Left Ventricular Wall Stress in Patients With Severe Aortic Insufficiency With Finite Element Analysis

Wollmuth, Jason; Bree, Douglas R.; Cupps, Brian P.; Krock, Marc D.; Pomerantz, Benjamin J.; Pasque, Robert P.; Howells, Analyn; Moazami, Nader; Kouchoukos, Nicholas T.; Pasque, Michael K.

doi:10.1016/j.athoracsur.2006.03.100

Cited by 13 publications

(6 citation statements)

References 17 publications

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“…The ability to create patient-specific finite element models would offer more accurate wall-stress results, as well as more insight into the ventricular pathophysiology. One of the earliest published finite element studies exploring the link between aortic valve pathology and LV stress was done on aortic insufficiency patients (Wollmuth et al, 2006). Patient-specific LV geometries were obtained from cardiac magnetic resonance imaging in patients with moderate-severe aortic insufficiency before and after aortic valve replacement, as well as in control volunteers without aortic valve disease.…”

Section: Discussionmentioning

confidence: 99%

Impact of Aortic Stenosis on Myofiber Stress: Translational Application of Left Ventricle-Aortic Coupling Simulation

et al. 2020

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The severity of aortic stenosis (AS) has traditionally been graded by measuring hemodynamic parameters of transvalvular pressure gradient, ejection jet velocity, or estimating valve orifice area. Recent research has highlighted limitations of these criteria at effectively grading AS in presence of left ventricle (LV) dysfunction. We hypothesized that simulations coupling the aorta and LV could provide meaningful insight into myocardial biomechanical derangements that accompany AS. A realistic finite element model of the human heart with a coupled lumped-parameter circulatory system was used to simulate AS. Finite element analysis was performed with Abaqus FEA. An anisotropic hyperelastic model was assigned to LV passive properties, and a time-varying elastance function governed the LV active response. Global LV myofiber peak systolic stress (mean ± standard deviation) was 9.31 ± 10.33 kPa at baseline, 13.13 ± 10.29 kPa for moderate AS, and 16.18 ± 10.59 kPa for severe AS. Mean LV myofiber peak systolic strains were −22.40 ± 8.73%, −22.24 ± 8.91%, and −21.97 ± 9.18%, respectively. Stress was significantly elevated compared to baseline for moderate (p < 0.01) and severe AS (p < 0.001), and when compared to each other (p < 0.01). Ventricular regions that experienced the greatest systolic stress were (severe AS vs. baseline) basal inferior (39.87 vs. 30.02 kPa; p < 0.01), mid-anteroseptal (32.29 vs. 24.79 kPa; p < 0.001), and apex (27.99 vs. 23.52 kPa; p < 0.001). This data serves as a reference for future studies that will incorporate patient-specific ventricular geometries and material parameters, aiming to correlate LV biomechanics to AS severity.

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Section: Discussionmentioning

confidence: 99%

Impact of Aortic Stenosis on Myofiber Stress: Translational Application of Left Ventricle-Aortic Coupling Simulation

et al. 2020

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“…The reduced hypertrophy occurred in the face of identical LV/aortic pressure gradients, and was likely due to the reduced LV wall stress in the CI group. The reduced wall stress is one mechanism by which LVEF was maintained in the CI group, since there is an inverse relationship between LV wall stress and LVEF [31]. The reduced LVH is another mechanism contributing to the preserved LV function, since LVH, per se, can impair cardiac function [17].…”

Section: Discussionmentioning

confidence: 99%

Novel mechanisms for caspase inhibition protecting cardiac function with chronic pressure overload

Park¹,

Vatner²,

Yan³

et al. 2013

Basic Res Cardiol

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Myocyte apoptosis is considered a major mechanism in the pathogenesis of heart failure. Accordingly, manipulations that inhibit apoptosis are assumed to preserve cardiac function by maintaining myocyte numbers. We tested this assumption by examining the effects of caspase inhibition (CI) on cardiac structure and function in C57BL/6 mouse with pressure overload model induced by transverse aortic constriction (TAC). CI preserved left ventricular (LV) function following TAC compared with the vehicle. TAC increased apoptosis in non-myocytes more than in myocytes and these increases were blunted more in non-myocytes by CI. Total myocyte number, however, did not differ significantly among control and TAC groups and there was no correlation between myocyte number and apoptosis, but there was a strong correlation between myocyte number and an index of myocyte proliferation, Ki67-positive myocytes. Despite comparable pressure gradients, LV hypertrophy was less in the CI group, likely attributable to decreased wall stress. Since changes in myocyte numbers did not account for protection from TAC, several other CI-mediated mechanisms were identified including: (a) lessening of TAC-induced fibrosis, (b) augmentation of isolated myocyte contractility, and (c) increased angiogenesis and Ki67-positive myocytes, which were due almost entirely to the non-myocyte apoptosis, but not myocyte apoptosis, with CI. CI maintained LV function following TAC not by protecting against myocyte loss, but rather by augmenting myocyte contractile function, myocyte proliferation, and angiogenesis resulting in reduced LV wall stress, hypertrophy, and fibrosis.

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“…Some groups have used CMR data to model wall stress and these types of analysis may ultimately yield novel insights into the pathophysiology of AR 43. The use of CMR can be also used to evaluate dynamic changes in peripheral vasculature such as aortic compliance, and may yield insights into some of the heterogeneity of the presentation of AR and why there can be discrepancies with the echocardiographic integrative approach 44…”

Section: Future Directionsmentioning

confidence: 99%

Evaluation of aortic regurgitation with cardiac magnetic resonance imaging: a systematic review

Lee

Branch

Hamilton-Craig

et al. 2017

Heart

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This review summaries the utility, application and data supporting use of cardiac magnetic resonance imaging (CMR) to evaluate and quantitate aortic regurgitation. We systematically searched Medline and PubMed for original research articles published since 2000 that provided data on the quantitation of aortic regurgitation by CMR and identified 11 articles for review. Direct aortic measurements using phase contrast allow quantitation of volumetric flow across the aortic valve and are highly reproducible and accurate compared with echocardiography. However, this technique requires diligence in prescribing the correct imaging planes in the aorta. Volumetric analytic techniques using differences in ventricular volumes are also highly accurate but less than phase contrast techniques and only accurate when concomitant valvular disease is absent. Comparison of both aortic and ventricular data for internal data verification ensures fidelity of aortic regurgitant data. CMR data can be applied to many types of aortic valve regurgitation including combined aortic stenosis with regurgitation, congenital valve diseases and post-transcatheter valve placement. CMR also predicts those patients who progress to surgery with high overall sensitivity and specificity. Future studies of CMR in patients with aortic regurgitation to quantify the incremental benefit over echocardiography as well as prediction of cardiovascular events are warranted.

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Left Ventricular Wall Stress in Patients With Severe Aortic Insufficiency With Finite Element Analysis

Cited by 13 publications

References 17 publications

Impact of Aortic Stenosis on Myofiber Stress: Translational Application of Left Ventricle-Aortic Coupling Simulation

Impact of Aortic Stenosis on Myofiber Stress: Translational Application of Left Ventricle-Aortic Coupling Simulation

Novel mechanisms for caspase inhibition protecting cardiac function with chronic pressure overload

Evaluation of aortic regurgitation with cardiac magnetic resonance imaging: a systematic review

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