Villarreal F J, Lew W Y, Waldman L K, Covell J W
Department of Medicine, Veterans Administration Medical Center, San Diego, Calif.
Circ Res. 1991 Feb;68(2):368-81. doi: 10.1161/01.res.68.2.368.
The myocardium is a complex three-dimensional structure consisting of myocytes interconnected by a dense collagen weave that courses in different directions. Regional ischemia can be expected to produce complex changes in ventricular deformation. In the present study, we examined the effects of ischemia on two- and three-dimensional finite strains during acute transmural myocardial ischemia in 13 open-chest anesthetized dogs. In contrast to systolic deformation observed during the control period in which circumferential shortening exceeded longitudinal shortening, our results indicate that after 5 minutes of acute ischemia, end-systolic in-plane lengthening across the left ventricular wall occurs in approximately equal amounts in the circumferential and longitudinal directions. Along with these changes in extensional strains, there were significant negative transverse shearing deformations during ischemia. Myocardial ischemia also resulted in a loss of the normal end-systolic transmural gradients of shortening and thickening. Three-dimensional end-diastolic strains indicate that the left ventricular wall undergoes a significant passive reconfiguration that varies transmurally with lengthening in the epicardial tangent plane and wall thinning increasing from the epicardium toward the endocardium. The large systolic changes in shearing deformations with ischemia could potentially influence collateral blood flow and certainly indicate that uniaxial measurements of deformation in the ischemic myocardium, which do not account for shearing deformation, are incomplete and must be interpreted with caution. Moreover, normal transmural systolic gradients in deformation, which would be anticipated on geometric grounds, are lost during ischemia, implying that the material properties of ischemic tissue or the loading conditions imposed on the ischemic region by partially impaired adjacent myocardium vary transmurally.
心肌是一种复杂的三维结构,由通过致密胶原纤维网相互连接的心肌细胞组成,这些纤维网呈不同方向分布。局部缺血预计会导致心室变形的复杂变化。在本研究中,我们在13只开胸麻醉犬的急性透壁心肌缺血过程中,研究了缺血对二维和三维有限应变的影响。与对照期观察到的收缩期变形相反,对照期圆周缩短超过纵向缩短,我们的结果表明,急性缺血5分钟后,左心室壁在收缩末期平面内的伸长在圆周方向和纵向方向上大致相等。随着这些拉伸应变的变化,缺血期间出现了显著的负横向剪切变形。心肌缺血还导致收缩末期正常的跨壁缩短和增厚梯度丧失。三维舒张末期应变表明,左心室壁发生了显著的被动重构,其跨壁变化表现为心外膜切线平面的伸长以及从心外膜向心内膜方向的壁变薄增加。缺血时剪切变形的大收缩期变化可能会影响侧支血流,并且肯定表明在缺血心肌中不考虑剪切变形的单轴变形测量是不完整的,必须谨慎解释。此外,基于几何原理预期的正常跨壁收缩期变形梯度在缺血期间丧失,这意味着缺血组织的材料特性或部分受损的相邻心肌施加在缺血区域的加载条件跨壁变化。