Role of subendocardial Purkinje network in triggering torsade de pointes arrhythmia in experimental long QT syndrome
Role of subendocardial Purkinje network in triggering torsade de pointes arrhythmia in experimental long QT syndrome
复制标题
DOI：
10.1093/europace/eun248
复制
发表时间：
2008-10-01
期刊：
影响因子：
6.1
通讯作者：
El-Sherif, Nabil
中科院分区：
文献类型：
--
作者：
Ben Caref, E.;Boutjdir, Mohamed;El-Sherif, Nabil
本研究解决了关于心内膜下浦肯野网络在长QT综合征（LQTS）中触发点扭转（TdP）室性心动过速（VAs）的“主要”作用的争议。方法与结果通过建立犬胸膜素- a （AP-A）替代LQT3模型，研究心内膜下浦肯野网络在触发VAs中的作用。利用64个插入针电极分析单极细胞外电图的三维激活和复极化模式。6只狗行体外循环，用Lugol's溶液对心内膜浦肯野网络进行化学消融。自发性VAs在AP-A输注后持续发展，并由心内膜下局灶活动触发，作用于复极化的空间三维弥散基底。在没有心室逸出节律的情况下，心内膜消融被认为是成功的，因为形成了完全的房室传导阻滞。心内膜消融后不再观察到自发性VAs。然而，适当的过早刺激持续诱导重新进入VAs。结论本研究强烈表明，在LQTS中，心内膜下浦肯野组织产生的局灶性活动是TdP VAs的主要触发因素，如果不是唯一的触发因素，它通过作用于心肌复极的三维弥散底物来诱导再入兴奋。
Aims The present study addresses the controversy regarding the 'primary' role of the subendocardial Purkinje network in triggering torsade de pointes (TdP) ventricular tachyarrhythmia (VAs) in the long QT syndrome (LQTS).Methods and results We investigated the well-established canine anthopleurin-A (AP-A) surrogate model of LQT3 to study the role of the subendocardial Purkinje network in triggering VAs. Three-dimensional activation and repolarization patterns were analysed from unipolar extracellular electrograms utilizing 64 plunge needle electrodes. In 6 dogs, the animals were placed on cardiopulmonary bypass and chemical ablation of the endocardial Purkinje network was obtained using Lugol's solution. Spontaneous VAs consistently developed in response to AP-A infusion and were triggered by a subendocardial focal activity acting on a substrate of spatial three-dimensional dispersion of repolarization. Endocardial ablation was considered successful by the development of complete atrioventricular block in the absence of ventricular escape rhythm. Following endocardial ablation spontaneous VAs were no longer observed. However, an appropriately coupled premature stimulus consistently induced re-entrant VAs.Conclusion The present study strongly suggests that in the LQTS, focal activity generated in subendocardial Purkinje tissue is the primary, if not the only, trigger for TdP VAs by acting on a substrate of three-dimensional dispersion of myocardial repolarization to induce re-entrant excitation.