Modeling mitral valve stenosis: A parametric study on the stenosis severity level

Fluid–Structure-Electrophysiology interaction (FSEI) in the left-heart: A multi-way coupled computational model

“…In fact, during the heart beat mitral and aortic valves open and close alternatively and their leaflets are pushed against each other, during the closing phase, to seal the valve. For this purpose a contact model has been developed [18] to account for the leaflet coaptation along arbitrary surfaces in space which are a-priori unknown. Specifically, at each time step, the cells of the fluidic domain (red box in Fig.…”

“…Some more recent studies have focussed on the left ventricular flow in presence of natural and prosthetic mitral valves. In particular, the effectiveness of the ventricle wash-out has been studied as function of the ventricle pumping efficiency [17], mitral valve geometry and possible presence of stenoses [17,18]. In these papers the full FSI between hemodynamics and deformable tissues was considered even if the contraction and relaxation of the ventricle was driven by an externally imposed flow rate rather than being determined by the active contraction of the myocardium.…”

Effects of stenotic aortic valve on the left heart hemodynamics: a fluid-structure-electrophysiology approach

“…Importantly, the expansion/contraction cycle of the heart chambers and the valve leaflets kinematic are not imposed but come as a part of the numerical solution. In particular, the AS induced by calcification is modeled in a similar fashion to [18] by preventing the mobility of a certain portion of the aortic leaflets close to the aortic root, where the only control parameter is the radius of the annular region identifying the calcific area setting the severity of the pathology. In addition to the normal case of healthy aortic valve (all portions of the valve leaflets can move), the model has been set so as to reproduce three different pathological configurations, namely (i) mild, (ii) moderate and (iii) severe stenosis, and for each case the hemodynamics has been solved in order to evidence the abnormal dynamics when the valve pathology occurs.…”

“…In order to reproduce such reduced mobility, AS is modeled by blocking a certain region of the leaflets next to the aortic root (corresponding the red area in figure 1c) to its initial position as a function of the disease severity, which can be progressively varied from moderate to acute by increasing the calcific area and, concurrently, reducing the AVA. A similar approach was adopted to model correctly the mitral valve stenosis in previous FSI numerical simulations [18]. Here, we have focused on four different cases: a normal valve corresponding to physiological conditions in which the valve leaflets can open freely according to the hydrodynamic loads; a mild stenosis, in which only 30 % of the orifice area is blocked; a moderate stenosis where 55% of the leaflet area is blocked and a severe stenosis corresponding to a calcific obstruction of 80 % the aortic orifice area.…”

“…As a consequence, the valve leaflets kinematics along with the inflow through the valvular orifices induced by the heart chambers expansion/contraction are not imposed but are obtained as a part of the numerical results. The hemodynamics of the whole system is thus investigated in physiological and pathological conditions to highlight the alterations of the ventricular flow produced by the AS, which is modelled as previously proposed for mitral valve stenosis [18] by progressively increasing the severity of the AS from moderate to acute, according to the current risk stratification [19]. The relevant clinical parameters introduced above to assess AS severity such as the AVA, the systolic jet velocity and mean TPD are measured numerically and validated against clinical observations before studying the wall shear stresses (WSS), which can not be measured in-vivo directly .…”