Fast V G, Kléber A G
Department of Physiology, University of Berne, Switzerland.
Cardiovasc Res. 1995 Sep;30(3):449-59.
Unidirectional conduction block in the heart can occur at a site where the impulse is transmitted from a small to a large tissue volume. The aim of this study was to evaluate the occurrence of conduction block in a 2-dimensional and 3-dimensional computer model of cardiac tissue consisting of a narrow strand abruptly emerging into a large area. In this structure, the strand diameter critical for the occurrence of block, hc, was evaluated as a function of changes in the active and passive electrical properties of both the strand and the large medium.
The effects of changes in the following parameters on hc were analysed: (1) maximum sodium conductance (gNamax), (2) longitudinal (Rx) and transverse (Ry) intracellular resistivities, and (3) inhomogeneities in gNamax and Rx and Ry between the strand and the large area. Three ionic models for cardiac excitation described by Beeler-Reuter, Ebihara-Johnson, and Luo-Rudy ionic current kinetics were compared.
In the 2-dimensional simulations, hc was 175 microns in Ebihara-Johnson and Beeler-Reuter models and 200 microns in the Luo-Rudy model. At the critical strand diameter, the site of conduction block was located beyond the transition, i.e. a small circular area was activated in the large medium, whereas with narrower strands conduction block occurred within the strands. The decrease of gNamax resulted in a large increase of hc. This increase was mainly due to the change of gNamax in the large area, while hc was almost independent of gNamax in the strand. Changing Rx had no effect on hc, whereas the increase of Ry decreased hc and reversed conduction block. Inhomogeneous changes of Rx and Ry in the strand versus the large medium had opposite effects on hc. When the resistivities of the strand alone were increased, hc also increased. In contrast, the increase of the resistivities in the large area reduced hc. In the 3-dimensional model, hc was 2.7 times larger than the corresponding 2-dimensional values at the various levels of gNamax and resistivity.
(1) At physiological values for active and passive electrical properties, hc in the 2D simulations is close to 200 microns in all three ionic models. In the 3-dimensional simulations, hc is 2.7 larger than in the 2-dimensional models. (2) The excitable properties of the large area but not of the strand modify hc. The decrease of intercellular coupling in the large medium facilitates impulse conduction and reduces hc, while the same change in the strand increases hc. (3) Occurrence of conduction block at an abrupt geometrical transition can be explained by both the impedance mismatch at the transition site and the critical curvature beyond the transition.
心脏中的单向传导阻滞可发生在冲动从较小组织体积传递到较大组织体积的部位。本研究的目的是评估在一个二维和三维心脏组织计算机模型中传导阻滞的发生情况，该模型由一条突然进入大面积区域的狭窄束状结构组成。在这种结构中，评估了对于传导阻滞发生至关重要的束状结构直径hc，它是束状结构和大面积介质的主动和被动电学特性变化的函数。
分析了以下参数变化对hc的影响：（1）最大钠电导（gNamax），（2）纵向（Rx）和横向（Ry）细胞内电阻率，以及（3）束状结构和大面积区域之间gNamax、Rx和Ry的不均匀性。比较了由Beeler-Reuter、Ebihara-Johnson和Luo-Rudy离子电流动力学描述的三种心脏兴奋离子模型。
在二维模拟中，Ebihara-Johnson模型和Beeler-Reuter模型中的hc为175微米，Luo-Rudy模型中的hc为200微米。在临界束状结构直径处，传导阻滞部位位于过渡区域之外，即大面积介质中有一个小圆形区域被激活，而束状结构较窄时，传导阻滞发生在束状结构内。gNamax的降低导致hc大幅增加。这种增加主要是由于大面积区域中gNamax的变化，而hc几乎与束状结构中的gNamax无关。改变Rx对hc没有影响，而Ry的增加会降低hc并逆转传导阻滞。束状结构与大面积介质中Rx和Ry的不均匀变化对hc有相反的影响。当仅增加束状结构的电阻率时，hc也会增加。相反，大面积区域中电阻率的增加会降低hc。在三维模型中，在不同的gNamax和电阻率水平下，hc比相应的二维值大2.7倍。
（1）在主动和被动电学特性的生理值下，二维模拟中所有三种离子模型的hc都接近200微米。在三维模拟中，hc比二维模型大2.7倍。（2）大面积区域而非束状结构的可兴奋特性会改变hc。大面积介质中细胞间耦合的降低促进冲动传导并降低hc，而束状结构中相同的变化会增加hc。（3）在几何形状突然转变处发生传导阻滞可由转变部位的阻抗失配和转变区域之外的临界曲率来解释。
