Endocardial ablation-resistant ivabradine-sensitive atrial tachycardia suggestive of an epicardial origin in the left atrial appendage

Q4 Medicine
Kohki Nakamura MD, PhD, FJCC , Takehito Sasaki MD , Kentaro Minami MD, PhD , Taiki Masuyama MD, PhD , Shingo Yoshimura MD , Keiji Hoshino MD , Akiko Kodama MD , Yuji Matsuo MD , Kenichi Kaseno MD, PhD , Suguru Nishiuchi MD, PhD , Shigeto Naito MD, PhD
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Abstract

A 23-year-old woman presented with 200,409 heart beats/day due to an atrial tachycardia (AT) lasting one year and tachycardia-induced cardiomyopathy. None of the antiarrhythmic or rate control drugs terminated the AT or sufficiently reduced the heart rate during the AT. Thus, she underwent radiofrequency catheter ablation of the AT. Ultra-high-resolution mapping suggested that the AT originated from the epicardial left atrial appendage (LAA), and endocardial radiofrequency ablation failed to eliminate the AT, although acceleration and transient termination of the AT during ongoing ablation in the endocardial LAA were observed. After the ablation, ivabradine monotherapy achieved both an optimal heart rate control during the AT and termination of the AT. Some ATs refractory to conventional antiarrhythmic drug therapy can be treated by ivabradine and are called ivabradine sensitive-ATs (ISATs). Left atrial ISATs often originate from the vicinity of the LAA and have been reported to be treated by endocardial radiofrequency ablation. This case report describes that a subset of ISATs originating from the LAA may be associated with epicardial abnormal automaticity and refractory to conventional endocardial radiofrequency ablation.

Learning objective

Some focal atrial tachycardias (ATs) refractory to conventional antiarrhythmic drug therapy are successfully treated by ivabradine and are called ivabradine sensitive-ATs (ISATs). ISATs originating from the left atrial appendage (LAA) have been reported to be eliminated by endocardial radiofrequency ablation, but a subset of LAA-ISATs may be associated with epicardial abnormal automaticity and may be refractory to endocardial radiofrequency ablation.
心内膜抗消融性伊伐布雷定敏感房性心动过速提示心外膜起源于左心房附件
一名23岁女性因持续一年的房性心动过速(AT)和心动过速引起的心肌病而出现200,409次/天的心跳。抗心律失常或控制心率的药物均不能终止AT或充分降低AT期间的心率。因此,她接受了射频导管消融AT。超高分辨率定位提示AT起源于心外膜左心耳(LAA),心内膜射频消融术未能消除AT,尽管在心内膜LAA持续消融术中观察到AT的加速和短暂终止。消融后,伊伐布雷定单药治疗获得了AT期间和AT终止时的最佳心率控制。一些对常规抗心律失常药物治疗难治的ATs可以用伊伐布雷定治疗,被称为伊伐布雷定敏感型ATs (ISATs)。左房isat通常起源于LAA附近,据报道可通过心内膜射频消融术治疗。本病例报告描述了起源于LAA的isat的一个亚群可能与心外膜异常自动性和传统的心内膜射频消融难治性有关。学习目的:一些常规抗心律失常药物治疗难治性局灶性房性心动过速(ATs)被伊伐布雷定成功治疗,称为伊伐布雷定敏感型心房过速(ISATs)。据报道,起源于左心耳(LAA)的isat可以通过心内膜射频消融术消除,但LAA- isat的一部分可能与心外膜异常自动性有关,并且可能对心内膜射频消融术无效。
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来源期刊
Journal of Cardiology Cases
Journal of Cardiology Cases Medicine-Cardiology and Cardiovascular Medicine
CiteScore
0.90
自引率
0.00%
发文量
177
审稿时长
59 days
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