Functionality of platelets after in vitro testing of pulsatile total artificial hearts.

Hemolysis is a metric of hemocompatibility in total artificial hearts (TAHs) but provides limited insight into platelet biology and thrombogenicity. We demonstrated reduced hemolysis with Realheart® TAH (RH) compared to FDA-approved SynCardia TAH (Sync). Here, we evaluated platelet function following exposure to both devices in a whole-blood in vitro system using a standardized ASTM F1830 protocol. Human blood (n = 5) was circulated for 360 min under controlled conditions (5 L/min, 100 mmHg, 37 °C) in RH, Sync, while matched static controls were maintained under identical temperature conditions. Platelets were assessed using metabolic (ATP, mitochondrial potential), phenotypic (surface markers, microparticles), and functional (agonist response, thromboelastometry) assays. Differences were observed between circulating and static conditions, including higher pH, increased lactate, and reduced platelet surface receptor expression, consistent with the non-physiological nature of static controls. Despite these changes, no evidence of increased platelet activation (CD62P), thrombogenicity (CD61+ microparticles), or mitochondrial damage (ATP, JC-1) was observed, and platelet function remained preserved by agonist stimulation and thromboelastometry. SynCardia increased mean platelet volume and reduced ATP levels, suggesting altered particle composition rather than intrinsic platelet dysfunction. These findings indicate preserved platelet integrity under clinically relevant TAH conditions and highlight that hemolysis and platelet responses represent distinct aspects of device hemocompatibility.