The bicuspid aortic valve (BAV) is the most common congenital cardiac anomaly and is present in 2% of the population. While a normal tricuspid aortic valve (TAV) consists of three leaflets, a BAV is formed with only two as a result of the fusion of two leaflets into a larger one1. This defect is associated with serious complications such as calcific aortic valve disease (CAVD), a condition characterized by the accumulation of calcium on the leaflets which contributes to the obstruction of the left ventricular outflow and progressive heart failure. Although studies have suggested similarities in the pathogenesis of CAVD in the BAV and TAV, the calcification of the BAV is more severe and its progression more rapid. Previous studies in our laboratory have evidenced the sensitivity of valve leaflets to their hemodynamic environment and the ability of fluid stress alterations to trigger an inflammatory response on the aortic surface of porcine aortic valve leaflets2. Although a similar mechano-etiology could contribute to the rapid calcification of the BAV, it is not clear how the particular BAV anatomy impacts on its hemodynamic environment and whether the hemodynamic stresses experienced by BAV leaflets differ from those present in TAV leaflets. Therefore, the aim of this study was to characterize BAV hemodynamics and to quantify its degree of abnormality relative to a TAV. A fluid-structure interaction (FSI) approach validated with respect to particle-image velocimetry (PIV) measurements was implemented to quantify TAV and BAV hemodynamics in terms of flow velocity field, valvular effective orifice area (EOA) and leaflet wall-shear stress. The large degree of hemodynamic abnormality predicted in the BAV model may contribute to the rapid progression of CAVD in that anatomy. This work lays the foundation for future mechanobiological studies aimed at investigating the isolated effects of native BAV hemodynamic stresses on the development of CAVD.

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