Wisneski Andrew D, Wang Yunjie, Deuse Tobias, Hill Arthur C, Pasta Salvatore, Sack Kevin L, Yao Jiang, Guccione Julius M
Department of Surgery, University of California, San Francisco, San Francisco, CA, United States.
Thornton Tomassetti Lifesciences Division, Santa Clara, CA, United States.
Front Physiol. 2020 Sep 8;11:574211. doi: 10.3389/fphys.2020.574211. eCollection 2020.
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 ( < 0.01) and severe AS ( < 0.001), and when compared to each other ( < 0.01). Ventricular regions that experienced the greatest systolic stress were (severe AS vs. baseline) basal inferior (39.87 vs. 30.02 kPa; < 0.01), mid-anteroseptal (32.29 vs. 24.79 kPa; < 0.001), and apex (27.99 vs. 23.52 kPa; < 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.
传统上,主动脉瓣狭窄(AS)的严重程度是通过测量跨瓣压力梯度、射血喷射速度等血流动力学参数,或估算瓣口面积来分级的。最近的研究强调了这些标准在左心室(LV)功能障碍情况下有效分级AS的局限性。我们假设,将主动脉和左心室耦合的模拟可以为伴随AS的心肌生物力学紊乱提供有意义的见解。使用具有耦合集总参数循环系统的真实人体心脏有限元模型来模拟AS。使用Abaqus有限元分析软件进行有限元分析。为左心室的被动特性指定了各向异性超弹性模型,并使用时变弹性函数来控制左心室的主动反应。左心室整体肌纤维的峰值收缩期应力(平均值±标准差)在基线时为9.31±10.33kPa,中度AS时为13.13±10.29kPa,重度AS时为16.18±10.59kPa。左心室肌纤维的平均峰值收缩期应变分别为-22.40±8.73%、-22.24±8.91%和-21.97±9.18%。与基线相比,中度(<0.01)和重度AS(<0.001)时应力显著升高,且两者之间相比(<0.01)也显著升高。经历最大收缩期应力的心室区域为(重度AS与基线相比)基底下部(39.87对30.02kPa;<0.01)、室间隔中部前壁(32.29对24.79kPa;<0.001)和心尖(27.99对23.52kPa;<0.001)。这些数据为未来的研究提供了参考,这些研究将纳入患者特异性的心室几何形状和材料参数,旨在将左心室生物力学与AS严重程度相关联。