ElectroCardioMaths Programme, Imperial Centre for Cardiac Engineering, Imperial College London, London, UK.
LIRYC Electrophysiology and Heart Modeling Institute, Bordeaux Fondation, Avenue du Haut-Lévèque, Pessac, France.
Europace. 2018 Nov 1;20(suppl_3):iii3-iii15. doi: 10.1093/europace/euy235.
Atrial fibrillation (AF) wavefront dynamics are complex and difficult to interpret, contributing to uncertainty about the mechanisms that maintain AF. We aimed to investigate the interplay between rotors, wavelets, and focal sources during fibrillation.
Arrhythmia wavefront dynamics were analysed for four optically mapped canine cholinergic AF preparations. A bilayer computer model was tuned to experimental preparations, and varied to have (i) fibrosis in both layers or the epicardium only, (ii) different spatial acetylcholine distributions, (iii) different intrinsic action potential duration between layers, and (iv) varied interlayer connectivity. Phase singularities (PSs) were identified and tracked over time to identify rotational drivers. New focal wavefronts were identified using phase contours. Phase singularity density and new wavefront locations were calculated during AF. There was a single dominant mechanism for sustaining AF in each of the preparations, either a rotational driver or repetitive new focal wavefronts. High-density PS sites existed preferentially around the pulmonary vein junctions. Three of the four preparations exhibited stable preferential sites of new wavefronts. Computational simulations predict that only a small number of connections are functionally important in sustaining AF, with new wavefront locations determined by the interplay between fibrosis distribution, acetylcholine concentration, and heterogeneity in repolarization within layers.
We were able to identify preferential sites of new wavefront initiation and rotational activity, in order to determine the mechanisms sustaining AF. Electrical measurements should be interpreted differently according to whether they are endocardial or epicardial recordings.
心房颤动(AF)的波阵面动力学复杂且难以解释,这导致维持 AF 的机制存在不确定性。我们旨在研究颤动过程中转子、波瓣和灶源之间的相互作用。
分析了四个光学映射犬胆碱能 AF 制剂的心律失常波阵面动力学。双层计算机模型根据实验制剂进行了调整,并进行了以下调整:(i)双层或心外膜均有纤维化;(ii)不同的空间乙酰胆碱分布;(iii)层间不同的固有动作电位持续时间;(iv)改变层间连接。随时间识别和跟踪相位奇点(PS),以识别旋转驱动因素。使用相位轮廓识别和跟踪新的焦点波前。在 AF 期间计算 PS 密度和新波前位置。在每个制剂中,维持 AF 的单一主导机制是旋转驱动因素或重复的新焦点波前。高密度 PS 位点优先存在于肺静脉交界处周围。四个制剂中的三个表现出稳定的新波前优先出现的位置。计算模拟预测,只有少数连接在维持 AF 中具有功能重要性,新波前的位置由纤维化分布、乙酰胆碱浓度和层内复极化异质性之间的相互作用决定。
我们能够确定新波前起始和旋转活动的优先部位,以确定维持 AF 的机制。电测量结果应根据是心内膜还是心外膜记录进行不同的解释。