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. 2019 Jan 11;9:1888. doi: 10.3389/fphys.2018.01888

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Copyright © 2019 Whittaker, Hancox and Zhang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Effects of class I drugs on human atrial electrophysiology in SQT1. Effects of (A) disopyramide (DISO), (B) quinidine (QUIN), and (C) propafenone (PROPAF) on (i) single human atrial cell action potentials (APs) under wild type (WT) conditions (blue, dashed line), drug-free WT-N588K (SQT1) conditions (green, solid line), and SQT1 + varying drug concentrations (purple, orange, and red solid lines). Corresponding fractional block of (ii) I_Kr and (iii) I_Na, and (iv) increase in APD₉₀ (red) and effective refractory period (ERP; blue). (D) Activation sequences in the 3D anatomical human atria model under (i) drug-free SQT1 (control – C), (ii) SQT1 + 2 μM DISO, (iii) SQT1 + 2 μM QUIN, and (iv) SQT1 + 0.5 μM PROPAF conditions, with corresponding (E) activation (ACT) time summarized as a barchart. All simulations performed at a basic cycle length of 1,000 ms.