TRANSMURAL DEFORMATION

心肌纤维取向经历了有序的转变 左心室的心外膜到心内膜。在前部 游离壁中壁纤维大致沿圆周方向运动 心内膜和心外膜上的方向和纤维是 更纵向的定向的。在顶端和底部，纤维 方向变化更快，相邻的阀环影响 局部肌纤维方向。不同深度的纤维和 室壁部位相互作用产生局部变形不完全 明白了。这些研究的总体目标将是 定义纤维方向和局部之间的关系 变形。我们已经开发出了一种方法，一种措施，三 双平面射线照相图像的有限维变形 植入的标记物界定了小体积的心肌。 自由壁的初步研究表明存在大量的相互作用 相邻纤维之间的应变，即主应变随 深度，显著的横向剪切伴随着正常应变， 和第一主轴的方向(方向 最大缩短)比纤维变化小得多 方向。此外，还可以修改应变方向 基本上通过心外膜激活，可能不是共线的 具有局部纤维方向。这些发现驳斥了这样的理论 心肌变形为一组非相互作用的嵌套 膜，每个膜都有自己的首选取向。这个 横向剪力的大小和方向 观察到的主要菌株要求要么细胞重排 根据Spotnitz或 细胞形状发生变化，以解决变形和 壁厚不能用细胞直径变化来解释 在收缩期间。本提案中的研究针对的是 量化肌纤维解剖可以解释观察到的 跨壁变形，应该提供新的洞察力 室壁增厚的机制。进一步的研究是 根据负荷条件的长期增加的影响而计划的 论跨壁变形。

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.