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JACC Clin Electrophysiol. 2017 Dec 26;3(13):1565-1576. doi: 10.1016/j.jacep.2017.06.016. Epub 2017 Dec 18.
2
Intramyocardial block in patients with atrioventricular block.心肌内阻滞在房室传导阻滞患者中的表现。
J Investig Med. 2018 Jun;66(5):1-4. doi: 10.1136/jim-2017-000682. Epub 2018 Mar 7.
3
Predicting the Unpredictable: Drug-Induced QT Prolongation and Torsades de Pointes.预测不可预测的:药物引起的 QT 间期延长和尖端扭转型室性心动过速。
J Am Coll Cardiol. 2016 Apr 5;67(13):1639-1650. doi: 10.1016/j.jacc.2015.12.063.
4
Electrocardiographic predictors of bradycardia-induced torsades de pointes in patients with acquired atrioventricular block.获得性房室传导阻滞患者中心动过缓诱导尖端扭转型室性心动过速的心电图预测因素。
Heart Rhythm. 2015 Mar;12(3):498-505. doi: 10.1016/j.hrthm.2014.11.018. Epub 2014 Nov 18.
5
Complex excitation dynamics underlie polymorphic ventricular tachycardia in a transgenic rabbit model of long QT syndrome type 1.复杂的兴奋动力学是1型长QT综合征转基因兔模型中多形性室性心动过速的基础。
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6
AV-block and conduction slowing prevail over TdP arrhythmias in the methoxamine-sensitized pro-arrhythmic rabbit model.在甲氧明致敏的致心律失常兔模型中,房室传导阻滞和传导减慢比尖端扭转型室性心动过速心律失常更为常见。
J Cardiovasc Electrophysiol. 2015 Jan;26(1):82-9. doi: 10.1111/jce.12533. Epub 2014 Sep 19.
7
Drug-induced torsade de pointes arrhythmias in the chronic AV block dog are perpetuated by focal activity.在慢性房室传导阻滞犬中,药物引起的尖端扭转型室性心动过速心律失常是由局灶性活动引起的。
Circ Arrhythm Electrophysiol. 2011 Aug;4(4):566-76. doi: 10.1161/CIRCEP.110.958991. Epub 2011 May 27.
8
The site of origin of torsade de pointes.尖端扭转型室性心动过速的起源部位。
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Risk factors for recurrent syncope and subsequent fatal or near-fatal events in children and adolescents with long QT syndrome.长 QT 综合征儿童和青少年复发性晕厥及随后的致死或近乎致死事件的危险因素。
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Torsades de pointes during complete atrioventricular block: Genetic factors and electrocardiogram correlates.尖端扭转型室性心动过速伴完全性房室传导阻滞:遗传因素和心电图相关性。
Can J Cardiol. 2010 Apr;26(4):208-12. doi: 10.1016/s0828-282x(10)70369-x.

碎裂心内膜信号与尖端扭转型室速的延迟后除极。

Fragmented endocardial signals and early afterdepolarizations during torsades de pointes tachycardia.

机构信息

Arrhythmia Unit, Department of Cardiovascular Medicine, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, P.R. China.

Institut de Cardiologie, Unité de Rythmologie, Groupe Hospitalier Pitié-Salpêtrière, Paris, France.

出版信息

Cardiol J. 2020;27(1):54-61. doi: 10.5603/CJ.a2018.0070. Epub 2018 Jul 16.

DOI:10.5603/CJ.a2018.0070
PMID:30009377
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8086491/
Abstract

BACKGROUND

Bradycardia-induced torsade de pointes (TdP) tachycardia in patients with spontaneous high-degree atrioventricular block (AVB) is common. The aim of this study was to analyze endocardial recordings during TdP in spontaneous high-degree AVB in humans to better understand the electrophysiological mechanisms underlying this phenomenon.

METHODS

The study group consisted of 5 patients with typical episodes of TdP during spontaneous high-degree AVB. A standard (USCI) temporary bipolar endocardial catheter positioned at the apex of the right ventricle (RV) and bipolar chest leads from two precordial leads V1 and V4 were used to record the tracings during TdP.

RESULTS

The presence of a wide spectrum of fragmentations was noted on endocardial electrograms (EGMs), which were invisible on the surface electrocardiogram (ECG) tracing. Endocardial signals indicated that TdP started in the proximity of the RV apex, since the local EGM began prior to the QRS complex on the surface ECG. Early afterdepolarizations (EADs) were observed in 2 out of 5 cases confirming a common opinion about the mechanism of TdP. However, this phenomenon was not observed in 3 other patients suggesting that the arrhythmia was the result of a different mechanism originating in proximity to the RV apex.

CONCLUSIONS

This work demonstrated early endocardial signals in the RV apex during TdP associated with high-degree AVB in humans, and exhibits a spectrum of fragmented signals in this area occurring on a single or multiple beats. These fragmentations indicate areas of poor conduction and various degrees of intramyocardial block, and therefore a new mechanism of TdP tachycardia in some patients with spontaneous high-degree AVB.

摘要

背景

患有自发性高度房室传导阻滞(AVB)的患者,心动过缓诱发尖端扭转型室性心动过速(TdP)较为常见。本研究旨在分析人类自发性高度 AVB 中 TdP 时的心内膜记录,以更好地理解这种现象的电生理机制。

方法

研究组包括 5 例典型的自发性高度 AVB 伴 TdP 发作的患者。使用标准(USCI)的临时双极心内膜导管置于右心室(RV)心尖部,以及来自两个前导导联 V1 和 V4 的双极胸导联来记录 TdP 期间的心内膜描记图。

结果

在心内膜电图(EGM)上注意到存在广泛的碎裂现象,而体表心电图(ECG)描记图上则不可见。心内膜信号表明 TdP 始于 RV 心尖部附近,因为局部 EGM 在心表 ECG 的 QRS 波群之前开始。在 5 例中的 2 例观察到早期后除极(EAD),证实了关于 TdP 机制的普遍观点。然而,在另外 3 例患者中未观察到这种现象,表明心律失常是源自 RV 心尖部附近的不同机制的结果。

结论

本工作在人类伴高度 AVB 的 TdP 期间在 RV 心尖部显示了早期的心内膜信号,并在该区域显示出发生在单个或多个搏动上的碎裂信号谱。这些碎裂表明存在传导不良区域和不同程度的心肌内阻滞,因此在一些患有自发性高度 AVB 的患者中存在 TdP 心动过速的新机制。