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In silico assessment of genetic variation in KCNA5 reveals multiple mechanisms of human atrial arrhythmogenesis

Fig 1

Effects of gain-of-function KCNA5 mutations.

A Effects of the mutations on the AP (i-iii) and APD-restitution (iv-vi) properties of human atrial myocytes elicited by updated Colman et al. model, Courtemanche et al. model and Grandi et al. model. B Effects of the mutations on the maximum sustained dominant frequency of excitation waves under the lone AF and chronic AF conditions using (i) Colman et al. model and (ii) Courtemanche et al. model. C Effects of the mutations on APD heterogeneity and tissue vulnerability window at the CT/PM junction in Colman et al. model. APD distribution among regional cells of whole atria and CT/PM for in (i) isolated single cells and (ii) in coupled tissue; the APD distribution in tissue is shown in boxplots with outlier limits of 1.5×IQR (interquartile range). (iii) Temporal vulnerability window to propagation wave break at the CT/PM junction.

Fig 1

doi: https://doi.org/10.1371/journal.pcbi.1005587.g001