JOURNAL ARTICLE

Computational fluid dynamics simulation of transcatheter aortic valve degeneration

Harry A Dwyer, Peter B Matthews, Ali Azadani, Nicolas Jaussaud, Liang Ge, T Sloane Guy, Elaine E Tseng
Interactive Cardiovascular and Thoracic Surgery 2009, 9 (2): 301-8
19414489

OBJECTIVES: Studied under clinical trials, transcatheter aortic valves (TAV) have demonstrated good short-term feasibility and results in high-risk surgical patients with severe aortic stenosis. However, their long-term safety and durability are unknown. The objective of this study is to evaluate hemodynamic changes within TAV created by bioprosthetic leaflet degeneration.

METHODS: Computational fluid dynamics (CFD) simulations were performed to evaluate the hemodynamics through TAV sclerosis (35% orifice reduction) and stenosis (78% orifice reduction). A three-dimensional surface mesh of the TAV within the aortic root was generated for each simulation. Leaflets were contained within an open, cylindrical body without attachment to the sinus commissures representing the stent. A continuous surface between the annulus and TAV excluded the geometry of the native calcified leaflets and prevented paravalvular leak. Unsteady control volume analysis throughout systole was used to calculate leaflet shear stress and total force on the TAV.

RESULTS: Sclerosis increased total force on the TAV by 63% (0.602-0.98 N). Advancement of degeneration from sclerosis to stenosis was accompanied by an 86% increase in total force (1.82 N) but only a 32% increase in peak wall shear stress on the leaflets. Of the total force exerted on the TAV, 99% was in the direction of axial flow. Shear stresses on the TAV were greatest during peak systolic flow with stress concentrations on the tips of the leaflets. In the normal TAV, the aortic root geometry and physiologic flow dominate location and magnitude of shear stress. Following leaflet degeneration, the specific geometry of the stenosis dictates the profile of axial velocity leaving the TAV and shear stress on the leaflets. A dramatic increase in peak leaflet shear stress was observed (115 Pa stenosis vs. 87 Pa sclerosis and 29 Pa normal).

CONCLUSIONS: CFD simulations in this study provide the first of its kind data quantifying hemodynamics within stenosed TAV. Stenosis leads to significant forces of TAV during systole; however, diastolic forces predominate even with significant stenosis. Substantial changes in peak shear stress occur with TAV degeneration. As the first implanted TAV begin to stenose, the authors recommend watchful examination for device failure.

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