Leffler C T, Saul J P
Division of Health Sciences and Technology, Harvard Medical School-Massachusetts Institute of Technology.
Pacing Clin Electrophysiol. 1994 Jan;17(1):113-30. doi: 10.1111/j.1540-8159.1994.tb01359.x.
Following atrial premature beats, the AV node may exhibit sustained reentrant tachyarrhythmias, isolated echo beats, or discontinuities in the recovery curve (the plot of conduction time versus atrial cycle length). A computer model was used to examine the hypothesis that spatial variation of AV nodal passive electrical resistance may account for these phenomena.
A computer model of a rectangular lattice of electrotonically linked elements whose ionic kinetics simulated nodal ionic flux was developed. The model showed that there exists a resistance value that minimizes the effective refractory period, because high resistance prevents depolarization of distal elements, while low resistance allows leakage of depolarizing current by electrotonic transmission, preventing activation of proximal elements. High resistances stabilized reentry by slowing conduction. Simulations incorporating equal resistance values between elements predicted increased AV nodal conduction times with increasing prematurity of atrial impulses. A model with a gradual change in resistance between fibers produced discontinuities and tachycardia, but not both simultaneously. Uniform anisotropy produced preferential transverse block, leading to echo beats and "fast-slow" tachycardia, but not recovery curve discontinuities. Nonuniform anisotropy could produce reentry, but tachycardia often occurred without discontinuities. Dividing the lattice into two electrotonically linked parallel pathways with different resistance values ("dual pathway model") predicted recovery curve discontinuities, echo beats, and tachycardia. At critical atrial cycle lengths, only the (high resistance) slow pathway conducted antegradely, while the fast pathway conducted retrogradely, to generate the typical "slow-fast" tachycardia. Responses of the dual pathway model to ablation were consistent with clinical data, including the previous observation of a decrease in fast pathway effective refractory period after slow pathway ablation.
Differences in passive electrical resistance of electronically linked dual pathways within the AV node may account for functional longitudinal dissociation, reentrant arrhythmias, and responses to catheter ablation therapy.
房性早搏后，房室结可能会出现持续性折返性快速心律失常、孤立性回波搏动或恢复曲线（传导时间与心房周期长度的关系图）的中断。使用计算机模型来检验房室结被动电阻的空间变化可能解释这些现象的假说。
建立了一个由电耦合元件组成的矩形晶格计算机模型，其离子动力学模拟了节点离子通量。该模型表明存在一个使有效不应期最小化的电阻值，因为高电阻会阻止远端元件的去极化，而低电阻会通过电紧张传导使去极化电流泄漏，从而阻止近端元件的激活。高电阻通过减慢传导来稳定折返。元件间电阻值相等的模拟预测，随着心房冲动提前程度增加，房室结传导时间会延长。纤维间电阻逐渐变化的模型产生了中断和心动过速，但并非同时出现。均匀各向异性产生优先横向阻滞，导致回波搏动和“快-慢”型心动过速，但不会出现恢复曲线中断。非均匀各向异性可产生折返，但心动过速往往在没有中断的情况下发生。将晶格分为具有不同电阻值的两条电耦合平行通路（“双径路模型”）预测会出现恢复曲线中断、回波搏动和心动过速。在临界心房周期长度时，只有（高电阻的）慢径路顺向传导，而快径路逆向传导，以产生典型的“慢-快”型心动过速。双径路模型对消融的反应与临床数据一致，包括先前观察到的慢径路消融后快径路有效不应期缩短。
房室结内电耦合双径路的被动电阻差异可能解释功能性纵向分离、折返性心律失常以及对导管消融治疗的反应。
