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. 2019 Aug 15;9:11893. doi: 10.1038/s41598-019-48174-5

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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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LEAP signals reproduce expected responses to ion channel blockers. Cardiomyocytes (iCell CM²) plated on Classic MEA 48-well plates were dosed with vehicle control or one of four doses of Nifedipine (a), E-4031 (b), and Verapamil (c). For each compound, amplitude normalized LEAP waveforms (averaged across 5 beats) from representative wells are overlaid for DMSO (black) and the four increasing concentrations of each compound (dark gray, light gray, orange, and teal). Triangles indicate automatically detected EADs. Bar plots represent the mean ± standard deviation of APD30, 50, and 90 across replicate wells (n = 8 for DMSO, n = 5 for each concentration of Nifedipine and E-4031, n = 3 for each concentration of Verapamil). The highest dose of Verapamil stopped cardiomyocyte beating.