<p>Precise monitoring of platelet function is fundamental to the effective management of cardiovascular diseases, yet conventional testing methodologies often overlook the influence of physiological fluid dynamics. Herein, we introduce and evaluate a microfluidics fabricated from 3D-Printed mold-based technique enabling the dynamic visualization and quantitative analysis of platelet adhesion and aggregation under simulated in vitro flow conditions. Using our model, we demonstrate that platelet aggregation is highly dependent on shear rate, with higher flow velocities leading to significantly larger and denser aggregates. Furthermore, at a single, physiologically relevant flow rate, we assessed the efficacy of common antiplatelet drugs—tirofiban, ticagrelor, and aspirin—revealing distinct potency hierarchies in their ability to inhibit platelet aggregation. Our demonstration of shear-sensitive platelet responses underscores a critical requirement: the evaluation of antiplatelet drugs must be conducted within a physiologically relevant hemodynamic context. Therefore, this microfluidic model represents a rapid, efficient, and powerful tool, not only for fundamental studies of platelet function but also as a promising platform for the personalized analysis of drug efficacy under simulated flow conditions.</p> Graphical abstract <p></p>

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Uniform shear-induced platelet aggregation analysis via microfluidics fabricated from 3D-printed mold: a rapid platform for antiplatelet drug assessment

  • Xuemei Gao,
  • Ling Ding,
  • Xuanrong Huan,
  • Fangyu Zhou,
  • Yonghua Mi,
  • Yuan Li

摘要

Precise monitoring of platelet function is fundamental to the effective management of cardiovascular diseases, yet conventional testing methodologies often overlook the influence of physiological fluid dynamics. Herein, we introduce and evaluate a microfluidics fabricated from 3D-Printed mold-based technique enabling the dynamic visualization and quantitative analysis of platelet adhesion and aggregation under simulated in vitro flow conditions. Using our model, we demonstrate that platelet aggregation is highly dependent on shear rate, with higher flow velocities leading to significantly larger and denser aggregates. Furthermore, at a single, physiologically relevant flow rate, we assessed the efficacy of common antiplatelet drugs—tirofiban, ticagrelor, and aspirin—revealing distinct potency hierarchies in their ability to inhibit platelet aggregation. Our demonstration of shear-sensitive platelet responses underscores a critical requirement: the evaluation of antiplatelet drugs must be conducted within a physiologically relevant hemodynamic context. Therefore, this microfluidic model represents a rapid, efficient, and powerful tool, not only for fundamental studies of platelet function but also as a promising platform for the personalized analysis of drug efficacy under simulated flow conditions.

Graphical abstract