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

Transcatheter aortic valve replacement has transformed the management of aortic stenosis; however, leaflet thrombosis and hypoattenuated leaflet thickening remain major clinical concerns. Flow disturbances from valve canting may alter local hemodynamics and promote thrombogenic conditions. We investigated how modest valve canting alters cusp-specific sinus flow and washout, and promotes thrombogenic microenvironments associated with leaflet thrombosis using particle image velocimetry, a physiologic blood loop, and tissue analysis.

A patient-derived aortic root model was used to evaluate the hemodynamic and thrombogenic effects of valve canting at -10° (anti-curvature), 0° (neutral), and +10° (along-curvature). Velocimetry quantified sinus flow and washout characteristics, and whole-blood loop experiments enabled histologic assessment of leaflet-associated thrombus.

Canting redistributed systolic jet orientation and sinus recirculation in a direction-dependent manner while preserving global hemodynamics. The most spatially constrained cusp showed the greatest stasis and the slowest washout. In the right coronary cusp, anticurvature canting increased regions within the sinus with velocity less than 0.05 m/s to 92% versus 43% in neutral and 10% in along-curvature deployments, and prolonged neo-sinus (T₉₀) washout to 4.7 versus 2.9 and 1.8 cycles. Histology localized surface-adherent thrombus to poorly washed regions, most prominently on the right coronary cusp leaflet in anticurvature deployments. Left and noncoronary cusp responses shifted with tilt direction, indicating redistribution rather than uniform worsening of thrombogenic conditions.

Modest noncoaxial deployment creates sinus-resolved thrombogenic microenvironments that are not captured by global measures such as transvalvular gradient or effective orifice area; therefore, it is a modifiable determinant of post-transcatheter aortic valve replacement leaflet thrombosis risk and a potential contributor to hypoattenuated leaflet thickening.