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The bidirectional relationship of thyroid disease and atrial fibrillation: Established knowledge and future considerations

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Abstract

Atrial fibrillation (AF) tends to occur frequently in patients with thyroid disease, primarily hyperthyroidism. In hyperthyroidism, increased levels of thyroid hormones, via intra- and extranuclear mechanisms, have profound effects on cardiac electrophysiology. Hypothyroidism carries a lower risk for AF and is mainly associated with the overtreatment of hypothyroid patients. New-onset AF is frequently the only manifestation of thyroid disease, which renders screening for thyroid dysfunction in that scenario clinically useful. Managing thyroid disease and comorbid AF is essential. This includes thyroid hormones control along with conventional AF therapy. However, there are several open issues with this comorbid duo. The optimal management of thyroid disease and its impact on AF burden remains obscure. There is scanty information on clear-cut benefits for therapy of subclinical thyroid disease and screening of asymptomatic patients. Furthermore, the immunogenetic overlap between the autoantibodies in Graves’ disease and AF genesis may lead to novel therapeutic implications. The objective of this review is to summarize the up-to-date epidemiology, pathogenesis, pathophysiology and management of interacting thyroid disease and AF.

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Abbreviations

AF:

Atrial Fibrillation

TSH:

Thyroid-stimulating hormone/ thyrotropin

T3:

Triiodothyronine

T4:

Thyroxine

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Acknowledgements

We want to thank Dr Stavros Zanos (Institute of Bioelectronic Medicine, Feinstein Institutes for Medical Research) for his significant scientific contribution to the manuscript. Dr Zanos thoroughly revised the manuscript and added substantial knowledge on the interaction between thyroid hormones and the autonomic nervous system, which predisposes to AF.

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Correspondence to George Giannakoulas.

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Bekiaridou, A., Kartas, A., Moysidis, D.V. et al. The bidirectional relationship of thyroid disease and atrial fibrillation: Established knowledge and future considerations. Rev Endocr Metab Disord 23, 621–630 (2022). https://doi.org/10.1007/s11154-022-09713-0

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