Transcatheter aortic valve canting creates cusp-specific thrombogenic microenvironments through altered sinus hemodynamics

Figures

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  Noncoaxial TAVR creates cusp-specific stasis and leaflet thrombogenicity.

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  Figure 1. Schematic of THV canting configurations in the patient-derived aortic root model. A, −10° canting of the THV axis toward the right coronary sinus relative to the annular plane normal. B, Neutral deployment (0°), with the THV axis aligned with the root axis. C, +10° canting of the THV axis toward the left and noncoronary sinus relative to the annular plane normal. The bottom panel shows the top view of the sinus of Valsalva with the different THV configurations canted with respect to the sinuses. LCC, Left coronary cusp; RCC, right coronary cusp.

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  Figure 2. Effect of THV canting on downstream flow patterns. A-C, Systolic velocity vector fields within the downstream plane for anticurvature (−10°), neutral (0°), and along-curvature (+10°) canting, respectively. D-F, Corresponding vorticity magnitude.

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  Figure 3. Percentage of aortic sinus area exhibiting low velocity (|v| < .05 m/s) quantified from phase-averaged PIV velocity fields averaged over 20 cardiac cycles. Anticurvature canting (−10°) markedly increased low-velocity area within the RCC, whereas along-curvature canting (+10°) reduced RCC stasis and shifted low-velocity regions toward the LCC and NCC. Neutral alignment (0°) produced a more uniform distribution across the 3 sinuses. LCC, Left coronary cusp; NCC, noncoronary cusp; RCC, right coronary cusp.

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  Figure 4. Effect of THV canting on RCC sinus flow patterns and RCC leaflet surface thrombosis. A-C, Systolic velocity vector fields within the RCC sinus plane for anticurvature (−10°), neutral (0°), and along-curvature (+10°) canting configurations, respectively. D-F, Corresponding vorticity magnitude maps highlighting enlarged shear layers and recirculation zones adjacent to the outflow leaflet belly under canted conditions. G-I, Representative Carstairs-stained histologic sections from the RCC leaflet outflow surface, with arrowheads indicating surface-adherent fibrin/platelet-rich thrombus that increases with canting, while underlying leaflet architecture remains preserved.

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  Figure 5. Effect of THV canting on LCC sinus flow patterns and LCC leaflet surface thrombosis. A-C, Systolic velocity vector fields within the LCC sinus plane for anticurvature (−10°), neutral (0°) and along-curvature (+10°) canting configurations, respectively. D-F, Corresponding vorticity magnitude maps highlighting enlarged shear layers and recirculation zones adjacent to the outflow leaflet belly under canted conditions. G-I, Representative Carstairs-stained histologic sections from the leaflet outflow surface, with arrowheads indicating surface-adherent fibrin/platelet-rich thrombus that increases with canting while underlying leaflet architecture remains preserved.

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  Figure 6. Effect of THV canting on NCC sinus flow patterns and NCC leaflet surface thrombosis. A-C, Systolic velocity vector fields within the NCC sinus plane for anticurvature (−10°), neutral (0°), and along-curvature (+10°) canting configurations, respectively. D-F, Corresponding vorticity magnitude maps highlighting enlarged shear layers and recirculation zones adjacent to the outflow leaflet belly under canted conditions. G-I, Representative Carstairs-stained histologic sections from the leaflet outflow surface, with arrowheads indicating surface-adherent fibrin/platelet-rich thrombus that increases with canting while underlying leaflet architecture remains preserved.

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  Figure 7. Sinus-specific washout dynamics across valve canting configurations. Normalized particle retention curves are shown for the RCC, NCC, and LCC neosinuses under anticurvature (−10°), neutral (0°), and along-curvature (+10°) canting configurations. The horizontal dashed line denotes 10% particle retention, corresponding to the time to 90% washout (T90). Across all sinuses, anticurvature canting consistently prolonged washout, evidenced by delayed T90 relative to neutral and along-curvature configurations. LCC, Left coronary cusp; NCC, noncoronary cusp; RCC, right coronary cusp.

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  Figure E1. Statistical shape modeling workflow for generation of representative cohort anatomies. Patient-specific anatomies were segmented from imaging data and processed using statistical shape modeling to establish pointwise correspondence across the cohort. The resulting shape distribution was used to generate virtual representative anatomies corresponding to the mean and ±2 SDs of the primary shape mode. These anatomies were subsequently fabricated using 3D printing and incorporated into a biocompatible flow chamber for experimental investigations. PDMS, Polydimethylsiloxane.

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  Figure E2. Representative images of a custom transcatheter valve fabrication. A, Laser-cut cobalt-chromium frame before leaflet mounting. B, High-magnification view of representative (red outlines) stent-strut edge demonstrating smooth, burr-free surface after electropolishing. C, Assembled valve consisting of the cobalt-chromium frame and trileaflet porcine pericardial tissue. D and E, Scanning electron microscopy of leaflet microstructure reveals a dense collagen fiber network, that is, fibrous side facing the ventricle (D) and serous side facing the aorta in (E), consistent with the microstructure of glutaraldehyde-treated pericardial bioprosthetic valve leaflets reported in prior studies.

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  Figure E3. Representative images of in-house THVs mounted over 3D-printed tapered disks to precisely maintain the canting angle. (A) Shows a control valve with no canting is shown, and (B), a tapered disk at –10 degrees.

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  Figure E4. Experimental platforms for hydrodynamic and biological assessment using a population-derived PDMS aortic model. A, Optical flow loop used for phase-averaged PIV. A pulsatile pump generated physiologic waveforms through a compliance chamber and mechanical mitral valve into the PDMS aortic root model. Flow rate was monitored with an inline probe, and velocity fields were acquired using a laser sheet and high-speed camera (inset). The working fluid was a refractive–index–matched glycerin solution. B, Blood loop configuration using the same PDMS aortic model. A linear piston actuator generated matched pulsatile flow, with upstream and downstream pressure transducers for hemodynamic monitoring. A compliance chamber and adjustable back-pressure regulator maintained physiologic loading conditions. The transparent PDMS model was perfused with porcine blood for biological assays (inset). PDMS, Polydimethylsiloxane.