Element Model Of Left Ventricle Research Articles

Recruitment from Myosin Off State Steepens ESPVR in Finite Element Model of Left Ventricle

Recruitment from Myosin Off State Steepens ESPVR in Finite Element Model of Left Ventricle

Effect of Transmural Differences in Excitation-Contraction Delay and Contraction Velocity on Left Ventricle Isovolumic Contraction: A Simulation Study.

Recent studies have shown that left ventricle (LV) exhibits considerable transmural differences in active mechanical properties induced by transmural differences in electrical activity, excitation-contraction coupling, and contractile properties of individual myocytes. It was shown that the time between electrical and mechanical activation of myocytes (electromechanical delay: EMD) decreases from subendocardium to subepicardium and, on the contrary, the myocyte shortening velocity (MSV) increases in the same direction. To investigate the physiological importance of this inhomogeneity, we developed a new finite element model of LV incorporating the observed transmural gradients in EMD and MSV. Comparative simulations with the model showed that when EMD or MSV or both were set constant across the LV wall, the LV contractility during isovolumic contraction (IVC) decreased significantly ((dp/dt)max⁡ was reduced by 2 to 38% and IVC was prolonged by 18 to 73%). This was accompanied by an increase of transmural differences in wall stress. These results suggest that the transmural differences in EMD and MSV play an important role in physiological contractility of LV by synchronising the contraction of individual layers of ventricular wall during the systole. Reduction or enhancement of these differences may therefore impair the function of LV and contribute to heart failure.

Quasi-static image-based immersed boundary-finite element model of left ventricle under diastolic loading.

Finite stress and strain analyses of the heart provide insight into the biomechanics of myocardial function and dysfunction. Herein, we describe progress toward dynamic patient-specific models of the left ventricle using an immersed boundary (IB) method with a finite element (FE) structural mechanics model. We use a structure-based hyperelastic strain-energy function to describe the passive mechanics of the ventricular myocardium, a realistic anatomical geometry reconstructed from clinical magnetic resonance images of a healthy human heart, and a rule-based fiber architecture. Numerical predictions of this IB/FE model are compared with results obtained by a commercial FE solver. We demonstrate that the IB/FE model yields results that are in good agreement with those of the conventional FE model under diastolic loading conditions, and the predictions of the LV model using either numerical method are shown to be consistent with previous computational and experimental data. These results are among the first to analyze the stress and strain predictions of IB models of ventricular mechanics, and they serve both to verify the IB/FE simulation framework and to validate the IB/FE model. Moreover, this work represents an important step toward using such models for fully dynamic fluid–structure interaction simulations of the heart. © 2014 The Authors. International Journal for Numerical Methods in Engineering published by John Wiley & Sons, Ltd.

Finite Element Analysis of Ventricular Wall Motion and Intra-Ventricular Blood Flow in Heart with Myocardial Infarction

To study the wall motion abnormality and characteristic flow distribution observed in the heart with myocardial infarction, we modified our finite element model of left ventricle and performed simulations at two different phases after the onset of the disease by applying characteristic material property to the infarcted region. The model could not only reproduce the hemodynamic change in myocardial infarction but also give mechanistic insight into the following complicating problems. 1) Stagnation of blood as the cause of clot formation 2) Extra energy wasted for the stretch of infarcted tissue. The effect of compensatory enhancement of the force generation in normal myocardial tissue is also discussed.

心筋梗塞における壁運動および心腔内血流の流体構造連成有限要素解析(OS20b 流体構造連成解析)

To study the wall motion abnormality and characteristic flow distribution observed in the heart with myocardial infarction, we modified our finite element model of left ventricle and performed simulations at two different phases after the onset of the disease by applying characteristic material property to the infarcted region. The model could not only reproduce the hemodynamic change in myocardial infarction but also give mechanistic insight into the following complicating problems. 1) Stagnation of blood as the cause of clot formation 2) Extra energy wasted for the stretch of infarcted tissue. The effect of compensatory enhancement of the force generation in normal myocardial tissue is also discussed.

Finite element model of left ventricle: Mechanical effects of acute ischemia: [formula omitted]. Depts. of Medicine and AMES/Bioengineering, Univ. of Calif., San Diego, La Jolla, CA 92093

Finite element model of left ventricle: Mechanical effects of acute ischemia: [formula omitted]. Depts. of Medicine and AMES/Bioengineering, Univ. of Calif., San Diego, La Jolla, CA 92093