Fluid structure interaction modelling of aortic valve stenosis: Effects of valve calcification on coronary artery flow and aortic root hemodynamics
Introduction
Aortic valve disease is the most common form of valvular heart disease (VHD) in the elderly and frequently coexists with coronary artery disease [38]. Contemporary registries suggest the prevalence of coronary artery disease increases with age and the presence of aortic stenosis such that over half of all patients require simultaneous coronary bypass during valve surgery [23]. Aortic valve disease of the elderly occurs when calcium deposits on aortic valve leaflets over time, thereby changing the geometry and material properties of the aortic valve leaflets [10,34,41]. Invasive studies demonstrate that changes in the geometry and material properties of the aortic valve leaflets not only affect hemodynamics within the aortic root but also have a significant impact on coronary blood flow [7,9,33]. The hemodynamic variations in coronary arteries due to calcification may lead to accelerated atherosclerosis and eventually result in coronary stenosis [16,31].
Clinical investigations [5] show that the wall shear stress plays a significant role in the initiation of atherosclerosis within the coronary arterial wall and the progression of the calcium deposition on the leaflets. Calcification and atherosclerosis are, however, complex multifactorial processes which are yet to be completely understood [9,13,28]. It is believed that blood flow-induced shear stress affects the endothelial cells, leading to endothelial dysfunction, inflammatory responses, oxidative stress which remodels the artery wall and valve structure, and eventually results in progression of calcification and initiation of atherosclerosis [17,18,40]. For example, a recent study carried out by Hatoum et al. [17] shows that the recirculation zone in the sinuses for a calcified aortic valve varies in terms of strength and number of vortices with that of for the healthy valve. They also demonstrated that the calcified aortic valve leaflet experiences a smaller range of shear stress with higher shear stress probabilities during the systole compared to that of a healthy valve.
During the past decades, researchers have investigated pathologies of aortic valve and coronary arteries using numerical [3,24], clinical (in-vivo), and experimental (in-vitro) methods [6,9,18,30,39]. In numerical modelling, finite element analysis (FEM) and computational fluid dynamics (CFD) have been used to investigate valve hemodynamics [12,36,37,42]. The FEM studies [12,22] considered only the structural domain and did not account for the effect of fluid in their simulations. Similarly, the CFD simulations are not able to capture the effect of the structural domain on the fluid one.
To overcome the limitations of the aforementioned works not being able to model the fluid and structure domain simultaneously, fluid structure interaction (FSI) modelling has been employed by researchers [14,15] to study the influence of the valve structure and the coronary wall on the fluid domain. For example, Weinberg et al. [43] developed a FSI model of the aortic valve with nonlinear, anisotropic material properties and investigated the effect of material properties on leaflet strain during the cardiac cycle, comparing the impact of trileaflet and bicuspid valve morphology. They found that nonlinearity in the material properties of the bicuspid aortic valve has a significant effect on leaflet strain compared to that of the trileaflet valve. Katayama et al. [19] developed a model of the aortic valve to investigate the impact of the presence of sinuses on hemodynamic parameters inside the aortic root, and found that the presence of the sinuses affect the opening time of the valve. These aforementioned studies have not considered coronary arteries in their model, although the presence of coronary flow is able to change the hemodynamic parameters inside the aortic root [4,32].
To consider the effect of coronary arteries, Kim et al. [21] developed an FSI model of the aortic root including coronary arteries. However, the model did not incorporate the leaflets and sinuses. Nobari et al. [32] extended the model of Kim et al. [21] by adding right and left coronary arteries. They also utilised the ALE approach to simulate an FSI model of the aortic valve. Mohammadi et al. [29] improved the previous model by considering the tapered shape and branches of the coronary arteries. They used the combined FD and ALE approaches to simulate the model of the aortic valve. They investigated the effect of narrowing of the coronary arteries on the wall shear stress inside the coronary arteries based on the explicit finite element method using LS-DYNA software. Cao et al. [4] presented a FSI model of the aortic valve with coronary arteries and investigated the impact of having coronary artery on leaflet wall shear stress. They found that vortex development in sinus due to the presence of coronary arteries can, in turn, changes the magnitude of the leaflet wall shear stress. However, the impact of aortic valve stenosis on the hemodynamic parameters inside the aortic root, flow features in sinuses, and wall shear stress on the leaflets were neglected.
In this paper, the effect of valve stenosis on the aortic root and coronary hemodynamic parameters as well as the shape of the vortices inside the sinuses and the aortic root hemodynamics were investigated. To do this, 2D models of the healthy, calcified and severely calcified aortic valves were developed in ANSYS Fluent based on the echocardiography images available in the literature. In order to capture the turbulent nature of the flow downstream of the leaflets, the k-ω SST turbulence model was used. The influence of the calcification of the aortic-valve leaflets on hemodynamic parameters inside the aortic root, such as transvalvular pressure gradient, valve orifice diameter, maximum jet velocity along the valve orifice, wall shear stress on the fibrosa and ventricularis layers of the leaflets, was investigated. The impact of calcification of the aortic valve leaflets on the flow pattern in the sinuses was also studied; the vorticity magnitude corresponding to different points behind the leaflets was calculated in order to show how strong vortices can become as a result of the stiffening of the aortic valve leaflets. Furthermore, the flow features such as velocity magnitude, and the wall shear stress on the coronary walls inside the coronary arteries were studied in order to show the significance of the calcification on coronary hemodynamics. Based on the calculated hemodynamic parameters, susceptible locations for the initiation of coronary artery disease were determined.
Section snippets
Methods
In this study, a model of a 2D healthy aortic valve was developed in a commercial software package, ANSYS Workbench 19.1. The model geometry was based on the 2D echocardiography images of a healthy tricuspid aortic valve available in the literature for a healthy person of 27 years of age [1]. The numerical model consists of two different domains: fluid (blood flow field) and structure (deformable leaflets). Fluid structure interaction methodology was used to model the interaction of the fluid
Validation of the model
For validation purposes, two hemodynamic parameters calculated for the healthy valve were compared against published data [11,20]. The calculated transvalvular pressure gradient TPGmax and average wall shear stress (AWSS) for the presented work and previous experiments [20,44] are given in Table. 3.
To further validate the model, the results were qualitatively compared against recently published PIV data by [17]. Fig. 5 shows a comparison of streamlines and flow features between the present
Conclusion
In this study the effect of calcification of the aortic valve leaflets on hemodynamic parameters inside the aortic root and coronary arteries was investigated. To do this, 2D models of healthy, calcified, and severely calcified aortic valves were developed in ANSYS Fluent and ANSYS Mechanical based on the echocardiography images available in the literature. Results revealed that calcification has significantly changed the hemodynamic parameters inside the aortic root and the coronary arteries,
Limitations
We are dealing with a complicated model, and consequently a number of assumptions and simplifications have been employed: an idealised 2D geometry of the aortic root, sinuses, and leaflets are considered instead of 3D tricuspid leaflets since we are investigating the global dynamic behaviour of the leaflets. The arterial walls have been considered solid compared to the natural arterial walls which have a complex multilayered structure in which the Young's modulus of the walls are a function of
Declaration of Competing Interest
There are no potential conflicts of interest with respect to the research, authorship, and publication of this article.
Acknowledgments
The authors gratefully acknowledge the financial support of the Australian Government Research Training Program, South Australian Health and Medical Research Institute (SAHMRI) and the University of Adelaide. The authors also would like to acknowledge the supercomputing resources provided by the Phoenix HPC service at the University of Adelaide.
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