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. 2023 Feb 22;44(27):2483–2494. doi: 10.1093/eurheartj/ehad086

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© The Author(s) 2023. Published by Oxford University Press on behalf of the European Society of Cardiology.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (https://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Structured Graphical Abstract — The reduction of L-type Ca²⁺-current in atrial myocytes promotes atrial fibrillation. Phosphodiesterase type 8B binds L-type Ca²⁺ channels and reduces local cAMP levels and PKA-dependent channel phosphorylation, thereby decreasing L-type Ca²⁺-current and abbreviating atrial action potential that promotes atrial fibrillation persistence. ADP, adenosine diphosphate; cAF, persistent (chronic) atrial fibrillation; cAMP, cyclic adenosine monophosphate; DAD, delayed afterdepolarization; I_Ca,L, L-type Ca²⁺ current; LTCC, L-type Ca²⁺ channel; PDE, phosphodiesterase; PLB, phospholamban; RyR2, ryanodine receptor type 2; SERCA2a, sarcoplasmic reticulum Ca^{2 +} ATPase type 2a; SLN, sarcolipin; SR, sinus rhythm.