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原位心脏移植采用心房-心房吻合术后晚期发生心房扑动的机制。

Mechanism of atrial flutter occurring late after orthotopic heart transplantation with atrio-atrial anastomosis.

作者信息

Marine Joseph E, Schuger Claudio D, Bogun Frank, Kalahasty Gautham, Arnaldo Fabian, Czerska Barbara, Krishnan Subramaniam C

机构信息

Henry Ford Heart and Vascular Institute, Detroit, Michigan 48202, USA.

出版信息

Pacing Clin Electrophysiol. 2005 May;28(5):412-20. doi: 10.1111/j.1540-8159.2005.40019.x.

Abstract

OBJECTIVE

We sought to better define the electrophysiologic mechanism of atrial flutter in patients after heart transplantation.

BACKGROUND

Atrial flutter is a recognized problem in the post-cardiac transplant population. The electrophysiologic basis of atrial flutter in this patient population is not completely understood.

METHODS

Six patients with cardiac allografts and symptoms related to recurrent atrial flutter underwent diagnostic electrophysiologic study with electroanatomic mapping and radiofrequency catheter ablation. Comparison was made with a control non-transplant population of 11 patients with typical counterclockwise right atrial flutter.

RESULTS

In each case, mapping showed typical counterclockwise activation of the donor-derived portion of the right atrium, with concealed entrainment shown upon pacing in the cavotricuspid isthmus (CTI). The anastomotic suture line of the atrio-atrial anastomosis formed the posterior barrier of the reentrant circuit. Ablation of the electrically active, donor-derived portion of the CTI was sufficient to terminate atrial flutter and render it noninducible. Comparison with the control population showed that the electrically active portion of the CTI was significantly shorter in patients with transplant-associated flutter and that ablation was accomplished with the same or fewer radiofrequency lesions.

CONCLUSIONS

Atrial flutter in cardiac transplant recipients is a form of typical counterclockwise, isthmus-dependent flutter in which the atrio-atrial anastomotic suture line forms the posterior barrier of the reentrant circuit. Ablation in the donor-derived portion of the CTI is sufficient to create bidirectional conduction block and eliminate this arrhythmia. Ablation or surgical division of the donor CTI at the time of transplantation could prevent this arrhythmia.

摘要

目的

我们试图更好地明确心脏移植术后患者心房扑动的电生理机制。

背景

心房扑动是心脏移植后人群中一个公认的问题。该患者群体中心房扑动的电生理基础尚未完全明确。

方法

6例心脏移植患者出现与复发性心房扑动相关的症状,接受了诊断性电生理研究,包括电解剖标测和射频导管消融。与11例典型逆时针方向右心房扑动的非移植对照人群进行了比较。

结果

在每例患者中,标测显示右心房供体来源部分典型的逆时针激动,在腔静脉峡部(CTI)起搏时显示隐匿性拖带。心房-心房吻合口的吻合缝线形成了折返环的后屏障。消融CTI电活动的供体来源部分足以终止心房扑动并使其不能被诱发。与对照人群相比,移植相关心房扑动患者的CTI电活动部分明显较短,且消融时使用的射频损伤相同或更少。

结论

心脏移植受者的心房扑动是一种典型的逆时针、峡部依赖型扑动,其中心房-心房吻合缝线形成折返环的后屏障。消融CTI的供体来源部分足以产生双向传导阻滞并消除这种心律失常。在移植时消融或手术分离供体CTI可预防这种心律失常。

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