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. 2017 Nov 21;7:15922. doi: 10.1038/s41598-017-16218-3

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© The Author(s) 2017

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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Transmural Dispersion. Absolute ∆APD80 was calculated in milliseconds from epi, mid, and endo areas of the transmural surface. (a) No significant difference was observed from ∆APD80 across the transmural surface post I_Ks blockade in protocol B. (b) ∆APD80 was calculated as the difference between post and pre-treatment. APD80 reduction from isoprenaline was significantly greater in the epicardium as compared to the endocardium. On the other hand, APD80 under I_Kr blockade increased more significantly in the midmyocardium and endocardium as compared to the epicardium. (c) Normalized ∆APD80 was calculated as the difference between post treatment and baseline. The transmural gradient was increased by both isoprenaline and E-4031, a trend which was also observed in comparing pre- and post-treatments.