Hemodynamic patterning of the avian atrioventricular valve - PubMed (original) (raw)

Hemodynamic patterning of the avian atrioventricular valve

Huseyin C Yalcin et al. Dev Dyn. 2011 Jan.

Abstract

In this study, we develop an innovative approach to rigorously quantify the evolving hemodynamic environment of the atrioventricular (AV) canal of avian embryos. Ultrasound generated velocity profiles were imported into Micro-Computed Tomography generated anatomically precise cardiac geometries between Hamburger-Hamilton (HH) stages 17 and 30. Computational fluid dynamic simulations were then conducted and iterated until results mimicked in vivo observations. Blood flow in tubular hearts (HH17) was laminar with parallel streamlines, but strong vortices developed simultaneous with expansion of the cushions and septal walls. For all investigated stages, highest wall shear stresses (WSS) are localized to AV canal valve-forming regions. Peak WSS increased from 19.34 dynes/cm(2) at HH17 to 287.18 dynes/cm(2) at HH30, but spatiotemporally averaged WSS became 3.62 dynes/cm(2) for HH17 to 9.11 dynes/cm(2) for HH30. Hemodynamic changes often preceded and correlated with morphological changes. These results establish a quantitative baseline supporting future hemodynamic analyses and interpretations.

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Figures

Fig. 1

Fig. 1

Stage specific AV orifice diameter (left) and peak velocity (right) as measured by ultrasound. Insets on right are representative original Doppler velocity recordings. A: HH17. B: HH23. C: HH 27. D: HH 30. Correlation of AV canal velocity with left atrial (LA) input velocity for stages E: HH27 and F: HH30.

Fig. 2

Fig. 2

Stage specific AV orifice flow profiles at peak velocity (left) and spatially averaged WSS throughout cardiac cycle (right) as calculated by CFD and from ultrasound with Poiseuille and Plug Flow (boundary layer 1/5th of the diameter) assumptions. A: HH17. B: HH23. C: HH 27. D: HH 30.

Fig. 3

Fig. 3

Change in pressure across the AV canal region.

Fig. 4

Fig. 4

A: 3D hemodynamic environment in the AV region - Stage HH 17. B: Spatially averaged WSS on the inner curvature versus outer curvature throughout the cardiac cycle. A is atria V is ventricle.

Fig. 5

Fig. 5

A: 3D hemodynamic environment in the AV region - Stage HH 23. Arrows at late cycle representation show location of vortices. B: Spatially averaged WSS on the right and left mural surfaces and ventral and dorsal midlines throughout cardiac cycle. RA is right atria, LA is left atria, RV is right ventricle, LV is left ventricle.

Fig. 6

Fig. 6

A: 3D hemodynamic environment in the AV region - Stage HH 27. B: Spatially averaged WSS on the inflow and outflow surfaces throughout cardiac cycle. LA is left atria, LV is left ventricle.

Fig. 7

Fig. 7

A: 3D hemodynamic environment in the AV region - Stage HH 30. B: Spatially averaged WSS on the inflow and outflow surfaces throughout cardiac cycle. LA is left atria, LV is left ventricle.

Fig. 8

Fig. 8

Stage dependent blood rheology. A: Hematocrit amounts for stages (adapted from (RYCHTER et al., 1955)). B: Hematocrit dependent blood density (Adapted from (Usami et al., 1970)). C: Nonlinear power law relationship for shear-rate dependent viscosity. Dots represent correlations generated based on hematocrit amounts and lines based on embryonic stages.

Fig. 9

Fig. 9

Cushion regions where the WSS were traced (shown with dotted lines). Inflow segments are blue, outflow are red for seperated regions. Trace colors match with plot colors for regions in Figures 4–7. At HH24, dorsal cushion is on the other side of the geometry. A is atria, V is ventricle, L is left, R is right.

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