Comparing Reentrant Drivers Predicted by Image-Based Computational Modeling and Mapped by Electrocardiographic Imaging in Persistent Atrial Fibrillation.

Comparing Reentrant Drivers Predicted by Image-Based Computational Modeling and Mapped by Electrocardiographic Imaging in Persistent Atrial Fibrillation.
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DOI:
10.3389/fphys.2018.00414
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发表时间:
2018
影响因子:
4
通讯作者:
Cochet H
Cochet H
中科院分区:
医学2区
文献类型:
--
作者:
Boyle PM;Hakim JB;Zahid S;Franceschi WH;Murphy MJ;Vigmond EJ;Dubois R;Haïssaguerre M;Hocini M;Jaïs P;Trayanova NA;Cochet H

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心电图测绘 (ECGI) 可检测导致持续性 AF (PsAF) 中心律失常持续的折返驱动因素 (RD)。来自晚期钆增强磁共振成像 (LGE-MRI) 的患者特定计算模型可识别纤维化基质中可能维持 RD 的所有潜在位点,而不仅仅是映射 AF 期间表现出的位点。本研究的目的是比较模拟和 ECGI (RDsim/RDECGI) 的 RD,并分析消融的影响。我们考虑了 12 名接受 RDECGI 消融术的 PsAF 患者。对于同一队列,我们​​模拟了 AF,并在患者特定模型中通过消融前 LGE-MRI 的几何形状和纤维化分布确定了 RDsim 部位。比较 RDsim 和 RDECGI 包含区域,并评估通过模拟和 ECGI 识别的 RD 宏观位置之间的一致性程度。分析了消融 RDECGI/RDsim 的效果。 RDsim 在 28 个心房区域进行预测(每个模型中位数 [四分位数范围 (IQR)] = 3.0 [1.0; 3.0])。 ECGI 检测到 42 个 RDECGI 隐藏区域(每位患者 4.0 [2.0; 5.0])。每个个体的 RDsim 和 RDECGI 区域数量没有显着相关(R = 0.46,P = ns)。正如预期的那样,基于 RDsim 和 RDECGI 不同的机制基础,区域一致性的总体比率是公平的(修正的 Cohen κ0 统计量 = 0.11)。研究发现 19 个区域同时存在 RDsim 和 RDECGI,这表明临床观察到的 RD 的一部分是由纤维化介导的。两种模式之间最常见的差异来源(23/32 区域)是 RDECGI 的存在,其通过纤维化基质以外的机制持续存在。在 6/12 例患者中,至少有一个区域在模拟中观察到潜在 RD,但在临床绘图中并未表现出来。与其他 RDECGI 靶标的消融相比,纤维化介导的 RDECGI(即也含有 RDsim 的区域中的靶标)的消融倾向于更高的阳性反应率(57% vs. 41%,P = ns)。我们的分析表明,人类 PsAF 中的 RD 至少部分是由纤维化介导的。基于基底的消融结合模拟与 ECGI 可以改善结果。
Electrocardiographic mapping (ECGI) detects reentrant drivers (RDs) that perpetuate arrhythmia in persistent AF (PsAF). Patient-specific computational models derived from late gadolinium-enhanced magnetic resonance imaging (LGE-MRI) identify all latent sites in the fibrotic substrate that could potentially sustain RDs, not just those manifested during mapped AF. The objective of this study was to compare RDs from simulations and ECGI (RDsim/RDECGI) and analyze implications for ablation. We considered 12 PsAF patients who underwent RDECGI ablation. For the same cohort, we simulated AF and identified RDsim sites in patient-specific models with geometry and fibrosis distribution from pre-ablation LGE-MRI. RDsim- and RDECGI-harboring regions were compared, and the extent of agreement between macroscopic locations of RDs identified by simulations and ECGI was assessed. Effects of ablating RDECGI/RDsim were analyzed. RDsim were predicted in 28 atrial regions (median [inter-quartile range (IQR)] = 3.0 [1.0; 3.0] per model). ECGI detected 42 RDECGI-harboring regions (4.0 [2.0; 5.0] per patient). The number of regions with RDsim and RDECGI per individual was not significantly correlated (R = 0.46, P = ns). The overall rate of regional agreement was fair (modified Cohen's κ0 statistic = 0.11), as expected, based on the different mechanistic underpinning of RDsim- and RDECGI. nineteen regions were found to harbor both RDsim and RDECGI, suggesting that a subset of clinically observed RDs was fibrosis-mediated. The most frequent source of differences (23/32 regions) between the two modalities was the presence of RDECGI perpetuated by mechanisms other than the fibrotic substrate. In 6/12 patients, there was at least one region where a latent RD was observed in simulations but was not manifested during clinical mapping. Ablation of fibrosis-mediated RDECGI (i.e., targets in regions that also harbored RDsim) trended toward a higher rate of positive response compared to ablation of other RDECGI targets (57 vs. 41%, P = ns). Our analysis suggests that RDs in human PsAF are at least partially fibrosis-mediated. Substrate-based ablation combining simulations with ECGI could improve outcomes.
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