The role of fibroblasts in complex fractionated electrograms during persistent/permanent atrial fibrillation: implications for electrogram-based catheter ablation.
The role of fibroblasts in complex fractionated electrograms during persistent/permanent atrial fibrillation: implications for electrogram-based catheter ablation.
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DOI：
10.1161/circresaha.111.255026
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发表时间：
2012-01-20
影响因子：
20.1
通讯作者：
Trayanova NA
中科院分区：
文献类型：
--
作者：
Ashihara T;Haraguchi R;Nakazawa K;Namba T;Ikeda T;Nakazawa Y;Ozawa T;Ito M;Horie M;Trayanova NA
基于电描记图的导管消融术针对复杂的分割心房电图 (CFAE)，根据经验已知可有效阻止持续性/永久性心房颤动 (AF)。然而，CFAE 和基于电描记图的消融的机制仍不清楚。由于心房纤维化与持续性/永久性 AF 相关，因此我们假设心房肌细胞和成纤维细胞之间的电紧张相互作用在 CFAE 发生和基于电图的导管消融中发挥重要作用。我们使用了心力衰竭的人体心房组织模型，并模拟了有或没有局部增殖的成纤维细胞的传播和螺旋波折返。成纤维细胞与心房肌细胞的偶联导致动作电位持续时间较短、传导速度较慢和兴奋性较低。因此，心肌片中的异质成纤维细胞增殖导致频繁的螺旋波破裂，并且在成纤维细胞增殖区域记录的双极电图表现出CFAE。模拟表明，针对此类成纤维细胞衍生的 CFAE 的消融终止了 AF，这是由于消融部位暂时钉住了螺旋波，然后将其推出成纤维细胞增殖区域。 CFAE 不能仅仅归因于胶原蛋白的积累。心房中的成纤维细胞增殖可能是持续性/永久性 AF 期间 CFAE 发生的原因。我们的研究结果可能有助于更好地理解 CFAE 靶向房颤消融的机制。
Electrogram-based catheter ablation, targeting complex fractionated atrial electrograms (CFAEs), is empirically known to be effective in halting persistent/permanent atrial fibrillation (AF). However, the mechanisms underlying CFAEs and electrogram-based ablation remain unclear. Because atrial fibrosis is associated with persistent/permanent AF, we hypothesized that electrotonic interactions between atrial myocytes and fibroblasts play an important role in CFAE genesis and electrogram-based catheter ablation. We used a human atrial tissue model in heart failure and simulated propagation and spiral wave reentry with and without regionally proliferated fibroblasts. Coupling of fibroblasts to atrial myocytes resulted in shorter action potential duration, slower conduction velocity, and lower excitability. Consequently, heterogeneous fibroblast proliferation in the myocardial sheet resulted in frequent spiral wave breakups, and the bipolar electrograms recorded at the fibroblast proliferation area exhibited CFAEs. The simulations demonstrated that ablation targeting such fibroblast-derived CFAEs terminated AF, resulting from the ablation site transiently pinning the spiral wave and then pushing it out of the fibroblast proliferation area. CFAEs could not be attributed to collagen accumulation alone. Fibroblast proliferation in atria might be responsible for the genesis of CFAEs during persistent/ permanent AF. Our findings could contribute to better understanding of the mechanisms underlying CFAE-targeted AF ablation.