波前场映射揭示消融终止心房颤动驱动因素之间的生理网络。

George Leef, F. Shenasa, N. Bhatia, A. Rogers, W. Sauer, John M. Miller, Mark Swerdlow, M. Tamboli, M. Alhusseini, E. Armenia, T. Baykaner, J. Brachmann, M. Turakhia, F. Atienza, W. Rappel, Paul J. Wang, S. Narayan
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引用次数: 9

摘要

从人类心房的光学成像和房颤的临床研究中,局部驱动因素被提出了持续性房颤(AF)的机制,但由于驱动因素波动和消融它们可能不会终止房颤,因此存在争议。我们使用波前场成像来验证房颤驱动因素的假设,即如果并发房颤驱动因素可能相互作用产生波动的控制区域,以解释它们的出现/消失和消融的急性影响。方法:我们从一个国际注册中心招募了54例通过靶向消融终止持续性房颤的患者。对64极篮的单极AF电图进行分析,以重建激活时间,绘制每20 ms的传播矢量,并创建非专有相位图。结果每例患者(63.6±8.5岁,女性29.6%)在3种类型的房颤中出现4.0±2.1个空间锚定的旋转或局灶点。首先,单一(I型;n=7),第二种是成对的手性-反手性(II型;N =5)旋转驱动器控制大部分心房面积。1 - 2个大驱动因素消融终止了所有I型或II型房颤病例。第三,3 - 5个驱动因素的相互作用(III型;N =42),随控制区域的变化而变化。在驱动中心靶向消融终止心房颤动,III型患者比I型患者需要更多的消融(左心房P=0.02)。结论:持续性房颤的波前场成像揭示了一个由少数空间锚定的旋转和病灶位点组成的病理生理网络,它们相互作用、波动并控制不同的区域。未来的工作应该确定控制更大心房区域的心房颤动驱动是否是有吸引力的消融目标。
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Wavefront Field Mapping Reveals a Physiologic Network Between Drivers Where Ablation Terminates Atrial Fibrillation.
BACKGROUND Localized drivers are proposed mechanisms for persistent atrial fibrillation (AF) from optical mapping of human atria and clinical studies of AF, yet are controversial because drivers fluctuate and ablating them may not terminate AF. We used wavefront field mapping to test the hypothesis that AF drivers, if concurrent, may interact to produce fluctuating areas of control to explain their appearance/disappearance and acute impact of ablation. METHODS We recruited 54 patients from an international registry in whom persistent AF terminated by targeted ablation. Unipolar AF electrograms were analyzed from 64-pole baskets to reconstruct activation times, map propagation vectors each 20 ms, and create nonproprietary phase maps. RESULTS Each patient (63.6±8.5 years, 29.6% women) showed 4.0±2.1 spatially anchored rotational or focal sites in AF in 3 patterns. First, a single (type I; n=7) or, second, paired chiral-antichiral (type II; n=5) rotational drivers controlled most of the atrial area. Ablation of 1 to 2 large drivers terminated all cases of types I or II AF. Third, interaction of 3 to 5 drivers (type III; n=42) with changing areas of control. Targeted ablation at driver centers terminated AF and required more ablation in types III versus I (P=0.02 in left atrium). CONCLUSIONS Wavefront field mapping of persistent AF reveals a pathophysiologic network of a small number of spatially anchored rotational and focal sites, which interact, fluctuate, and control varying areas. Future work should define whether AF drivers that control larger atrial areas are attractive targets for ablation.
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