Berenfeld O, Jalife J
Department of Pharmacology, SUNY Health Science Center at Syracuse, NY 13210, USA.
Circ Res. 1998 Jun 1;82(10):1063-77. doi: 10.1161/01.res.82.10.1063.
Multiple electrode mapping of the ventricles during complex tachyarrhythmias has revealed focal subendocardial activation whose mechanism remains unexplained. We hypothesized that reentry involving the Purkinje-muscle junctions (PMJs) may be a mechanism for such focal excitations. We have constructed an anatomically appropriate computerized 3-dimensional model of the mammalian ventricles that includes the Purkinje conduction system and 214 PMJs distributed throughout the endocardium. Isochronal maps during normal excitation, as well as during right or left bundle branch block, resembled experimental measurements and compared well with isochronal maps of propagation in the human heart. Activity observed at both sides of a PMJ in the model showed that propagation from Purkinje fibers to muscle was slower than in the opposite direction. Under these realistic and normal conditions, the evolution of reentrant activity involving muscle and the Purkinje network was simulated. The reentry pattern was independent of the initiation site. It evolved with drifting epicardial breakthroughs and transformed on the endocardium from focal activity to figure-of-8 reentry. In addition, the ECG amplitude undulated during the evolution, and decrease in the cycle period, apparent wavelength, and propagation velocity were observed. Finally, the reentry was terminated if the Purkinje system was disconnected from the muscle before it reached a relative steady state. The simulation results suggest the following: (1) Epicardial breakthroughs and endocardial focal activity may originate at the PMJs. (2) The ECG amplitude may decrease as the reentry stabilizes and the excitation wavelength decreases. (3) The Purkinje system may have a double role in the evolution of reentry: first, it is essential to the reentry at the initial stage; second, it may lead to the establishment of intramyocardial reentry, at which time the Purkinje system becomes irrelevant.
在复杂快速心律失常期间对心室进行的多电极标测显示，心内膜下局灶性激动的机制仍未得到解释。我们推测，涉及浦肯野纤维 - 心肌连接（PMJ）的折返可能是这种局灶性激动的一种机制。我们构建了一个解剖结构合适的哺乳动物心室计算机三维模型，该模型包括浦肯野传导系统以及分布于心内膜各处的214个PMJ。正常激动期间以及右束支或左束支传导阻滞期间的等时图类似于实验测量结果，并且与人类心脏中的传播等时图比较良好。在模型中观察到PMJ两侧的活动表明，从浦肯野纤维到心肌的传播比相反方向更慢。在这些现实且正常的条件下，模拟了涉及心肌和浦肯野网络的折返活动的演变。折返模式与起始部位无关。它随着心外膜突破点的漂移而演变，并在心内膜上从局灶性活动转变为8字形折返。此外，在演变过程中心电图振幅呈波浪状变化，并且观察到周期、视波长和传播速度减小。最后，如果浦肯野系统在达到相对稳定状态之前与心肌断开连接，折返就会终止。模拟结果表明：（1）心外膜突破点和心内膜局灶性活动可能起源于PMJ。（2）随着折返稳定且激动波长减小，心电图振幅可能降低。（3）浦肯野系统在折返演变过程中可能具有双重作用：第一，它在初始阶段对折返至关重要；第二，它可能导致心肌内折返的建立，此时浦肯野系统变得无关紧要。
