Image-Based Computational Evaluation of the Effects of Atrial Wall Thickness and Fibrosis on Re-entrant Drivers for Atrial Fibrillation.

Image-Based Computational Evaluation of the Effects of Atrial Wall Thickness and Fibrosis on Re-entrant Drivers for Atrial Fibrillation.
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DOI:
10.3389/fphys.2018.01352
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发表时间:
2018
影响因子:
4
通讯作者:
Aslanidi O
Aslanidi O
中科院分区:
医学2区
文献类型:
--
作者:
Roy A;Varela M;Aslanidi O

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导读:导管消融(CA)是房颤(AF)的一种常用治疗方法,但对最佳消融部位的了解以及由此产生的临床结果并不理想。越来越多的证据表明,基于患者特异性底物信息的消融策略,如纤维化分布和心房壁厚度(AWT),可用于改善治疗。我们假设,大AWT梯度和纤维化贴片对心房组织传导特性的竞争影响可以确定维持房颤的再入驱动因素(rd)的位置。方法:使用两组模型:(1)AWT阶变的简单3D心房组织板模型和合成纤维化贴片;(2)基于患者特异性右心房(RA)和左心房(LA)几何形状的3D模型。后者分别来自4名健康志愿者和2名房颤患者,使用磁共振成像(MRI)获得。在RA中添加合成纤维化贴片,并通过同一患者的钆增强MRI获得LA中的纤维化分布。在所有模型中,3D几何形状与Fenton-Karma心房细胞模型相结合来模拟rd。结果:在平板内,RDs先向AWT台阶漂移,然后沿AWT台阶漂移。然而,随着额外的纤维化,rd定位在步骤和纤维化之间的区域。在RA中,rd向终端嵴(CT)区域和周围心房壁之间的大AWT梯度漂移并锚定。如果没有这样的梯度,rd会向上腔静脉(SVC)或三尖瓣(TSV)漂移。随着进一步的纤维化,rd起源于远离固定在纤维化贴片上的CT,而rd起源于靠近CT区域,仍然定位在两个结构之间。在洛杉矶,AWT更均匀,rd向肺静脉(pv)漂移。然而,有了额外的纤维化斑块,rd要么固定在它们上,要么繁殖。结论:在RA中,RD的位置由CT区域的纤维化和AWT梯度决定。在LA中,它们是由纤维化决定的,因为没有大的AWT梯度。这些结果阐明了维持房颤的rd稳定背后的机制,并有助于指导消融治疗。
Introduction: Catheter ablation (CA) is a common treatment for atrial fibrillation (AF), but the knowledge of optimal ablation sites, and hence clinical outcomes, are suboptimal. Increasing evidence suggest that ablation strategies based on patient-specific substrates information, such as distributions of fibrosis and atrial wall thickness (AWT), may be used to improve therapy. We hypothesized that competing influences of large AWT gradients and fibrotic patches on conductive properties of atrial tissue can determine locations of re-entrant drivers (RDs) sustaining AF. Methods: Two sets of models were used: (1) a simple model of 3D atrial tissue slab with a step change in AWT and a synthetic fibrosis patch, and (2) 3D models based on patient-specific right atrial (RA) and left atrial (LA) geometries. The latter were obtained from four healthy volunteers and two AF patients, respectively, using magnetic resonance imaging (MRI). A synthetic fibrotic patch was added in the RA and fibrosis distributions in the LA were obtained from gadolinium-enhanced MRI of the same patients. In all models, 3D geometry was combined with the Fenton-Karma atrial cell model to simulate RDs. Results: In the slab, RDs drifted toward, and then along the AWT step. However, with additional fibrosis, the RDs were localized in regions between the step and fibrosis. In the RA, RDs drifted toward and anchored to a large AWT gradient between the crista terminalis (CT) region and the surrounding atrial wall. Without such a gradient, RDs drifted toward the superior vena cava (SVC) or the tricuspid valve (TSV). With additional fibrosis, RDs initiated away from the CT anchored to the fibrotic patch, whereas RDs initiated close to the CT region remained localized between the two structures. In the LA, AWT was more uniform and RDs drifted toward the pulmonary veins (PVs). However, with additional fibrotic patches, RDs either anchored to them or multiplied. Conclusion: In the RA, RD locations are determined by both fibrosis and AWT gradients at the CT region. In the LA, they are determined by fibrosis due to the absence of large AWT gradients. These results elucidate mechanisms behind the stabilization of RDs sustaining AF and can help guide ablation therapy.
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