Abstract 14543: Diminished Aortic Flow in Fetus and Its Implications in Development of Aortic Coarctation and Arch Interruption: A 3d/4d Fetal Echocardiography and Computational Fluid Dynamics Study

Abstract

Background and Objectives: During critical windows of cardiac morphogenesis and remodeling, altered intrauterine hemodynamics may lead to congenital heart defects, such as aortic arch abnormalities. We sought to investigate the effects of diminished flow in the fetal aorta to understand the cause, improved diagnosis, and prognosis of coarctation of aorta (CoA) and interrupted aortic arch (IAA). Methods: Computational fluid dynamics (CFD) model of aortic and ductal arches was built based on dynamic 3D/4D spatiotemporal image correlation (STIC) fetal echocardiography (FE) and Doppler images from a normal fetus. Pulsatile hemodynamics, including velocity, pressure gradient, and wall shear stress (WSS), were stimulated as aortic flow decreased from 100% to 80%, 60%, 40%, and 20% by CFD, with accompanying ductal flow increased proportionally to maintain combined cardiac output (Figure). Results: As aortic flow diminished from 100% to 20% progressively, velocity, pressure, and WSS decreased in systole and diastole in aortic arch and isthmus. As aortic flow decreased, the flow structures changed, resulting in a reduction of WSS in the aortic isthmus, especially on the posterior wall. There was a “zero flow zone” between the left carotid and subclavian arteries when aortic flow decreased to 40% of baseline, and another one between innominate and left carotid arteries when it decreased to 20%. Pearson correlation analysis showed significant correlations between aortic flow, pressure, velocity, and WSS (r=0.883 - 1.000, P=0.047 - 0.001) at aortic isthmus. Conclusions: It is feasible to create a hemodynamic model of human fetal aortic arch using 3D/4D FE and CFD. The alterations of flow variables, especially WSS, and the “zero flow zones" in the aorta from progressive aortic flow reduction suggest the "flow-dependency” of the fetal aortic arch development and a unifying hypothesis of diminished flow in the pathogenesis of CoA and IAA.