Title

Augmented mitral valve leaflet area decreases leaflet stress: a finite element simulation.

Publication/Presentation Date

4-1-2012

Abstract

BACKGROUND: Using human mitral valve (MV) models derived from three-dimensional echocardiography, finite element analysis was used to predict mechanical leaflet and chordal stress. Subsequently, valve geometries were altered to examine the effects on stresses of the following: (1) varying coaptation area; (2) varying noncoapted leaflet tissue area; and (3) varying interleaflet coefficient of friction (μ).

METHODS: Three human MV models were loaded with a transvalvular pressure of 80 mm Hg using finite element analysis. Initially leaflet coaptation was set to 10%, 50%, or 100% of actual coaptation length to test the influence of coaptation length on stress distribution. Next, leaflet surface areas were augmented by 1% overall and by 2% in the noncoapted "belly" region to test the influence of increased leaflet billowing without changing the gross geometry of the MV. Finally, the coefficient of friction between the coapted leaflets was set to μ = 0, 0.05, or 0.3, to assess the influence of friction on MV function.

RESULTS: Leaflet coaptation length did not affect stress distribution in either the coapted or noncoapted leaflet regions; peak leaflet stress was 0.36 ± 0.17 MPa at 100%, 0.35 ± 0.14 MPa at 50%, and 0.35 ± 0.15 MPa at 10% coaptation lengths (p = 0.85). Similarly, coaptation length did not affect peak chordal tension (p = 0.74). Increasing the noncoapted leaflet area decreased the peak valvular stresses by 5 ± 2% (p = 0.02). Varying the coefficient of friction between leaflets did not alter leaflet or chordal stress distribution (p = 0.18).

CONCLUSIONS: Redundant MV leaflet tissue reduces mechanical stress on the noncoapted leaflets; the extent of coaptation or frictional interleaflet interaction does not independently influence leaflet stresses. Repair techniques that increase or preserve noncoapted leaflet area may decrease mechanical stresses and thereby enhance repair durability.

Volume

93

Issue

4

First Page

1141

Last Page

1145

ISSN

1552-6259

Disciplines

Medicine and Health Sciences

PubMedID

22397985

Department(s)

Department of Medicine, Cardiology Division

Document Type

Article

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