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. 2017 Jul 5;37(5):780–789. doi: 10.1007/s40846-017-0257-x

Fig. 2.

Fig. 2

Simulated WT and heterozygous V141M KCNQ1 action potentials (AP) and the IKs and ICaL during the AP in endocardial (Endo), epicardial (Epi) and midmyocardial (Mid) myocytes with and without isoproterenol (ISO). A modified O’Hara-Rudy (ORd) human ventricular myocyte model was used in the simulations. The cycle length was 1000 ms. Baseline APs (in grey) and APs with ISO challenge (in black) were simulated for WT (dash lines) and V141M KCNQ1 (solid lines) respectively. APs were shortened significantly by the V141M KCNQ1 mutation with and without ISO. In all V141M cases, IKs and ICaL increased relative to WT during the AP