Simulation of diffuse and stringy fibrosis in a bilayer interconnected cable model of the left atrium

Aims The aim of this study is to design a computer model of the left atrium for investigating fibre-orientation-dependent microstructure such as stringy fibrosis. Methods and results We developed an approach for automatic construction of bilayer interconnected cable models from left atrial geometry and epi- and endocardial fibre orientation. The model consisted of two layers (epi- and endocardium) of longitudinal and transverse cables intertwined-like fabric threads, with a spatial discretization of 100 mu m. Model validation was performed by comparison with cubic volumetric models in normal conditions. Then, diffuse (n = 2904), stringy (n = 3600), and mixed fibrosis patterns (n = 6840) were randomly generated by uncoupling longitudinal and transverse connections in the interconnected cable model. Fibrosis density was varied from 0% to 40% and mean stringy obstacle length from 0.1 to 2 mm. Total activation time, apparent anisotropy ratio, and local activation time jitter were computed during normal rhythm in each pattern. Non-linear regression formulas were identified for expressing measured propagation parameters as a function of fibrosis density and obstacle length (stringy and mixed patterns). Longer obstacles (even below tissue space constant) were independently associated with prolonged activation times, increased anisotropy, and local fluctuations in activation times. This effect was increased by endo-epicardial dissociation and mitigated when fibrosis was limited to the epicardium. Conclusion Interconnected cable models enable the study of microstructure in organ-size models despite limitations in the description of transmural structures.

Automated summary

The study aims to design a computer model of the left atrium to investigate microstructure dependent on fiber orientation like stringy fibrosis. Through an interconnected cable model, different fibrosis patterns were generated and it was found that longer obstacles in the model led to prolonged activation times, increased anisotropy, and local activation time jitter. The study concludes that the presence and length of fibrosis can impact the conduction parameters of the heart.