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阵发性心房颤动的驱动机制分析:左心房体与肺静脉之间的激活顺序比较。

Analysis of the driving mechanism in paroxysmal atrial fibrillation: comparison of the activation sequence between the left atrial body and pulmonary vein.

机构信息

Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.

Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan; Department of Cardiac Arrhythmias, Kumamoto University, Kumamoto, Japan.

出版信息

J Cardiol. 2020 Jun;75(6):673-681. doi: 10.1016/j.jjcc.2020.01.004. Epub 2020 Feb 7.

Abstract

BACKGROUND

It has been shown that most paroxysmal atrial fibrillation (AF) can be terminated by pulmonary vein (PV) isolation alone, suggesting that rapid discharges from PV drive AF. To define the driving mechanism of AF, we compared the activation sequence in the body of left atrium (LA) to that within PV.

METHODS

Endocardial noncontact mapping of LA body (LA group; n = 16) and selective endocardial mapping of left superior PV (LSPV) (PV group; n = 13) were performed in 29 paroxysmal AF patients. The frequency of pivoting activation, wave breakup, and wave fusion observed in LA were compared to those in LSPV to define the driving mechanism of AF. Circumferential ablation lesion around left PV was performed after right PV isolation to examine the effect of linear lesion around PV on AF termination both in LA and PV groups.

RESULTS

The frequency of pivoting activation, wave breakup, and wave fusion in PV group were significantly higher than those in LA group (36.5 ± 17.7 vs 5.0 ± 2.2 times/seconds, p < 0.001, 10.1 ± 4.3 vs 5.0 ± 2.2 times/seconds, p = 0.004, 18.1 ± 5.7 vs 11.0 ± 5.2, p = 0.002). Especially in the PV group, the frequency of pivoting activation was significantly higher than that of wave breakup and wave fusion (36.5 ± 17.7 vs 10.1 ± 4.3 times/seconds, p < 0.001, 36.5 ± 17.7 vs 18.1 ± 5.7 times/seconds, p < 0.001). These disorganized activations in LSPV were eliminated by the circumferential ablation lesion around left PV (pivoting activation; 36.5 ± 17.7 vs 9.3 ± 2.3 times/seconds, p < 0.001, wave breakup; 10.1±1.3 times/seconds, p = 0.003, wave fusion; 18.1 ± 5.7 vs 5.7 ± 1.8, p < 0.001), resulted in AF termination in all patients in both LA and PV groups.

CONCLUSIONS

Activation sequence within PV was more disorganized than that in LA body. Frequent episodes of pivoting activation rather than wave breakup and fusion observed within PV acted as the driving sources of paroxysmal AF.

摘要

背景

已经证明,大多数阵发性心房颤动(AF)可以仅通过肺静脉(PV)隔离来终止,这表明快速放电来自 PV 驱动 AF。为了定义 AF 的驱动机制,我们比较了左心房(LA)体内心内膜非接触式标测(LA 组;n=16)和左优势 PV(LSPV)选择性心内膜标测(PV 组;n=13)中的激活序列。在 29 例阵发性 AF 患者中比较 LA 内观察到的枢轴激活、波破裂和波融合的频率,以定义 AF 的驱动机制。在右 PV 隔离后,在左 PV 周围进行环形消融损伤,以检查 PV 周围线性损伤对 LA 和 PV 组中 AF 终止的影响。

结果

PV 组的枢轴激活、波破裂和波融合的频率明显高于 LA 组(36.5±17.7 比 5.0±2.2 次/秒,p<0.001,10.1±4.3 比 5.0±2.2 次/秒,p=0.004,18.1±5.7 比 11.0±5.2,p=0.002)。特别是在 PV 组中,枢轴激活的频率明显高于波破裂和波融合的频率(36.5±17.7 比 10.1±4.3 次/秒,p<0.001,36.5±17.7 比 18.1±5.7 次/秒,p<0.001)。左 PV 周围的环形消融损伤消除了 LSPV 中的这些不规则激活(枢轴激活;36.5±17.7 比 9.3±2.3 次/秒,p<0.001,波破裂;10.1±1.3 次/秒,p=0.003,波融合;18.1±5.7 比 5.7±1.8,p<0.001),导致两组患者的 LA 和 PV 中均终止了 AF。

结论

PV 内的激活序列比 LA 体内心内膜更紊乱。在 PV 内观察到的频繁枢轴激活而不是波破裂和融合作为阵发性 AF 的驱动源。

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