Journal
CARDIOVASCULAR ENGINEERING AND TECHNOLOGY
Volume 12, Issue 4, Pages 438-453Publisher
SPRINGER
DOI: 10.1007/s13239-021-00536-9
Keywords
Aortic valve stenosis; Large-eddy simulation; Computational fluid dynamics; Turbulence; Kinetic energy; Wall shear stress; Energy loss
Funding
- University of Edinburgh
- EPSRC [EP/P020267/1, EP/R512540/1]
- UK Medical Research Council [MC-A651-53301]
- National Institute for Health Research Biomedical Research Centre based at Imperial College Healthcare NHS Trust
- Imperial College London 1939
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This study investigated the turbulence effects in aortic valve stenosis (AVS) using large-eddy simulation (LES) and magnetic resonance imaging (MRI). Turbulence in AVS was found to be induced by a combination of high velocity jet impinging on the arterial wall and a dilated ascending aorta. The turbulent wall shear stress (WSS) accounted for a significant portion of the total WSS in the aorta, highlighting the importance of considering turbulence in assessing aortic hemodynamics in patients with AVS.
Blood flow in the aorta is often assumed laminar, however aortic valve pathologies may induce transition to turbulence and our understanding of turbulence effects is incomplete. The aim of the study was to provide a detailed analysis of turbulence effects in aortic valve stenosis (AVS). Methods Large-eddy simulation (LES) of flow through a patient-specific aorta with AVS was conducted. Magnetic resonance imaging (MRI) was performed and used for geometric reconstruction and patient-specific boundary conditions. Computed velocity field was compared with 4D flow MRI to check qualitative and quantitative consistency. The effect of turbulence was evaluated in terms of fluctuating kinetic energy, turbulence-related wall shear stress (WSS) and energy loss. Results Our analysis suggested that turbulence was induced by a combination of a high velocity jet impinging on the arterial wall and a dilated ascending aorta which provided sufficient space for turbulence to develop. Turbulent WSS contributed to 40% of the total WSS in the ascending aorta and 38% in the entire aorta. Viscous and turbulent irreversible energy losses accounted for 3.9 and 2.7% of the total stroke work, respectively. Conclusions This study demonstrates the importance of turbulence in assessing aortic haemodynamics in a patient with AVS. Neglecting the turbulent contribution to WSS could potentially result in a significant underestimation of the total WSS. Further work is warranted to extend the analysis to more AVS cases and patients with other aortic valve diseases.
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