论文标题
在存在微观纤维化结构的情况下,单域模型的均质化
Homogenisation for the monodomain model in the presence of microscopic fibrotic structures
论文作者
论文摘要
心脏电生理学中的计算模型对于长期运行时间臭名昭著,限制了用于解决方案的数值离散量中的节点和网格元素的数量。这使得在较小的空间尺度上纳入结构异质性,从而完全理解诸如心脏纤维化等疾病的关键心律失常作用,这一点尤其具有挑战性。在这项工作中,我们通过体积平均探索均质化的技术,以将非导电微结构包含到具有较小的计算开销的大规模心脏网格中。重要的是,我们的方法不仅限于周期性模式,从而使同质模型可以代表例如不同类型的纤维化中存在的胶原沉积的复杂模式。我们首先强调了适当的边界条件选择对于定义同质模型参数的封闭问题的重要性。然后,我们证明了该技术能够正确地将纤维化模式的效果(空间分辨率为10 $ $ m m)提高到更大的数值网格尺寸为100-250 $μ$ m的能力。使用这些更粗的网格的均质模型正确预测了纤维化的关键促性心律失常作用,包括传导减慢,源/接收器不匹配以及稳定重点激活模式。因此,这种同质化方法代表了迈出整个器官模拟的重要一步,该模拟揭示了微观心脏组织异质性的影响。
Computational models in cardiac electrophysiology are notorious for long runtimes, restricting the numbers of nodes and mesh elements in the numerical discretisations used for their solution. This makes it particularly challenging to incorporate structural heterogeneities on small spatial scales, preventing a full understanding of the critical arrhythmogenic effects of conditions such as cardiac fibrosis. In this work, we explore the technique of homogenisation by volume averaging for the inclusion of non-conductive micro-structures into larger-scale cardiac meshes with minor computational overhead. Importantly, our approach is not restricted to periodic patterns, enabling homogenised models to represent, for example, the intricate patterns of collagen deposition present in different types of fibrosis. We first highlight the importance of appropriate boundary condition choice for the closure problems that define the parameters of homogenised models. Then, we demonstrate the technique's ability to correctly upscale the effects of fibrotic patterns with a spatial resolution of 10 $μ$m into much larger numerical mesh sizes of 100-250 $μ$m. The homogenised models using these coarser meshes correctly predict critical pro-arrhythmic effects of fibrosis, including slowed conduction, source/sink mismatch, and stabilisation of re-entrant activation patterns. As such, this approach to homogenisation represents a significant step towards whole organ simulations that unravel the effects of microscopic cardiac tissue heterogeneities.