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BACKGROUND

Recent researches have suggested that the complex three-dimensional structures caused by structural remodeling play a key role in atrial fibrillation (AF) substrates. Here we aimed to investigate this hypothesis using a multi-layer model representing intramural microstructural features.

METHODS

The proposed multi-layer model was composed of the endocardium, connection wall, and epicardium. In the connection wall, intramural fibrosis was simulated using fibrotic patches randomly scattered in the myocardial tissue of fibrotic layers, while endo-epicardial dissociation was simulated using myocardial patches randomly scattered in the fibrotic tissue of isolation layers. Multiple simulation groups were generated to quantitatively analyze the effects of endo-epicardial dissociation and intramural fibrosis on AF stability, including a stochastic group, interrelated groups, fibrosis-degree-controlled groups, and dissociation-degree-controlled groups.

RESULTS

Stable intramural re-entries were observed to move along complete re-entrant circuits inside the transmural wall in four of 65 simulations in the stochastic group. 2. About 21 of 23 stable simulations in the stochastic group were distributed in the areas with high endo-epicardial dissociation and intramural fibrosis. 3. The difference between fibrosis-degree-controlled groups and dissociation-degree-controlled groups suggested that some distributions of connection areas may affect AF episodes despite low intramural fibrosis and endo-epicardial dissociation. 4. The overview of tracking phase singularities revealed that endo-epicardial dissociation played a visible role in AF substrates.

CONCLUSION

The complex intramural microstructure is positively correlated with critical components of AF maintenance mechanisms. The occurrence of intramural re-entry further indicates the complexity of AF wave-dynamics.

BACKGROUND

METHODS

RESULTS

Stable intramural re-entries were observed to move along complete re-entrant circuits inside the transmural wall in four of 65 simulations in the stochastic group. 2. About 21 of 23 stable simulations in the stochastic group were distributed in the areas with high endo-epicardial dissociation and intramural fibrosis. 3. The difference between fibrosis-degree-controlled groups and dissociation-degree-controlled groups suggested that some distributions of connection areas may affect AF episodes despite low intramural fibrosis and endo-epicardial dissociation. 4. The overview of tracking phase singularities revealed that endo-epicardial dissociation played a visible role in AF substrates.

CONCLUSION

背景

最近的研究表明，结构重塑引起的复杂三维结构在心房颤动（AF）基质中起着关键作用。在这里，我们旨在使用代表壁内微观结构特征的多层模型来研究这一假设。

方法

所提出的多层模型由心内膜、连接壁和心外膜组成。在连接壁中，使用随机散布在纤维化层心肌组织中的纤维化斑块模拟壁内纤维化，而使用随机散布在隔离层纤维化组织中的心肌斑块模拟心内膜-心外膜分离。生成了多个模拟组来定量分析心内膜-心外膜分离和壁内纤维化对 AF 稳定性的影响，包括随机组、相关组、纤维化程度控制组和分离程度控制组。

结果

在随机组的 65 次模拟中有 4 次观察到稳定的壁内折返沿着透壁壁内的完整折返环移动。2. 在随机组的 23 次稳定模拟中，约有 21 次分布在高心内膜-心外膜分离和壁内纤维化的区域。3. 纤维化程度控制组和分离程度控制组之间的差异表明，尽管壁内纤维化和心内膜-心外膜分离程度低，但连接区域的某些分布可能会影响 AF 发作。4. 跟踪相位奇点的概述表明，心内膜-心外膜分离在 AF 基质中起着明显的作用。