Omens J H, Covell J W
Department of Medicine, University of California San Diego, La Jolla 92093-0613.
Circulation. 1991 Sep;84(3):1235-45. doi: 10.1161/01.cir.84.3.1235.
Although chronic volume overload is thought to induce uniform cardiac enlargement, the stimulus for tissue growth has not been defined. Changes in diastolic and systolic stress or strain have been proposed as mechanical factors that may stimulate hypertrophy. Since there are thought to be transmural variations in these stresses and strains, three-dimensional patterns of myocardial tissue growth may provide insight into the role of these factors.
To assess the transmural variation in tissue growth after volume overload, the configurations of three columns of four to six gold beads (1-mm diameter) implanted in the left ventricular anterior free wall were recorded in five dogs before and after cardiac enlargement induced by creating a systemic arteriovenous fistula. Data were obtained with end-diastolic pressures adjusted to the same level in the control and hypertrophic states. End-diastolic wall thickness remained constant, whereas left ventricular diameter increased. Small increases in transmural systolic strain were seen. The volumes defined by four beads (a tetrahedron) at end diastole showed increases in myocardial mass of 20-27% after 3.6 (mean) weeks of hypertrophy and were uniform across the wall of the left ventricle. The edges of single bilinear-quadratic finite elements were fitted to the three columns of the bead set at end diastole in control and at end diastole after hypertrophy at equal end-diastolic pressures. Thus, continuous transmural strain distribution were obtained at the hypertrophic state with respect to the control state. The transmural distributions of these end-diastolic growth strains were uniform and positive for both the circumferential and longitudinal components measured in a cardiac coordinate system, with small radial growth strain indicating that growth was predominantly parallel to the epicardial tangent plane. Moreover, when strains were transformed (rotated) to fiber coordinates, in-plane fiber and cross-fiber growth strains were both positive at all locations across the wall and approximately equal in magnitude, indicating considerable growth in the cross-fiber direction.
These results indicate that the stimulus for volume-overload hypertrophy may be constant across the wall and that substantial cross-fiber growth occurs during volume-overload hypertrophy.
尽管慢性容量超负荷被认为会导致心脏均匀性增大,但组织生长的刺激因素尚未明确。舒张期和收缩期应力或应变的变化被认为是可能刺激心肌肥大的机械因素。由于这些应力和应变被认为存在跨壁差异,心肌组织生长的三维模式可能有助于深入了解这些因素的作用。
为了评估容量超负荷后组织生长的跨壁差异,在五只犬建立体循环动静脉瘘导致心脏增大前后,记录植入左心室前游离壁的三列四至六个金珠(直径1毫米)的构型。在对照和肥厚状态下,将舒张末期压力调整到相同水平获取数据。舒张末期壁厚保持不变,而左心室直径增加。观察到跨壁收缩期应变有小幅增加。在肥厚3.6(平均)周后,舒张末期由四个珠子(一个四面体)定义的体积显示心肌质量增加了20 - 27%,且在左心室壁上是均匀的。在相同的舒张末期压力下,将单双线性 - 二次有限元的边缘拟合到对照状态下舒张末期和肥厚后舒张末期的珠子组的三列上。因此,获得了相对于对照状态的肥厚状态下的连续跨壁应变分布。在心脏坐标系中测量的这些舒张末期生长应变对于圆周和纵向分量的跨壁分布都是均匀且为正的,小的径向生长应变表明生长主要平行于心外膜切线平面。此外,当应变转换(旋转)到纤维坐标系时,壁上所有位置的面内纤维和跨纤维生长应变均为正,且大小近似相等,表明跨纤维方向有显著生长。
这些结果表明,容量超负荷性肥大的刺激因素在整个心室壁上可能是恒定的,并且在容量超负荷性肥大过程中会发生大量的跨纤维生长。