TRANSMURAL DEFORMATION

心肌纤维取向经历了有序的转变， 从心外膜到左心室内膜 垂体前 游离壁中壁纤维层通常沿周向 心内膜和心外膜上的方向和纤维， 更纵向地定向。 在顶端和基部，纤维 方向变化更快，相邻的阀环影响 局部肌纤维方向。 不同深度的纤维 心室部位相互作用产生局部变形， 明白 这些研究的总目标是， 定义纤维方向和局部 变形 我们发明了一种方法第三步- 来自双平面射线照相图像的三维有限变形 植入标记物来划分小体积的心肌。 对自由壁的初步研究表明， 在相邻光纤之间，即，主应变增加， 深度，显著的横向剪切伴随着法向应变， 以及第一主轴的取向（第二主轴的方向）。 最大缩短）的跨壁变化远小于纤维 方向 此外，应变方向可以被修改 基本上通过心外膜激活 具有局部纤维方向。 这些发现驳斥了 心肌变形为一组非相互作用的嵌套 膜，每个膜都有自己的优选取向。 的 横向剪切的大小和方向 观察到的主要菌株要求细胞重排 Spotnitz提出的心外膜切面外，或 细胞形状的变化，以解释变形和 细胞壁增厚不能用细胞直径的变化来解释 心脏收缩期。 本建议中的研究针对的是 定量肌纤维解剖结构可以解释观察到的 透壁变形，并应提供新的见解， 心室壁增厚的机制。 进一步的研究 计划在负荷条件的慢性增加的影响 关于透壁变形

Myocardial fiber orientation undergoes an orderly transition from epicardium to endocardium in the left ventricle. In the anterior free wall midwall fibers course in a generally circumferential direction and fibers on the endocardium and epicardium are oriented more longitudinally. At the apex and base, fiber direction changes more rapidly and adjacent valve rings influence local myofiber direction. How fibers at different depths and ventricular sites interact to produce local deformation is not fully understood. It will be the general objective of these studies to define the relationship between fiber direction and local deformation. We have developed a method a measure three- dimensional finite deformations from biplane radiographic images of implanted markers demarcating small volumes of myocardium. Initial studies in the free wall indicate substantial interaction between adjacent fibers, i.e., principal strains increase with depth, significant transverse shear accompanies normal strains, and the orientation of the first principal axis (direction of greatest shortening) varies transmurally much less than fiber direction. Moreover, strain direction can be modified substantially by epicardial activation and may not be colinear with local fiber direction. These findings refute the theory that myocardium deforms as a set of noninteracting nested membranes, each with its own preferred orientation. The magnitudes of the transverse shears and directions of the principal strains observed demand either cellular rearrangements out of the epicardial tangent plane as proposed by Spotnitz or cellular shape changes to account for the deformations and the wall thickening not explained by cell diameter changes occurring during systole. The studies in the present proposal are directed at quantitating the myofiber anatomy can account for the observed transmural deformation and should provide new insight into the mechanism of ventricular wall thickening. Further studies are planned on the effects of chronic increases in loading conditions on transmural deformation.