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. 2019 Sep 10;9:12997. doi: 10.1038/s41598-019-49450-0

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Simulation of the effect of drugs on human atrial action potential. (A) The virtual AP from virtual human atrial myocytes harboring WT SCN5A was compared with that from A1656D mutant harboring cells after 60 sec of stimulation at 1 Hz. The virtual human atrial myocyte with A1656D mutation exhibited prolonged APs with higher plateau and delayed after-depolarizations (DADs), compared with that of WT. (B–D) The simulated effects of mexiletine (B), flecainide (C), and ranolazine (D) on the AP of virtual human atrial myocytes with A1656D mutation.