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The efficacy of reduced order modeling for transstenotic pressure drop in the coronary arteries is presented. Coronary artery disease is a leading cause of death worldwide and the computation of pressure drop in the coronary arteries has become a standard for evaluating the functional significance of a coronary stenosis. Comprehensive models typically employ three-dimensional (3D) computational fluid dynamics (CFD) to simulate coronary blood flow in order to compute transstenotic pressure drop at the arterial stenosis. In this study, we evaluate the capability of different hydrodynamic models to compute transstenotic pressure drop. Models range from algebraic formulae to one-dimensional (1D), two-dimensional (2D), and 3D time-dependent CFD simulations. Although several algebraic pressure-drop formulae have been proposed in the literature, these models were found to exhibit wide variation in predictions. Nonetheless, we demonstrate an algebraic formula that provides consistent predictions with 3D CFD results for various changes in stenosis severity, morphology, location, and flow rate. The accounting of viscous dissipation and flow separation were found to be significant contributions to accurate reduce order modeling of transstenotic coronary hemodynamics.

Background Hemostasis studies performed in vivo have shown that hemostatic plugs formed after penetrating injuries are characterized by a core of highly activated, densely packed platelets near the injury site, covered by a shell of less activated and loosely packed platelets. Thrombin production occurs near the injury site, further activating platelets and starting the process of platelet mass retraction. Tightening of interplatelet gaps may then prevent the escape and exchange of solutes. Objectives To reconstruct the hemostatic plug macro- and micro-architecture and examine how platelet mass contraction regulates solute transport and solute concentration in the gaps between platelets. Methods Our approach consisted of three parts. First, platelet aggregates formed in vitro under flow were analyzed using scanning electron microscopy to extract data on porosity and gap size distribution. Second, a three-dimensional (3-D) model was constructed with features matching the platelet aggregates formed in vitro. Finally, the 3-D model was integrated with volume and morphology measurements of hemostatic plugs formed in vivo to determine how solutes move within the platelet plug microenvironment. Results The results show that the hemostatic mass is characterized by extremely narrow gaps, porosity values even smaller than previously estimated and stagnant plasma velocity. Importantly, the concentration of a chemical species released within the platelet mass increases as the gaps between platelets shrink. Conclusions Platelet mass retraction provides a physical mechanism to establish steep chemical concentration gradients that determine the extent of platelet activation and account for the core-and-shell architecture observed in vivo.

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