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ANALYSIS OF PASSIVE FILLING WITH FIBROTIC MYOCARDIAL INFARCTION

机译:纤维性心肌梗死的被动填充分析

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Cardiovascular diseases account for one third of all deaths worldwide, more than 33% of which are related to ischemic heart disease, involving a myocardial infarction (MI). Following myocardial infarction, the injured region and ventricle undergo structural changes which are thought to be caused by elevated stresses and reduction of strains in the infarcted wall. The fibrotic phase is defined as the period when the amount of new collagen and number of fibroblasts rapidly increase in the infarcted tissue. We studied through finite element analysis the mechanics of the infarcted and remodeling rat heart during diastolic filling. Biventricular geometries of healthy and infarcted rat hearts reconstructed from magnetic resonance images were imported in Abaqus©. The passive myocardium was modelled as a nearly incompressible, hyperelastic, transversely isotropic material represented by the strain energy function W = 1/2C(e~Q - 1) with Q = b_f E_(11)~2 + b_t(E_(22)~2 + E_(33)~2 + E_(32)~2) + b_(fs)(E_(12)~2 + E_(21)~2 + E_(13)~2 + E_(31)~2). Material parameters were obtained from literature. As boundary conditions, the circumferential and longitudinal displacements at the base were set to zero. The radial displacements at the base were left free. A linearly increasing pressure from 0 to 3.80 kPa and 0.86 kPa, respectively, was applied to the endocardial surfaces of left and right ventricle. Average radial, circumferential and longitudinal strains during passive filling were -0.331, 0.135, 0.042 and -0.250, -0.078 and 0.046 for the healthy heart and the infarcted heart, respectively. The average radial, circumferential and longitudinal stresses were -1.196 kPa, 3.87 kPa in the healthy heart and 0.424 kPa and -1.90 kPa, 8.74 kPa and 1.69 kPa in the infarcted heart. The strains were considerable lower in the infarcted heart compared to the health heart whereas stresses were higher in the presence of an infarct compared to the healthy case. The results of this study indicate the feasibility of the models developed for a more comprehensive assessment of mechanics of the infarcted ventricle including extension to account for cardiac contraction.
机译:心血管疾病占全世界所有死亡的三分之一,其中超过33%与缺血性心脏病有关,涉及心肌梗塞(MI)。心肌梗塞后,受伤区域和心室发生结构变化,这被认为是由于应力增加和梗死壁应变降低而引起的。纤维化期定义为梗塞组织中新胶原蛋白的数量和成纤维细胞数量迅速增加的时期。我们通过有限元分析研究了舒张期充盈过程中梗塞和重塑大鼠心脏的力学。根据磁共振图像重建的健康和梗死大鼠心脏的双心室几何结构已导入Abaqus©。被动心肌被建模为由应变能函数W = 1 / 2C(e〜Q-1)表示的几乎不可压缩的超弹性横向各向同性材料,其中Q = b_f E_(11)〜2 + b_t(E_(22) 〜2 + E_(33)〜2 + E_(32)〜2)+ b_(fs)(E_(12)〜2 + E_(21)〜2 + E_(13)〜2 + E_(31)〜2 )。材料参数是从文献中获得的。作为边界条件,将基座的周向和纵向位移设置为零。底部的径向位移保持自由状态。分别向左心室和右心室的心内膜表面施加从0到3.80 kPa和0.86 kPa的线性增加的压力。对于健康的心脏和梗塞的心脏,被动填充过程中的平均径向,周向和纵向应变分别为-0.331、0.135、0.042和-0.250,-0.078和0.046。在健康心脏中,平均径向,圆周和纵向应力分别为-1.196 kPa,3.87 kPa和在梗死心脏中分别为0.424 kPa和-1.90 kPa,8.74 kPa和1.69 kPa。与健康心脏相比,梗死心脏中的应变要低得多,而在存在梗死区域中,应力要高得多。这项研究的结果表明,为更全面地评估梗塞心室力学机制(包括扩展以解决心脏收缩)而开发的模型的可行性。

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