Mechanical circulatory support (MCS) devices developed for end-stage heart failure or as a bridge-to-transplant include total artificial hearts (TAH) and ventricular assist devices (VAD) and utilize prosthetic heart valves (PHV) or rotary impellers to control blood recirculation [1]. These devices are currently not optimized to reduce the incidence of pathological flow patterns that cause elevated stresses leading to platelet activation and thrombosis. Although the latter is partially mitigated by lifelong anticoagulation therapy, it dramatically increases the risk of uncontrolled bleeding. For instance thromboembolic stroke-related complications (∼2%) were relatively less with the TAH-t compared to uncontrolled bleeding due to anticoagulation use (∼20%) [2]. Platelet activation should therefore be quantified and optimized based on patient-specific cardiac outputs in device prototypes before clinical use.

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