Optical mapping of drug-induced polymorphic arrhythmias and torsade de pointes in the isolated rabbit heart
Optical mapping of drug-induced polymorphic arrhythmias and torsade de pointes in the isolated rabbit heart
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DOI：
10.1016/s0735-1097(96)00588-8
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发表时间：
1997-03-15
影响因子：
24
通讯作者：
Jalife, J
中科院分区：
文献类型：
--
作者：
Asano, Y;Davidenko, JM;Jalife, J
目标.本研究旨在：1）检验以下假设：在心动过缓和药物诱导的动作电位延长的情况下，早期后除极（埃兹）的多个病灶导致兴奋波前的起源和方向的逐搏变化，并负责多态性心律失常;（2）确定埃兹是否可以启动非平稳再入，引起典型的尖端扭转型室性心动过速（TDP）。在过去，很难将埃兹或折返与TDP的波形心电图（EGG）起搏联系起来。一种电压敏感的染料用于高分辨率的视频成像的电波上的心外膜和内膜表面的Langendorff灌注兔心脏。同时记录右室间隔区的心电图和单相动作电位。消融房室结可诱发心动过缓。低氯化钾台氏液加奎尼丁灌流引起动作电位和QT间期延长，最终出现埃兹和触发活动，引起间歇性多形性心律失常。在一个实验中，触发活动之后是一个长时间的漩涡状折返，具有TDP特征的ECG模式。然而，在大多数实验中，观察到不同起源和传播模式的病灶活动。触发反应也表现出不同程度的局部阻滞。用E-4031获得了类似的结果。在控制条件下和奎尼丁存在下的快速起搏一致导致涡旋样折返，其ECG模式类似TDP。然而，奎尼丁组心律失常的周期长度比对照组长（[平均值+/- SEM] 194 +/- 12 vs. 132 +/- 8 ms，p < 0.03）。药物诱导的多形性室性心律失常可能是由埃兹或EAD诱导的非平稳折返活动引起的波传播模式的搏动变化引起的。相反，在有或无药物的情况下，爆发式起搏诱导的多态性心动过速是非稳态折返活动的结果。(C)1997年，美国心脏病学会。
Objectives. This study sought to 1) test the hypothesis that in the setting of bradycardia and drug-induced action potential prolongation, multiple foci of early afterdepolarizations (EADs) result in beat to beat changes in the origin and direction of the excitation wave front and are responsible for polymorphic arrhythmias; and 2) determine whether EADs may initiate nonstationary reentry, giving rise to the typical torsade de pointes (TDP) pattern.Background. In the past, it has been difficult to associate EADs or reentry with the undulating electrocardiographic (EGG) pat terns of TDP.Methods. A voltage-sensitive dye was used for high resolution video imaging of electrical waves on the epicardial and endocardial surface of the Langendorff-perfused rabbit heart. ECG and monophasic action potentials from the right septal region were also recorded. Bradycardia was induced by ablation of the atrioventricular node.Results. Perfusion of low potassium chloride Tyrode solution plus quinidine led to prolongation of the action potential and the QT interval, Eventually, EADs and triggered activity ensued, giving rise to intermittent episodes of polymorphic arrhythmia. In one experiment, triggered activity was followed by a long episode of vortex like reentry with an ECG pattern characteristic of TDP. However, in most experiments, focal activity of varying origins and propagation patterns was observed. Triggered responses also showed varying degrees of local block. Similar results were obtained with E-4031. Burst pacing both at control conditions and in the presence of quinidine consistently led to vortex-like reentry whose ECG pattern resembled TDP. However, the cycle length of the arrhythmia with quinidine was longer than that for control ([mean +/- SEM] 194 +/- 12 vs. 132 +/- 8 ms, p < 0.03).Conclusions. Drug induced polymorphic ventricular arrhythmias may result from beat to beat changes in wave propagation patterns initiated by EADs or EAD-induced nonstationary reentrant activity. In contrast, burst pacing-induced polymorphic tachycardia in the presence or absence of drugs is the result of nonstationary reentrant activity. (C) 1997 by the American College of Cardiology.