TRANSMURAL DEFORMATION

描述（改编自申请人摘要）：细胞增厚 占正常左室壁的不到三分之一 增厚沿着解理面的Sycester变形 纹层将产生横向剪切应变。显著的径向 纵向和径向周向收缩剪切变形， 最近发现，使用有限变形方法开发的 调查员的实验室。在最近的研究中， 这些纹层之间的剪切变形产生 壁增厚他利用了这个事实， 隔膜和左心室上不同方向的行程 自由墙研究者发现，剪切变形是 两个部位的符号相反，壁增厚与 初始解理面角。这些结果有力地支持了他的 心肌细胞放射状板层运动假说 产生壁增厚。在这个建议中，建模和实验 研究将被用来探索这种独特的机制墙 增厚研究人员将检验这一假设，即它是 独特的非轴对称心室结构和心内膜- 心外膜激活序列产生剪切。进一步研究 将探讨血流动力学因素对横向剪切的调节作用 以及在中观察到的卵裂平面解剖结构变化的影响， 心室重构和肥厚对室壁的这种机制 增厚

DESCRIPTION (adapted from the applicant's abstract): Cell thickening accounts for less then one third of normal left ventricular wall thickening. Systolic deformation along the cleavage planes separating the laminae would produce transverse shear strains. Significant radial longitudinal and radial circumferential systolic shearing deformation has recently been found using a finite deformation approach developed in the investigator s laboratory. In recent studies the investigator explored the hypothesis that shearing deformation between these laminae produces wall thickening. He took advantage of the fact that the cleavage planes course in different directions on the septum and the left ventricular free wall. The investigator found that shearing deformation was of the opposite sign at the two sites and wall thickening was proportional to the initial cleavage plane angle. These results strongly support his hypothesis that motion of radially orientated laminae of myocytes produces wall thickening. In this proposal, modeling and experimental studies will be used to explore this unique mechanism of wall thickening. The investigator will test the hypothesis that it is the unique nonaxisymmetric ventricular architecture and endocardial-to- epicardial activation sequence that produce the shears. Further studies will explore the regulation of transverse shears by hemodynamic factors and the effects of changes in cleavage plane anatomy observed in ventricular remodeling and hypertrophy on this mechanism of wall thickening.