Patients with aortic stenosis present with calcium deposits on the native aortic valve, which can result in non-concentric expansion of Transcatheter Aortic Valve Replacement (TAVR) stents. The objective of this study is to evaluate whether eccentric deployment of TAVRs lead to turbulent blood flow and blood cell damage. Particle Image Velocimetry was used to quantitatively characterize fluid velocity fields, shear stress and turbulent kinetic energy downstream of TAVRs deployed in circular and eccentric orifices representative of deployed TAVRs in vivo. Effective orifice area (EOA) and mean transvalvular pressure gradient (TVG) values did not differ substantially in circular and eccentric deployed valves, with only a minor decrease in EOA observed in the eccentric valve (2.0 cm(2) for circular, 1.9 cm(2) for eccentric). Eccentric deployed TAVR lead to asymmetric systolic jet formation, with increased shear stresses (circular = 97 N/m(2) vs. eccentric = 119 N/m(2)) and regions of turbulence intensity (circular = 180 N/m(2) vs. eccentric = 230 N/m(2)) downstream that was not present in the circular deployed TAVR. The results of this study indicate that eccentric deployment of TAVRs can lead to altered flow characteristics and may potentially increase the hemolytic potential of the valve, which were not captured through hemodynamic evaluation alone.
Aortic valve (AV) calcification is a highly prevalent disease with serious impact on mortality and morbidity. Although exact causes and mechanisms of AV calcification are unclear, previous studies suggest that mechanical forces play a role. Since calcium deposits occur almost exclusively on the aortic surfaces of AV leaflets, it has been hypothesized that adverse patterns of fluid shear stress on the aortic surface of AV leaflets promote calcification. The current study characterizes AV leaflet aortic surface fluid shear stresses using Laser Doppler velocimetry and an in vitro pulsatile flow loop. The valve model used was a native porcine valve mounted on a suturing ring and preserved using 0.15% glutaraldehyde solution. This valve model was inserted in a mounting chamber with sinus geometries, which is made of clear acrylic to provide optical access for measurements. To understand the effects of hemodynamics on fluid shear stress, shear stress was measured across a range of conditions: varying stroke volumes at the same heart rate and varying heart rates at the same stroke volume. Systolic shear stress magnitude was found to be much higher than diastolic shear stress magnitude due to the stronger flow in the sinuses during systole, reaching up to 20 dyn/cm2 at mid-systole. Upon increasing stroke volume, fluid shear stresses increased due to stronger sinus fluid motion. Upon increasing heart rate, fluid shear stresses decreased due to reduced systolic duration that restricted the formation of strong sinus flow. Significant changes in the shear stress waveform were observed at 90 beats/ min, most likely due to altered leaflet dynamics at this higher heart rate. Overall, this study represents the most well-resolved shear stress measurements to date across a range of conditions on the aortic side of the AV. The data presented can be used for further investigation to understand AV biological response to shear stresses.
The congenital bicuspid aortic valve (BAV) is associated with increased leaflet calcification, ascending aortic dilatation, aortic stenosis (AS) and regurgitation (AR). Although underlying genetic factors have been primarily implicated for these complications, the altered mechanical environment of BAVs could potentially accelerate these pathologies. The objective of the current study is to characterize BAV hemodynamics in an in vitro system. Two BAV models of varying stenosis and jet eccentricity and a trileaflet AV (TAV) were constructed from excised porcine AVs. Particle Image Velocimetry (PIV) experiments were conducted at physiological flow and pressure conditions to characterize fluid velocity fields in the aorta and sinus regions, and ensemble averaged Reynolds shear stress and 2D turbulent kinetic energy were calculated for all models. The dynamics of the BAV and TAV models matched the characteristics of these valves which are observed clinically. The eccentric and stenotic BAV showed the strongest systolic jet (V = 4.2 m/s), which impinged on the aortic wall on the non-fused leaflet side, causing a strong vortex in the non-fused leaflet sinus. The magnitudes of TKE and Reynolds stresses in both BAV models were almost twice as large as comparable values for TAV, and these maximum values were primarily concentrated around the central jet through the valve orifice. The in vitro model described here enables detailed characterization of BAV flow characteristics, which is currently challenging in clinical practice. This model can prove to be useful in studying the effects of altered BAV geometry on fluid dynamics in the valve and ascending aorta. These altered flows can be potentially linked to increased calcific responses from the valve endothelium in stenotic and eccentric BAVs, independent of concomitant genetic factors.
Aortic valve (AV) calcification is a highly prevalent disease with serious impact on mortality and morbidity. The exact causes and mechanisms of AV calcification are unclear, although previous studies suggest that mechanical forces play a role. It has been clinically demonstrated that calcification preferentially occurs on the aortic surface of the AV. This is hypothesized to be due to differences in the mechanical environments on the two sides of the valve. It is thus necessary to characterize fluid shear forces acting on both sides of the leaflet to test this hypothesis. The current study is one of two studies characterizing dynamic shear stress on both sides of the AV leaflets. In the current study, shear stresses on the ventricular surface of the AV leaflets were measured experimentally on two prosthetic AV models with transparent leaflets in an in vitro pulsatile flow loop using two-component Laser Doppler Velocimetry (LDV). Experimental measurements were utilized to validate a theoretical model of AV ventricular surface shear stress based on the Womersley profile in a straight tube, with corrections for the opening angle of the valve leaflets. This theoretical model was applied to in vivo data based on MRI-derived volumetric flow rates and valve dimension obtained from the literature. Experimental results showed that ventricular surface shear stress was dominated by the streamwise component. The systolic shear stress waveform resembled a half-sinusoid during systole and peaks at 64–71 dyn/cm2, and reversed in direction at the end of systole for 15–25 ms, and reached a significant negative magnitude of 40–51 dyn/cm2. Shear stresses from the theoretical model applied to in vivo data showed that shear stresses peaked at 77–92 dyn/cm2 and reversed in direction for substantial period of time (108–110 ms) during late systole with peak negative shear stress of 35–38 dyn/cm2.
Background This study was undertaken to evaluate an in vitro mitral valve simulator's ability to mimic the systolic leaflet coaptation, regurgitation, and leaflet mechanics of a healthy and chronic ischemic mitral regurgitation (IMR) ovine model. Methods Mitral valve size and geometry of both healthy and chronic IMR ovine animals was used to recreate systolic mitral valve function in vitro. A2-P2 coaptation length, coaptation depth, tenting area, anterior leaflet strain, and mitral regurgitation were compared between the animal groups and valves simulated in the bench-top model. Results For the control conditions, no differences were observed between the healthy animals and simulator in coaptation length (p=.681), coaptation depth (p=.559), tenting area (p=.199), and anterior leaflet strain in the radial (p=.230) and circumferential (p=.364) directions. For the chronic IMR conditions, no differences were observed between the models in coaptation length (p=.596), coaptation depth (p=.621), tenting area (p=.879), and anterior leaflet strain in the radial (p=.151) and circumferential (p=.586) directions. Mitral regurgitation was similar between IMR models with an asymmetric jet originating from the tethered A3-P3 leaflets. Conclusion This study is the first to demonstrate the effectiveness of an in vitro simulator to emulate the systolic valvular function and mechanics of a healthy and chronic IMR ovine model. The in vitro IMR model provides the capability to recreate intermediary and exacerbated levels of annular and subvalvular distortion at which IMR repairs can be simulated. This system provides a realistic and controllable test platform for the development and evaluation of current and future IMR repairs.
Numerical models of the mitral valve have been used to elucidate mitral valve function and mechanics. These models have evolved from simple two-dimensional approximations to complex three-dimensional fully coupled fluid structure interaction models. However, to date these models lack direct one-to-one experimental validation. As computational solvers vary considerably, experimental benchmark data are critically important to ensure model accuracy. In this study, a novel left heart simulator was designed specifically for the validation of numerical mitral valve models. Several distinct experimental techniques were collectively performed to resolve mitral valve geometry and hemodynamics. In particular, micro-computed tomography was used to obtain accurate and high-resolution (39 µm voxel) native valvular anatomy, which included the mitral leaflets, chordae tendinae, and papillary muscles. Threedimensional echocardiography was used to obtain systolic leaflet geometry for direct comparison of resultant leaflet kinematics. Stereoscopic digital particle image velocimetry provided all three components of fluid velocity through the mitral valve, resolved every 25 ms in the cardiac cycle. A strong central filling jet was observed during peak systole, with minimal out-of-plane velocities (V~0.6m/s). In addition, physiologic hemodynamic boundary conditions were defined and all data were synchronously acquired through a central trigger. Finally, the simulator is a precisely controlled environment, in which flow conditions and geometry can be systematically prescribed and resultant valvular function and hemodynamics assessed. Thus, these data represent the first comprehensive database of high fidelity experimental data, critical for extensive validation of mitral valve fluid structure interaction simulations.
The mitral valve is a complex apparatus with multiple constituents that work cohesively to ensure unidirectional flow between the left atrium and ventricle. Disruption to any or all of the components-the annulus, leaflets, chordae, and papillary muscles-can lead to backflow of blood, or regurgitation, into the left atrium, which deleteriously effects patient health. Through the years, a myriad of surgical repairs have been proposed; however, a careful appreciation for the underlying structural mechanics can help optimize long-term repair durability and inform medical device design. In this review, we aim to present the experimental methods and significant results that have shaped the current understanding of mitral valve mechanics. Data will be presented for all components of the mitral valve apparatus in control, pathological, and repaired conditions from human, animal, and in vitro studies. Finally, current strategies of patient specific and noninvasive surgical planning will be critically outlined.
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