, an amorphous metal based on palladium (Pd) is scrutinized and reveals substantial thrombogenic resistance compared to a state-of-the-art titanium alloy. In vitro assessment with human whole blood shows that the Pd glass provokes reduced platelet activation (lower expression of CD62P, CD41/CD61) and greatly retarded fibrin formation, but pronounced platelet spreading therewith challenging the dogma that platelet spreading equals activation. Mechanistic analysis of the early biomaterial-blood interactions reveals that conformational changes of adhered fibrinogen, and modified alpha(IIb)beta(3) integrin expression and distribution across adhered platelets, underlay the superior performance of Pd glass. The study is accompanied by structural and thermophysical bulk investigations and physicochemical surface characterization to link the materials properties with the observed blood response. The results reveal a remarkable potential of Pd-based glass as direct blood-contacting bulk material without the need for coating.