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心房壁厚度和拉伸的非均一性促进心房颤动时的-scroll 波锚定。

Heterogeneous atrial wall thickness and stretch promote scroll waves anchoring during atrial fibrillation.

机构信息

Center for Arrhythmia Research, Department of Internal Medicine, University of Michigan, 5025 Venture Drive, Ann Arbor, MI 48108, USA.

出版信息

Cardiovasc Res. 2012 Apr 1;94(1):48-57. doi: 10.1093/cvr/cvr357. Epub 2012 Jan 6.

Abstract

AIMS

Atrial dilatation and myocardial stretch are strongly associated with atrial fibrillation (AF). However, the mechanisms by which the three-dimensional (3D) atrial architecture and heterogeneous stretch contribute to AF perpetuation are incompletely understood. We compared AF dynamics during stretch-related AF (pressure: 12 cmH(2)O) in normal sheep hearts (n = 5) and in persistent AF (PtAF, n = 8)-remodelled hearts subjected to prolonged atrial tachypacing. We hypothesized that, in the presence of stretch, meandering 3D atrial scroll waves (ASWs) anchor in regions of large spatial gradients in wall thickness.

METHODS AND RESULTS

We implemented a high-resolution optical mapping set-up that enabled simultaneous epicardial- and endoscopy-guided endocardial recordings of the intact atria in Langendorff-perfused normal and PtAF (AF duration: 21.3 ± 11.9 days) hearts. The numbers and lifespan of long-lasting ASWs (>3 rotations) were greater in PtAF than normal (lifespan 0.9 ± 0.5 vs. 0.4 ± 0.2 s/(3 s of AF), P< 0.05). Than normal hearts, focal breakthroughs interacted with ASWs at the posterior left atrium and left atrial appendage to maintain AF. In PtAF hearts, ASW filaments seemed to span the atrial wall from endocardium to epicardium. Numerical simulations using 3D atrial geometries (Courtemanche-Ramirez-Nattel human atrial model) predicted that, similar to experiments, filaments of meandering ASWs stabilized at locations with large gradients in myocardial thickness. Moreover, simulations predicted that ionic remodelling and heterogeneous distribution of stretch-activated channel conductances contributed to filament stabilization.

CONCLUSION

The heterogeneous atrial wall thickness and atrial stretch, together with ionic and anatomic remodelling caused by AF, are the main factors allowing ASW and AF maintenance.

摘要

目的

心房扩张和心肌拉伸与心房颤动(AF)密切相关。然而,三维(3D)心房结构和不均匀拉伸如何导致 AF 持续存在的机制尚不完全清楚。我们比较了在正常绵羊心脏(n = 5)和持续性 AF(PtAF,n = 8)-重塑心脏中与拉伸相关的 AF(压力:12cmH2O)期间的 AF 动力学。我们假设,在拉伸存在的情况下,蜿蜒的 3D 心房滚动波(ASW)会在壁厚度空间梯度较大的区域固定。

方法和结果

我们实施了一种高分辨率光学映射设置,该设置使我们能够同时对 Langendorff 灌注的正常和 PtAF(AF 持续时间:21.3 ± 11.9 天)心脏的完整心房进行心外膜和内窥镜引导的心内膜记录。PtAF 中的长时 ASW(>3 次旋转)的数量和寿命长于正常(寿命 0.9 ± 0.5 与 0.4 ± 0.2 s/(3 s 的 AF),P<0.05)。与正常心脏相比,局灶性突破与左心房后侧壁和左心耳的 ASW 相互作用以维持 AF。在 PtAF 心脏中,ASW 纤维似乎跨越了从心内膜到心外膜的心房壁。使用 3D 心房几何形状(Courtemanche-Ramirez-Nattel 人类心房模型)的数值模拟预测,与实验相似,蜿蜒 ASW 的纤维在心肌厚度梯度较大的位置稳定。此外,模拟预测离子重塑和拉伸激活通道电导的不均匀分布有助于纤维稳定。

结论

不均匀的心房壁厚度和心房拉伸,以及由 AF 引起的离子和解剖重塑,是允许 ASW 和 AF 维持的主要因素。

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