de Groot Natasja M S, Zeppenfeld Katja, Wijffels Maurits C, Chan Wing King, Blom Nico A, Van der Wall Ernst E, Schalij Martin J
Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands.
Heart Rhythm. 2006 May;3(5):526-35. doi: 10.1016/j.hrthm.2006.01.011. Epub 2006 Feb 28.
In patients late after surgical repair of congenital heart disease (CHD), areas with abnormal electrophysiologic properties may serve as slow conducting pathways within a macroreentrant circuit or may be the source of focal atrial tachycardia.
The purpose of this study was to evaluate the role of abnormal areas during focal atrial tachycardia prior to ablation.
Electroanatomic activation mapping of 62 atrial tachycardias was performed in 43 consecutive patients (37 +/- 12 years) after surgical repair of CHD. The mechanism of atrial tachycardia was scar related intra-atrial reentry (n = 27), cavotricuspid-related atrial flutter (n = 21), atrial fibrillation (n = 2), or focal atrial tachycardia (n = 10). During intra-atrial reentry, channels of slow conduction could be identified in all patients. Subsequent ablation was directed toward connecting two nonconductive borders. The site of origin during focal atrial tachycardia showed fractionated potentials and/or continuous electrical activity.
Ablation directed at isolating the source area resulted in termination of focal atrial tachycardia in all cases. In two patients, ablation of an area showing continuous electrical activity giving rise to fibrillatory conduction resulted in termination of atrial fibrillation. Ablation of intra-atrial reentry was successful in 70%. Atrial flutter and focal atrial tachycardia were successfully ablated in all patients. No complications were observed.
In patients with surgically corrected CHD, atrial tachycardia most often is caused by a macroreentrant mechanism but in some is the result of a focal mechanism. Areas of abnormal conduction may serve not only as a zone of slow conduction within a macroreentrant circuit but also as the site of origin of a focal atrial arrhythmia. Catheter ablation directed at "source isolation" is effective in eliminating focal atrial tachycardia in patients with CHD.
在先天性心脏病(CHD)手术修复后的晚期患者中,具有异常电生理特性的区域可能作为大折返环路内的缓慢传导通路,或者可能是局灶性房性心动过速的起源部位。
本研究的目的是评估在消融术前局灶性房性心动过速期间异常区域的作用。
对43例连续的先天性心脏病手术修复后的患者(37±12岁)进行了62次房性心动过速的电解剖激动标测。房性心动过速的机制为瘢痕相关的房内折返(n = 27)、腔静脉 - 三尖瓣相关房扑(n = 21)、房颤(n = 2)或局灶性房性心动过速(n = 10)。在房内折返期间,所有患者均可识别出缓慢传导通道。随后的消融旨在连接两个非传导边界。局灶性房性心动过速的起源部位显示出碎裂电位和/或持续性电活动。
针对隔离起源区域的消融在所有病例中均导致局灶性房性心动过速终止。在2例患者中,对显示持续性电活动并引发颤动传导的区域进行消融导致房颤终止。房内折返的消融成功率为70%。所有患者的房扑和局灶性房性心动过速均成功消融。未观察到并发症。
在先天性心脏病手术矫正后的患者中,房性心动过速最常见的原因是大折返机制,但在某些情况下是局灶性机制的结果。异常传导区域不仅可作为大折返环路内的缓慢传导区,还可作为局灶性房性心律失常的起源部位。针对“起源隔离”的导管消融对消除先天性心脏病患者的局灶性房性心动过速有效。