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. 2020 Nov 30;115(6):72. doi: 10.1007/s00395-020-00827-7

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — General mechanisms of atrial fibrillation and the potential involvement of disturbed mitochondrial Ca²⁺ handling. Re-entry requires a vulnerable substrate and trigger for initiation. Ectopic activity can maintain re-entry behaviour. APD, action potential duration; DAD, delayed afterdepolarisation

(adapted from Heijman et al. [48])