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。在前游离壁 左心室中壁纤维走行的一般圆周方向 心内膜和心外膜上的方向和纤维是定向的 纵向的。心脏纤维的尖端和底部的方向发生变化 更快和相邻的瓣环影响局部肌纤维方向。 位于心肌不同深度和不同位置的纤维 相互作用产生局部变形尚不清楚。一种理论认为 单独的纤维就像滑杆一样，不会对纤维施加压力。 在心壁的不同方向。然而，心外膜变形 受其他纤维层功能的影响，以及功能的丧失 心内膜下纤维影响跨壁功能。这将是 这些研究的总体目标是定义纤维之间的关系 方向和局部变形。我们建议使用高速双翼飞机 X光和三排铅珠植入整个左心室 麻醉犬的墙。的无穷小理论的假设 将避免轴对称薄膜，并且更完整的理论 将利用三维有限变形。测量的 穿壁变形表现为0.5克四面体的主应变 会与确定的局部纤维方向进行比较 组织学上。研究将在左侧正常心脏中进行。 室壁游离壁，位于室间隔和心尖和心底附近 纤维方向变化很快。此外，研究计划在下列项目下进行 已显示为修改区域功能的条件(异常 激活序列，缺血)和慢性条件下左 脑室的形状发生了很大的变化(容量或压力过载 肥大)。预计这些研究将提供 对解剖学排列之间的关系的重大洞察 正常人和病变者的肌纤维与局部室壁变形 心。

Myocardial fiber orientation undergoes an orderly transition from epicardium to endocardium in the left ventricle. In the anterior free wall of the left ventricle midwall fibers course in a general circumferential direction and fibers on the endocardium and epicardium are oriented longitudinally. At the apex and base of the heart fiber direction changes more rapidly and adjacent valve rings influence local myofiber direction. How fibers lying at different depths and locations in the myocardium interact to produce local deformation is not known. One theory holds that individual fibers act as slippery rods and exert no force on fibers lying at different directions in the heart wall. However, epicardial deformation is influenced by the function of other fiber layers, and loss of function of subendocardial fibers effects transmural function. It will be the general objective of these studies to define the relationship between fiber direction and local deformation. We propose to utilize high speed biplane X-ray and three rows of lead beads implanted across the left ventricular wall of anesthetized dogs. Assumptions of the infinitesimal theory of axisymmetric membranes will be avoided, and the more complete theory of finite deformation in three dimensions will be utilized. Measured transmural deformation expresses as principal strains in .5 gm tetrahedron of muscle will be compared to local fiber direction determined histologically. Studies will be conducted in the normal heart in the left ventricular free wall, in the septum, and near the apex and base where fiber direction changes rapidly. Moreover, studies are planned under conditions which have been shown to modify regional function (abnormal activation sequence, ischemia) and under chronic conditions where the left ventricle undergoes large changes in shape (volume or pressure overload hypertrophy). It is anticipated that these studies will provide significant insight into the relationship between anatomic arrangement of myofibers and local ventricular deformation in the normal and diseased heart.