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. 2017 Dec 28;18(Suppl 14):497. doi: 10.1186/s12859-017-1895-2

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© The Author(s). 2017

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 1 — Schematic changes in ventricular action potential at the molecular level within the cardiomyocytes. The resting membrane potential of cardiomyocytes is about −90 mV (mV) while at the full depolarization it can be gradually shifted to +20 mV. In the repolarization stage, membrane potential will return to −90 mV. Some drugs can prolong the duration of normal action potential (lengthened action potential in green) which eventually can lead to drug-induced arrhythmia. Consequently, production of lengthened action potential (long QT syndrome) may initiate TdP arrhythmia (Adapted with permission from [31])