Davidenko J M, Salomonsz R, Pertsov A M, Baxter W T, Jalife J
Department of Pharmacology, State University of New York Health Science Center at Syracuse 13210, USA.
Circ Res. 1995 Dec;77(6):1166-79. doi: 10.1161/01.res.77.6.1166.
It is well known that electrical pacing may either terminate or change the rate and/or ECG appearance of reentrant ventricular tachycardia. However, the dynamics of interaction of reentrant waves with waves initiated by external pacing are poorly understood. Prevailing concepts are based on simplistic models in which propagation occurs in one-dimensional rings of cardiac tissue. Since reentrant activation in the ventricles occurs in two or three dimensions, such concepts might be insufficient to explain the mechanisms of pacing-induced effects. We used numerical and biological models of cardiac excitation to explore the phenomena, which may take place as a result of electrical pacing during functionally determined reentry. Computer simulations of a two-dimensional array of electrically coupled FitzHugh-Nagumo cells were used to predict the response patterns expected from thin slices of sheep ventricular epicardial muscle, in which self-sustaining reentrant activity in the form of spiral waves was consistently initiated by premature stimulation and monitored by means of video mapping techniques. The results show that depending on their timing and shape, externally induced waves may collide with the self-sustaining spiral and result in one of three possible outcomes: (1) direct annihilation of the spiral, (2) multiplication of the spiral, or (3) shift of the spiral center (ie, core). Multiplication and shift of the spiral core were attended by changes in rate and morphology of the arrhythmia as seen by "pseudo-ECGs." Furthermore, delayed termination (ie, termination of the activity one to three cycles after the stimulus) occurred after both multiplication and shift of the spiral center. Both numerical predictions and experimental results support the hypothesis that whether a pacing stimulus will terminate a reentrant arrhythmia or modify its ECG appearance depends on whether the interactions between the externally induced wave and the spiral wave result in the de novo formation of one or more "wavebreaks." The final outcome depends on the stimulus parameters (ie, position and size of the electrodes and timing of the stimulus) as well as on the position of the newly formed wavebreak(s) in relation to that of the original wave.
众所周知，电起搏可能会终止或改变折返性室性心动过速的速率和/或心电图表现。然而，对于折返波与外部起搏引发的波之间相互作用的动力学，人们了解甚少。目前流行的概念基于简单模型，即传播发生在心脏组织一维环中。由于心室中的折返激活发生在二维或三维空间，这样的概念可能不足以解释起搏诱导效应的机制。我们使用心脏兴奋的数值和生物学模型来探索在功能确定的折返期间电起搏可能导致的现象。通过对二维电耦合FitzHugh-Nagumo细胞阵列进行计算机模拟，来预测从绵羊心室心外膜肌肉薄片预期得到的反应模式，在该薄片中，通过过早刺激持续引发以螺旋波形式的自持折返活动，并借助视频映射技术进行监测。结果表明，根据其时间和形状，外部诱发的波可能与自持螺旋波碰撞，并导致三种可能结果之一：（1）螺旋波直接湮灭，（2）螺旋波倍增，或（3）螺旋波中心（即核心）移位。从“伪心电图”可见，螺旋波核心的倍增和移位伴随着心律失常速率和形态的变化。此外，在螺旋波中心倍增和移位之后均出现延迟终止（即刺激后一至三个周期活动终止）。数值预测和实验结果均支持这一假设，即起搏刺激是否会终止折返性心律失常或改变其心电图表现，取决于外部诱发波与螺旋波之间的相互作用是否导致一个或多个“波裂”的重新形成。最终结果取决于刺激参数（即电极的位置和大小以及刺激时间），以及新形成的波裂相对于原始波的位置。
