Vortex dynamics in trabeculated embryonic ventricles

TL;DR

This study uses computational fluid dynamics to analyze vortex formation in embryonic zebrafish hearts, revealing how trabecular structures influence intracardial flow, shear stress, and potentially gene expression during heart development.

Contribution

It introduces a detailed CFD analysis of vortex dynamics in trabeculated ventricles, linking morphology to flow patterns and gene regulation during early heart development.

Findings

Vortex formation occurs in intertrabecular regions at relevant developmental stages.

Trabecular morphology significantly alters intracardial flow and shear stress.

Flow disturbances may influence gene expression like Notch1, affecting heart morphogenesis.

Abstract

Proper heart morphogenesis requires a delicate balance between hemodynamic forces, myocardial activity, morphogen gradients, and epigenetic signaling, all of which are coupled with genetic regulatory networks. Recently both in vivo and in silico studies have tried to better understand hemodynamics at varying stages of vertebrate cardiogenesis. In particular, the intracardial hemodynamics during the onset of trabeculation is notably complex - the inertial and viscous fluid forces are approximately equal at this stage and small perturbations in morphology, scale, and steadiness of the flow can lead to significant changes in bulk flow structures, shear stress distributions, and chemical morphogen gradients. The immersed boundary method was used to solve the computational fluid dynamics problem involving fluid flow moving through the trabeculated ventricles of 72, 80, and 120 hours post fertilization wild type zebrafish embryos and ErbB2-inhibited embryos at 7 days post fertilization. An idealized trabeculated ventricular model was explored to map the bifurcations in flow structure that occur as a result of the unsteadiness of flow, trabeculae height, and fluid scale ($Re$). Vortex formation occurred in intertrabecular regions for biologically relevant parameter spaces, wherein flow velocities increased. This indicates that trabecular morphology may alter intracardial flow patterns and hence ventricular shear stresses and morphogen gradients. A potential implication of this work is that the onset of vortical (disturbed) flows can upregulate Notch1 expression in endothelial cells in vitro and hence impacts chamber morphogensis, valvulogenesis, and the formation of the trabeculae themselves.