In silico assessment of genetic variation in KCNA5 reveals multiple mechanisms of human atrial arrhythmogenesis
A Effects of the mutations on 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 in the lone AF and chronic AF conditions using (i) Colman et al. model and (ii) Courtemanche et al. model. C Effects of KCNA5 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 wave propagation break at the CT/PM junction. In panel B, * indicates cases in which re-entrant waves could not be sustained.