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Andrew W. Siefert

Bio: Andrew W. Siefert is an academic researcher from The Wallace H. Coulter Department of Biomedical Engineering. The author has contributed to research in topics: Mitral valve & Mitral valve repair. The author has an hindex of 12, co-authored 28 publications receiving 323 citations. Previous affiliations of Andrew W. Siefert include Exponent & Georgia Institute of Technology.

Papers
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Journal ArticleDOI
TL;DR: 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 ovine model and one with chronic IMR.

33 citations

Journal ArticleDOI
TL;DR: This review aims to present the experimental methods and significant results that have shaped the current understanding of mitral valve mechanics and current strategies of patient specific and noninvasive surgical planning.
Abstract: 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.

31 citations

Journal ArticleDOI
TL;DR: In this paper, a ground-truth data set was generated by quantifying the isolated effects of IMR and mitral annuloplasty on leaflet coaptation, regurgitation, and tethering forces of the anterior strut and posterior intermediary chordae tendineae.
Abstract: Computational models of the heart’s mitral valve (MV) exhibit potential for preoperative surgical planning in ischemic mitral regurgitation (IMR) However challenges exist in defining boundary conditions to accurately model the function and response of the chordae tendineae to both IMR and surgical annuloplasty repair Towards this goal, a ground-truth data set was generated by quantifying the isolated effects of IMR and mitral annuloplasty on leaflet coaptation, regurgitation, and tethering forces of the anterior strut and posterior intermediary chordae tendineae MVs were excised from ovine hearts (N = 15) and mounted in a pulsatile heart simulator which has been demonstrated to mimic the systolic MV geometry and coaptation of healthy and chronic IMR sheep Strut and intermediary chordae from both MV leaflets (N = 4) were instrumented with force transducers Tested conditions included a healthy control, IMR, oversized annuloplasty, true-sized annuloplasty, and undersized mitral annuloplasty A2-P2 leaflet coaptation length, regurgitation, and chordal tethering were quantified and statistically compared across experimental conditions MR was successfully simulated with significant increases in MR, tethering forces for each of the chordae, and decrease in leaflet coaptation (p < 05) Compared to the IMR condition, increasing levels of downsized annuloplasty significantly reduced regurgitation, increased coaptation, reduced posteromedial papillary muscle strut chordal forces, and reduced intermediary chordal forces from the anterolateral papillary muscle (p < 05) These results provide for the first time a novel comprehensive data set for refining the ability of computational MV models to simulate IMR and varying sizes of complete rigid ring annuloplasty

28 citations

Journal ArticleDOI
TL;DR: Despite lower cyclic loading on posterior sutures, the weaker posterior mitral annular tissue creates higher risk of dehiscence, apparently because of reduced collagen content.

28 citations

Journal ArticleDOI
TL;DR: Differences in force magnitude and rate for increasing levels of LVP between the septal-lateral and transverse directions have strong implications in the development of future mitral devices.

25 citations


Cited by
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Journal ArticleDOI
TL;DR: The current understanding of flow phenomena induced by heart valves are summarized, their linkage with disease pathways are discussed, and the research advances required to translate in-depth understanding of valvular hemodynamics into effective patient treatment are emphasized.
Abstract: As the pulsatile cardiac blood flow drives the heart valve leaflets to open and close, the flow in the vicinity of the valve resembles a pulsed jet through a nonaxisymmetric orifice with a dynamically changing area. As a result, three-dimensional vortex rings with intricate topology emerge that interact with the complex cardiac anatomy and give rise to shear layers, regions of recirculation, and flow instabilities that could ultimately lead to transition to turbulence. Such complex flow patterns, which are inherently valve- and patient-specific, lead to mechanical forces at scales that can cause blood cell damage and thrombosis, increasing the likelihood of stroke, and can trigger the pathogenesis of various life-threatening valvular heart diseases. We summarize the current understanding of flow phenomena induced by heart valves, discuss their linkage with disease pathways, and emphasize the research advances required to translate in-depth understanding of valvular hemodynamics into effective patient ther...

114 citations

Journal ArticleDOI
TL;DR: The developed computational framework may be useful in optimizing TAV design parameters to improve leaflet durability, and assessing the effects of underexpanded, elliptical, or non-uniformly expanded stent deployment on TAV durability.

94 citations

Journal ArticleDOI
TL;DR: This study identifies the in vivo material parameters for three common hyperelastic models for mitral valve tissue, an isotropic one and two anisotropic ones, using an inverse finite element approach and shows that the identified parameter values are highly sensitive to prestrain.
Abstract: Alterations in mitral valve mechanics are classical indicators of valvular heart disease, such as mitral valve prolapse, mitral regurgitation, and mitral stenosis. Computational modeling is a powerful technique to quantify these alterations, to explore mitral valve physiology and pathology, and to classify the impact of novel treatment strategies. The selection of the appropriate constitutive model and the choice of its material parameters are paramount to the success of these models. However, the in vivo parameters values for these models are unknown. Here, we identify the in vivo material parameters for three common hyperelastic models for mitral valve tissue, an isotropic one and two anisotropic ones, using an inverse finite element approach. We demonstrate that the two anisotropic models provide an excellent fit to the in vivo data, with local displacement errors in the sub-millimeter range. In a complementary sensitivity analysis, we show that the identified parameter values are highly sensitive to prestrain, with some parameters varying up to four orders of magnitude. For the coupled anisotropic model, the stiffness varied from 119,021 kPa at 0 % prestrain via 36 kPa at 30 % prestrain to 9 kPa at 60 % prestrain. These results may, at least in part, explain the discrepancy between previously reported ex vivo and in vivo measurements of mitral leaflet stiffness. We believe that our study provides valuable guidelines for modeling mitral valve mechanics, selecting appropriate constitutive models, and choosing physiologically meaningful parameter values. Future studies will be necessary to experimentally and computationally investigate prestrain, to verify its existence, to quantify its magnitude, and to clarify its role in mitral valve mechanics.

76 citations

OtherDOI
TL;DR: Various mechanical models to determine wall stress and cardiac function in normal and diseased hearts with both systolic and diastolic dysfunction are discussed and the results have enhanced the understanding of the biomechanical mechanism in the development and remodeling of normal and dysfunctional hearts.
Abstract: The heart pumps blood to maintain circulation and ensure the delivery of oxygenated blood to all the organs of the body. Mechanics play a critical role in governing and regulating heart function under both normal and pathological conditions. Biological processes and mechanical stress are coupled together in regulating myocyte function and extracellular matrix structure thus controlling heart function. Here, we offer a brief introduction to the biomechanics of left ventricular function and then summarize recent progress in the study of the effects of mechanical stress on ventricular wall remodeling and cardiac function as well as the effects of wall mechanical properties on cardiac function in normal and dysfunctional hearts. Various mechanical models to determine wall stress and cardiac function in normal and diseased hearts with both systolic and diastolic dysfunction are discussed. The results of these studies have enhanced our understanding of the biomechanical mechanism in the development and remodeling of normal and dysfunctional hearts. Biomechanics provide a tool to understand the mechanism of left ventricular remodeling in diastolic and systolic dysfunction and guidance in designing and developing new treatments.

67 citations