The antiarrhythmic effect of verapamil on atrioventricular re-entry in the Wolff-Parkinson-White syndrome: a computer model study

Paul H. Fleischmann , Gerhard Stark , Paul Wach
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引用次数: 4

Abstract

Verapamil is supposed to suppress the initiation of circus movement supraventricular tachycardia by affecting the atrioventricular node. In electrophysiological tests, programmed stimulation is usually performed by using the same location for pacing and premature stimulus. Spontaneous ectopic activity starts from a different location than the sinus node and can therefore find altered re-entry conditions. In this study a 3D computer model based on Huygen's principle is used for simulation of the spread of excitation in the human heart in combination with a posterobasal, right or left lateral accessory pathway (AP). The effect of verapamil on properties of the atrioventricular node were modelled by prolonging the effective refractory period and basal conduction time. For each of the three APs, ectopic foci at the atrial base and between sinus node and AP were modelled at various coupling intervals for investigating re-entrant activation. In the control state (without verapamil) only orthodromic echoes were found. The maximum echo zone (EZ) range was found near the AP. If stimuli were selected further away from the AP on the atrial basis, the EZ range decreased until no EZ was found. The EZ range decreased from it's maximum value near the AP. towards the difference of the effective refractory periods between AP and AV-node near the sinus node. Verapamil abolished the EZ in case of a posteroscptal AP. For a lateral AP the administration of verapamil resulted in an orthodromic and antidromic EZ depending on the atrial premature activation site. A maximum orthodromic EZ was found for premature stimuli near the AP. As stimulus site moved away from the AP. the EZ range first decreased continuously to zero leading eventually to an antidromic EZ. These findings suggest the important influence of the site of premature stimuli with respect to the accessory pathway and AV-node on the inducibility of atrial re-entry.

维拉帕米对Wolff-Parkinson-White综合征房室再入的抗心律失常作用:计算机模型研究
维拉帕米通过影响房室结抑制马戏运动室上性心动过速的发生。在电生理试验中,程控刺激通常采用起搏和过早刺激的相同位置。自发性异位活动开始于不同于窦房结的位置,因此可以发现改变的再入条件。在本研究中,基于Huygen原理的三维计算机模型用于模拟人类心脏中结合后基底、右或左外侧副通路(AP)的兴奋传播。维拉帕米通过延长有效不应期和基础传导时间来模拟其对房室结性质的影响。对于这三种AP,在不同的耦合间隔内对心房基底和窦结与AP之间的异位灶进行建模,以研究再入激活。在对照状态下(不使用维拉帕米)只发现正交回波。最大回声区(EZ)范围在AP附近发现。如果在心房基础上选择远离AP的刺激,则EZ范围减小,直到没有发现EZ。EZ范围由AP附近的最大值向AP与av淋巴结有效不应期的差异减小。维拉帕米在脑后AP的情况下消除了EZ。对于侧位AP,维拉帕米的给药导致正侧和反侧的EZ取决于心房过早激活位点。在AP附近发现了一个最大的正交EZ。随着刺激部位远离AP, EZ范围首先连续下降到零,最终导致反正交EZ。这些结果表明,相对于辅助通路和房室结的过早刺激位置对心房再入的诱导性有重要影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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