Material-Driven Clinical Complications in Mechanical Circulatory Support: From Blood–Material Interactions to Device-Related Adverse Events

Mechanical circulatory support (MCS) has transformed the management of advanced heart failure; however, device-related morbidity remains substantially driven by adverse interactions occurring at the blood–material and tissue–device interfaces. Despite progressive miniaturization and the evolution from first-generation pulsatile systems to contemporary continuous-flow devices, thrombotic, hemorrhagic, infectious, and inflammatory complications continue to limit long-term outcomes. This review examines the mechanistic contribution of material properties, surface architecture, and hemodynamic conditions to the pathogenesis of major MCS-associated complications, with particular emphasis on thrombogenicity, biomaterial-induced inflammatory activation, driveline and cannulation-associated infections, hemocompatibility disturbances, and device-related structural failure. The interplay between protein adsorption, platelet activation, complement cascade dysregulation, disturbed shear profiles, and biofilm formation is analyzed as a central determinant of adverse clinical events. Special attention is given to pediatric MCS, in which the continued reliance on extracorporeal pulsatile systems, unique anatomical constraints, and narrow therapeutic margins intensify susceptibility to both thromboembolic and infectious sequelae. Furthermore, the review addresses how material and surface modifications, and emerging biomimetic and anti-thrombogenic coatings may influence complication mitigation. By integrating clinical, engineering, and biomaterials perspectives, this work highlights that many complications traditionally regarded as secondary clinical phenomena are fundamentally rooted in device–material interactions and flow-mediated biological responses. Improved understanding of these mechanisms is essential for optimizing device design, enhancing hemocompatibility, and reducing complication burden in both adult and pediatric MCS populations.