NASPE Young Investigator Awardee-1993. Computer model of the atrioventricular node predicts reentrant arrhythmias.
NASPE Young Investigator Awardee-1993. Computer model of the atrioventricular node predicts reentrant arrhythmias.
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1993 年 NASPE 青年研究员奖获得者。
DOI：
10.1111/j.1540-8159.1994.tb01359.x
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Saul,JP
中科院分区：
文献类型：
--
作者：
Leffler,CT;Saul,JP
简介房性早搏后，房室结可能表现出持续的折返性快速心律失常、孤立的回声搏动或恢复曲线（传导时间与心房周期长度的关系图）的不连续性。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设。方法和结果开发了电子连接元件的矩形晶格的计算机模型，其离子动力学模拟结点离子通量。该模型表明，存在一个使有效不应期最小化的电阻值，因为高电阻可防止远端元件去极化，而低电阻则允许通过电紧张传输泄漏去极化电流，从而防止近端元件激活。高电阻通过减慢传导来稳定再入。元件之间采用相等电阻值的模拟预测，随着心房冲动早熟的增加，房室结传导时间也会增加。纤维之间阻力逐渐变化的模型会产生不连续性和心动过速，但不会同时产生两者。均匀的各向异性产生优先横向传导阻滞，导致回波搏动和“快慢”心动过速，但不会导致恢复曲线不连续。不均匀的各向异性可能会产生折返，但心动过速通常会在不连续的情况下发生。将晶格分成两个具有不同电阻值的电紧张连接的平行通路（“双通路模型”）预测恢复曲线不连续性、回声搏动和心动过速。在临界心房周期长度时，只有（高阻力）慢通路顺行传导，而快通路逆行传导，产生典型的“慢-快”心动过速。双通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通路消融后快通路有效不应期缩短。 结论 房室结内电紧张连接双通路的被动电阻差异可能是功能性纵向分离、折返性心律失常和对导管消融治疗的反应的原因。
IntroductionFollowing atrial premature beats, the AV node may exhibit sustained reentrant tachyarrhyth‐mias, 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.Methods and ResultsA computer model of a rectangular lattice of elecirotonically 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.ConclusionDifferences in passive electrical resistance of electrotonically linked dual pathways within the AV node may account for functional longitudinal dissociation, reentrant arrhythmias, and responses to catheter ablation therapy.