Steady Flow Hemodynamic and Energy Loss Measurements in Normal and Simulated Calcified Tricuspid and Bicuspid Aortic Valves

Abstract

The bicuspid aortic valve (BAV), which forms with two leaflets instead of three as in the normal tricuspid aortic valve (TAV), is associated with a spectrum of secondary valvulopathies and aortopathies potentially triggered by hemodynamic abnormalities. While studies have demonstrated an intrinsic degree of stenosis and the existence of a skewed orifice jet in the BAV, the impact of those abnormalities on BAV hemodynamic performance and energy loss has not been examined. This steady-flow study presents the comparative in vitro assessment of the flow field and energy loss in a TAV and type-I BAV under normal and simulated calcified states. Particle-image velocimetry (PIV) measurements were performed to quantify velocity, vorticity, viscous, and Reynolds shear stress fields in normal and simulated calcified porcine TAV and BAV models at six flow rates spanning the systolic phase. The BAV model was created by suturing the two coronary leaflets of a porcine TAV. Calcification was simulated via deposition of glue beads in the base of the leaflets. Valvular performance was characterized in terms of geometric orifice area (GOA), pressure drop, effective orifice area (EOA), energy loss (EL), and energy loss index (ELI). The BAV generated an elliptical orifice and a jet skewed toward the noncoronary leaflet. In contrast, the TAV featured a circular orifice and a jet aligned along the valve long axis. While the BAV exhibited an intrinsic degree of stenosis (18% increase in maximum jet velocity and 7% decrease in EOA relative to the TAV at the maximum flow rate), it generated only a 3% increase in EL and its average ELI (2.10 cm2/m2) remained above the clinical threshold characterizing severe aortic stenosis. The presence of simulated calcific lesions normalized the alignment of the BAV jet and resulted in the loss of jet axisymmetry in the TAV. It also amplified the degree of stenosis in the TAV and BAV, as indicated by the 342% and 404% increase in EL, 70% and 51% reduction in ELI and 48% and 51% decrease in EOA, respectively, relative to the nontreated valve models at the maximum flow rate. This study indicates the ability of the BAV to function as a TAV despite its intrinsic degree of stenosis and suggests the weak dependence of pressure drop on orifice area in calcified valves.

Three-dimensional macro-scale assessment of regional and temporal wall shear stress characteristics on aortic valve leaflets

“…Laser Doppler velocimetry (LDV) measurements carried out in a polyurethane trileaflet valve indicated a maximum WSS of 79 dyn/cm 2 near the tip of the leaflets (Weston et al 1999). Particle image velocimetry measurements in native porcine valves suggested a maximum fluid shear stress of 30 dyn/cm 2 in the shear layer extending from the tip of the leaflets (Seaman et al 2014). LDV measurements on prosthetic AV leaflets subjected to pulsatile flow suggested the existence of a high WSS ranging between 2 51 and þ 71 dyn/cm 2 on the leaflet ventricularis (i.e., surface facing the left ventricle) and a low WSS ranging between 0 and þ 20 dyn/cm 2 on the leaflet fibrosa (i.e., surface facing the aorta) .…”

Fluid–Structure Interaction Models of Bicuspid Aortic Valves: The Effects of Nonfused Cusp Angles

“…Both experimental and numerical studies have been previously performed on the BAV. Experimental studies characterized the BAV with a limited valve opening orifice, increased turbulent flow, and asymmetric jet flow toward the NFC [14][15][16][17]. Numerical models were used to analyze the structural and fluid dynamic aspects of the BAV, which cannot be captured in experimental studies.…”

Simulations of morphotype-dependent hemodynamics in non-dilated bicuspid aortic valve aortas

“…The dependence of the expression of aortopathy on the BAV subtype has suggested a role for hemodynamics in the etiology of BAV disease . Flow eccentricity, skewness, helicity and wall shear stress (WSS) have been shown to be systematically higher in BAV aortas than in tricuspid aortic valve (TAV) aortas and to exhibit abnormalities in dilated BAV aorta regions (Barker et al, 2012;Bissell et al, 2013;Bonomi et al, 2015;Burris and Hope, 2015;Chandra et al, 2012;Mahadevia et al, 2014;Pasta et al, 2013;Seaman et al, 2014;van Ooij et al, 2015). While all these flow abnormalities may play different roles in BAV disease, they all impact the tissue via the interfacial fluid shear stress imposed on the endothelium.…”