Boyle Patrick M, Hakim Joe B, Zahid Sohail, Franceschi William H, Murphy Michael J, Vigmond Edward J, Dubois Rémi, Haïssaguerre Michel, Hocini Mélèze, Jaïs Pierre, Trayanova Natalia A, Cochet Hubert
Department of Biomedical Engineering, Institute for Computational Medicine, Johns Hopkins University, Baltimore, MD, United States.
L'Institut de RYthmologie et Modélisation Cardiaque (IHU-LIRYC), Pessac-Bordeaux, France.
Front Physiol. 2018 Apr 19;9:414. doi: 10.3389/fphys.2018.00414. eCollection 2018.
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 (RD/RD) and analyze implications for ablation. We considered 12 PsAF patients who underwent RD ablation. For the same cohort, we simulated AF and identified RD sites in patient-specific models with geometry and fibrosis distribution from pre-ablation LGE-MRI. RD- and RD-harboring regions were compared, and the extent of agreement between macroscopic locations of RDs identified by simulations and ECGI was assessed. Effects of ablating RD/RD were analyzed. RD were predicted in 28 atrial regions (median [inter-quartile range (IQR)] = 3.0 [1.0; 3.0] per model). ECGI detected 42 RD-harboring regions (4.0 [2.0; 5.0] per patient). The number of regions with RD and RD per individual was not significantly correlated ( = 0.46, = ns). The overall rate of regional agreement was fair (modified Cohen's κ statistic = 0.11), as expected, based on the different mechanistic underpinning of RD- and RD. nineteen regions were found to harbor both RD and RD, 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 RD 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 RD (i.e., targets in regions that also harbored RD) trended toward a higher rate of positive response compared to ablation of other RD targets (57 vs. 41%, = 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.
心电图标测(ECGI)可检测出导致持续性房颤(PsAF)心律失常持续存在的折返驱动因素(RDs)。从延迟钆增强磁共振成像(LGE-MRI)得出的患者特异性计算模型可识别纤维化基质中所有可能维持折返驱动因素的潜在部位,而不仅仅是在标测房颤期间表现出来的那些部位。本研究的目的是比较模拟和ECGI得出的折返驱动因素(RD/RD),并分析其对消融的影响。我们纳入了12例接受了折返驱动因素消融的PsAF患者。对于同一队列,我们模拟了房颤,并在具有消融前LGE-MRI的几何形状和纤维化分布的患者特异性模型中识别出折返驱动因素部位。比较了折返驱动因素和含有折返驱动因素的区域,并评估了模拟和ECGI识别出的折返驱动因素宏观位置之间的一致程度。分析了消融折返驱动因素/折返驱动因素的效果。在28个心房区域预测到了折返驱动因素(每个模型中位数[四分位间距(IQR)]=3.0[1.0;3.0])。ECGI检测到42个含有折返驱动因素的区域(每位患者4.0[2.0;5.0])。个体中含有折返驱动因素和折返驱动因素的区域数量无显著相关性(=0.46,=无显著性差异)。基于折返驱动因素和折返驱动因素不同的机制基础,区域一致性的总体比率一般(修正的科恩κ统计量=0.11)。发现19个区域同时含有折返驱动因素和折返驱动因素,这表明临床观察到的一部分折返驱动因素是由纤维化介导的。两种方法之间最常见的差异来源(32个区域中的23个)是存在由纤维化基质以外的机制维持的折返驱动因素。在12例患者中的6例中,至少有一个区域在模拟中观察到潜在的折返驱动因素,但在临床标测期间未表现出来。与消融其他折返驱动因素靶点相比,消融由纤维化介导的折返驱动因素(即也含有折返驱动因素的区域中的靶点)的阳性反应率有升高趋势(57%对41%,=无显著性差异)。我们的分析表明,人类PsAF中的折返驱动因素至少部分是由纤维化介导的。将模拟与ECGI相结合的基于基质的消融可能会改善治疗效果。