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Pathophysiology and clinical relevance of atrial myopathy

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Abstract

Atrial myopathy is a condition that consists of electrical, structural, contractile, and autonomic remodeling of the atria and is the substrate for development of atrial fibrillation, the most common arrhythmia. Pathophysiologic mechanisms driving atrial myopathy are inflammation, oxidative stress, atrial stretch, and neurohormonal signals, e.g., angiotensin-II and aldosterone. These mechanisms initiate the structural and functional remodeling of the atrial myocardium. Novel therapeutic strategies are being developed that target the pathophysiologic mechanisms of atrial myopathy. In this review, we will discuss the pathophysiology of atrial myopathy, as well as diagnostic and therapeutic strategies.

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Funding

This work was supported by a Geconcerteerde onderzoeksactie grant (GOA, PID36444) of the University of Antwerp; by a Senior Clinical Investigator fellowship (to VFS) and research grants of the Fund for Scientific Research Flanders (Application Nos. 1842219N, G021019N, and G021420N; VLIR/iBOF Grant 20-VLIR-iBOF-027 (to VFS and GWDK).

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None of the authors has any personal conflicts of interest. MRLT, GWDK, and VFMS are acknowledged in a pending patent application without financial interest for their work on a Neuregulin-1 fusion protein to treat fibrosis and arrhythmia. This is unrelated to the content of this manuscript. HH received unconditional research support through the University of Hasselt or University of Antwerp from Bayer, Daiichi-Sankyo, Boehringer-Ingelheim, Bracco Imaging Europe, Medtronic, Boston-Scientific, Biotronik, and St Jude Medical, all outside the scope of this work.

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Tubeeckx, M.R.L., De Keulenaer, G.W., Heidbuchel, H. et al. Pathophysiology and clinical relevance of atrial myopathy. Basic Res Cardiol 119, 215–242 (2024). https://doi.org/10.1007/s00395-024-01038-0

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