Leaflet Stress and Strain Distributions Following Incomplete Transcatheter Aortic Valve Expansion

Publication Date

8-21-2015

Document Type

Article

Organizational Units

Daniel Felix Ritchie School of Engineering and Computer Science, Center for Orthopaedic Biomechanics, Mechanical and Materials Engineering

Keywords

Transcatheter aortic valve replacement, Finite element modeling, Oversizing, Incomplete stent expansion, Stress and strain

Abstract

Transcatheter aortic valve replacement (TAVR) is an established treatment alternative to surgical valve replacement in high-risk patients with severe symptomatic aortic stenosis. The current guidelines for TAVR are to upsize transcatheter aortic valve (TAV) relative to the native annulus to secure the device and minimize paravalvular leakage. Unlike surgical stented bioprosthetic valves where leaflets are attached to a rigid frame, TAVs must expand to fit within the native annulus. Fully-expanded circular TAVs have consistent leaflet kinematics; however, subtle variations in the degree of stent expansion may affect leaflet coaptation. The objective of this study was to determine the impact of incomplete TAV expansion on leaflet stress and strain distributions. In this study, we developed finite element models of a 23 mm homemade TAV expanded to diameters ranging from 18 to 23 mm in 1 mm increments. Through dynamic finite element simulations, we found that leaflet stress and strain distributions were dependent on the diameter of the inflated TAV. After complete expansion of the TAV to 23 mm, high stress and strain regions were observed primarily in the commissures during diastole. However, 2–3 mm incomplete TAV stent expansion induced localized high stress regions within the TAV commissures, while 4–5 mm incomplete stent expansion induced localized high stress regions within the belly of the TAV leaflets during the diastolic phase of the cardiac cycle. Increased mechanical stress and flexural deformation on TAV leaflets due to incomplete stent expansion may lead to accelerated tissue degeneration and diminished long-term valve durability.

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