A three-dimensional computational fluid dynamics (CFD) method has been developed to simulate the flow in a pumping left ventricle. The proposed method uses magnetic resonance imaging (MRI) technology to provide a patient specific, time dependent geometry of the ventricle to be simulated. Standard clinical imaging procedures were used in this study. A two-dimensional time-dependent orifice representation of the heart valves was used. The location and size of the valves is estimated based on additional long axis images through the valves. A semi-automatic grid generator was created to generate the calculation grid. Since the time resolution of the MR scans does not fit the requirements of the CFD calculations a third order bezier approximation scheme was developed to realize a smooth wall boundary and grid movement. The calculation was performed by a Navier-Stokes solver using the arbitrary Lagrange-Euler (ALE) formulation. Results show that during diastole, blood flow through the mitral valve forms an asymmetric jet, leading to an asymmetric development of the initial vortex ring. These flow features are in reasonable agreement with in vivo measurements but also show an extremely high sensitivity to the boundary conditions imposed at the inflow. Changes in the atrial representation severely alter the resulting flow field. These shortcomings will have to be addressed in further studies, possibly by inclusion of the real atrial geometry, and imply additional requirements for the clinical imaging processes.

The fluid-structure coupled simulation of the heart, though at its developing stage, has shown great prospect in heart function investigations and clinical applications. The purpose of this paper is to verify a commercial software based fluid-structure interaction scheme for the left ventricular filling. The scheme applies the finite volume method to discretize the arbitrary Lagrangian-Eulerian formulation of the Navier-Stokes equations for the fluid while using the nonlinear finite element method to model the structure. The coupling of the fluid and structure is implemented by combining the fluid and structure equations as a unified system and solving it simultaneously at every time step. The left ventricular filling flow in a three-dimensional ellipsoidal thin-wall model geometry of the human heart is simulated, based on a prescribed time-varying Young's modulus. The coupling converges smoothly though the deformation is very large. The pressure-volume relation of the model ventricle, the spatial and temporal distributions of pressure, transient velocity vectors as well as vortex patterns are analyzed, and they agree qualitatively and quantitatively well with the existing data. This preliminary study has verified the feasibility of the scheme and shown the possibility to simulate the left ventricular flow in a more realistic way by adding a myocardial constitutive law into the model and using a more realistic heart geometry.

No abstract

2021). Three-dimensional single framework multi-component lattice Boltzmann equation method for vesicle hydrodynamics. Physics of Fluids, 33 (7), 077110.

"Heart rate reduction with ivabradine promotes shear stress-dependent anti-inflammatory mechanisms in arteries", Thrombosis and Haemostasis, 2016: 116/1 (July) pp. [181][182][183][184][185][186][187][188][189][190]., is available online at: https://doi.org/10.1160/TH16-03-0214.eprints@whiterose.ac.uk https://eprints.whiterose.ac.uk/ Reuse Unless indicated otherwise, fulltext items are protected by copyright with all rights reserved. The copyright exception in section 29 of the Copyright, Designs and Patents Act 1988 allows the making of a single copy solely for the purpose of non-commercial research or private study within the limits of fair dealing. The publisher or other rights-holder may allow further reproduction and re-use of this version -refer to the White Rose Research Online record for this item. Where records identify the publisher as the copyright holder, users can verify any specific terms of use on the publisher's website. TakedownIf you consider content in White Rose Research Online to be in breach of UK law, please notify us by emailing eprints@whiterose.ac.uk including the URL of the record and the reason for the withdrawal request. 2 SUMMARY AimsBlood flow generates wall shear stress (WSS) which alters endothelial cell (EC) function. Low WSS promotes vascular inflammation and atherosclerosis whereas high uniform WSS is protective. Ivabradine decreases heart rate leading to altered hemodynamics. Besides its cardio-protective effects, ivabradine protects arteries from inflammation and atherosclerosis via unknown mechanisms. We hypothesised that ivabradine protects arteries by increasing WSS to reduce vascular inflammation. Methods and ResultsHypercholesterolemic mice were treated with ivabradine for 7 weeks in drinking water or remained untreated as a control. En face immunostaining demonstrated that treatment with ivabradine reduced the expression of pro-inflammatory VCAM-1 (p<0.01) and enhanced the expression of anti-inflammatory eNOS (p<0.01) at the inner curvature of the aorta. We concluded that ivabradine alters EC physiology indirectly via modulation of flow because treatment with ivabradine had no effect in ligated carotid arteries in vivo, and did not influence the basal or TNF -induced expression of inflammatory (VCAM-1, MCP-1) or protective (eNOS, HMOX1, KLF2, KLF4) genes in cultured EC. We therefore considered whether ivabradine can alter WSS which is a regulator of EC inflammatory activation. Computational fluid dynamics demonstrated that ivabradine treatment reduced heart rate by 20% and enhanced WSS in the aorta. ConclusionsIvabradine treatment altered hemodynamics in the murine aorta by increasing the magnitude of shear stress. This was accompanied by induction of eNOS and suppression of VCAM-1, whereas ivabradine did not alter EC that could not respond to flow. Thus ivabradine protects arteries by altering local mechanical conditions to trigger an anti-inflammatory response.