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心房颤动驱动部位与同时患有房性心律失常患者房性心动过速的空间关系。

Spatial relationship of sites for atrial fibrillation drivers and atrial tachycardia in patients with both arrhythmias.

机构信息

Stanford University Medical Center, Palo Alto, CA, United States.

Stanford University Medical Center, Palo Alto, CA, United States.

出版信息

Int J Cardiol. 2017 Dec 1;248:188-195. doi: 10.1016/j.ijcard.2017.07.003. Epub 2017 Jul 14.

Abstract

INTRODUCTION

Atrial fibrillation (AF) often converts to and from atrial tachycardia (AT), but it is undefined if these rhythms are mechanistically related in such patients. We tested the hypothesis that critical sites for AT may be related to regional AF sources in patients with both rhythms, by mapping their locations and response to ablation on transitions to and from AF.

METHODS

From 219 patients undergoing spatial mapping of AF prior to ablation at 3 centers, we enrolled 26 patients in whom AF converted to AT by ablation (n=19) or spontaneously (n=7; left atrial size 42±6cm, 38% persistent AF). Both atria were mapped in both rhythms by 64-electrode baskets, traditional activation maps and entrainment.

RESULTS

Each patient had a single mapped AT (17 reentrant, 9 focal) and 3.7±1.7 AF sources. The mapped AT spatially overlapped one AF source in 88% (23/26) of patients, in left (15/23) or right (8/23) atria. AF transitioned to AT by 3 mechanisms: (a) ablation anchoring AF rotor to AT (n=13); (b) residual, unablated AF source producing AT (n=6); (c) spontaneous slowing of AF rotor leaving reentrant AT at this site without any ablation (n=7). Electrogram analysis revealed a lower peak-to-peak voltage at overlapping sites (0.36±0.2mV vs 0.49±0.2mV p=0.03).

CONCLUSIONS

Mechanisms responsible for AT and AF may arise in overlapping atrial regions. This mechanistic inter-relationship may reflect structural and/or functional properties in either atrium. Future work should delineate how acceleration of an organized AT may produce AF, and whether such regions can be targeted a priori to prevent AT recurrence post AF ablation.

摘要

简介

心房颤动(AF)常转换为房性心动过速(AT),但这些节律在这些患者中是否存在机制相关性尚不清楚。我们通过在 AF 转复和维持期间对其定位和消融反应进行标测,来检验这样一个假设,即 AT 的关键部位可能与两种节律患者的局部 AF 源有关。

方法

我们从 3 个中心的 219 例接受 AF 消融前空间标测的患者中,入选了 26 例 AF 通过消融(n=19)或自发(n=7;左房大小 42±6cm,38%持续性 AF)转为 AT 的患者。通过 64 电极篮、传统激活图和拖带对两种节律进行双侧心房标测。

结果

每位患者均有 1 个可标测的 AT(17 个折返性,9 个局灶性)和 3.7±1.7 个 AF 源。在 26 例患者中,有 23 例(88%)的可标测 AT 与 1 个 AF 源的空间重叠,位于左房(15/23)或右房(8/23)。AF 通过 3 种机制转为 AT:(a)消融使 AF 转子锚定于 AT(n=13);(b)残留未消融的 AF 源产生 AT(n=6);(c)AF 转子自发性减速,使折返性 AT 在此部位而无需任何消融(n=7)。电描记图分析显示重叠部位的峰峰值电压较低(0.36±0.2mV 比 0.49±0.2mV,p=0.03)。

结论

AT 和 AF 的发生机制可能起源于重叠的心房区域。这种机制上的相互关系可能反映了左右心房的结构和/或功能特性。未来的工作应该阐明如何加速有组织的 AT 可能产生 AF,以及这些区域是否可以预先作为靶点来预防 AF 消融后 AT 的复发。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db56/5865446/1c0ac7df4ef7/nihms947350f1.jpg

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Int J Cardiol. 2019 Mar 1;278:151-152. doi: 10.1016/j.ijcard.2018.12.002. Epub 2018 Dec 5.

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