Lorange M, Gulrajani R M
Research Center, Hôpital du Sacré-Coeur, Montreal, Quebec, Canada.
J Electrocardiol. 1993 Oct;26(4):245-61. doi: 10.1016/0022-0736(93)90047-h.
Present-day computer models of the entire heart, capable of simulating the activation isochrones and subsequently the body surface potentials, focus on considerations of myocardial anisotropy. Myocardial anisotropy enters into play at two levels, first by affecting the spatial pattern of activation owing to faster propagation along cardiac fibers and second by altering the equivalent dipole sources used to calculate the surface potentials. The construction of a new and detailed model of the human heart is described, based on 132 transverse sections obtained following a computed tomography scan of a frozen human heart whose chambers were inflated with pressurized air. The entire heart anatomy was reconstructed as a three-dimensional array of approximately 250,000 points spaced 1 mm apart. Conduction in the thin-walled atria was assumed isotropic from the sinus node region to the atrioventricular node, where it was subject to a 50 ms delay. A two-tier representation of the specialized conduction system was used, with the initial segments of the left and right bundles represented by a system of cables that feeds to the second tier, which is a sheet of conduction tissue representing the distal Purkinje system. Approximately 1,120 "Purkinje-myocardium" junctions present at the terminations of the cables and sprinkled uniformly over the sheet, transmit the excitation to the ventricles. A stylized representation of myocardial fiber rotation was incorporated into the ventricles and the local fiber direction at each model point used to compute the velocity of propagation to its nearest neighbors. Accordingly, the activation times of the entire ventricular myocardium could be determined using the 1,120 or so Purkinje-myocardium junctions as start points. While myocardial anisotropy was considered in the ventricular propagation process, it was ignored in the computation of the equivalent dipole sources. Nevertheless, the computed electrocardiogram, vectorcardiogram, and body surface potential maps obtained with the new heart model properly positioned inside an inhomogeneous torso model were all within normal limits.
目前能够模拟激活等时线并随后模拟体表电位的全心脏计算机模型，主要关注心肌各向异性。心肌各向异性在两个层面发挥作用，首先是由于沿心肌纤维的更快传播影响激活的空间模式，其次是通过改变用于计算表面电位的等效偶极子源。本文描述了一个新的详细人体心脏模型的构建，该模型基于对一个冷冻人体心脏进行计算机断层扫描后获得的132个横断面，该心脏的腔室用压缩空气充气。整个心脏解剖结构被重建为一个三维阵列，由大约250,000个间距为1毫米的点组成。薄壁心房从窦房结区域到房室结的传导被假定为各向同性，在房室结处有50毫秒的延迟。使用了特殊传导系统的两层表示法，左右束支的起始段由一个电缆系统表示，该系统连接到第二层，第二层是代表远端浦肯野系统的传导组织片。在电缆末端均匀分布在该片上的大约1,120个“浦肯野-心肌”连接点将兴奋传递到心室。心室中纳入了心肌纤维旋转的程式化表示，并使用每个模型点处的局部纤维方向来计算向其最近邻点的传播速度。因此，可以使用大约1,120个浦肯野-心肌连接点作为起点来确定整个心室心肌的激活时间。虽然在心室传播过程中考虑了心肌各向异性，但在等效偶极子源的计算中忽略了这一点。尽管如此，将新心脏模型正确放置在非均匀躯干模型内所获得的计算心电图、向量心电图和体表电位图均在正常范围内。
