Pathophysiology of Takotsubo syndrome - a joint scientific statement from the Heart Failure Association Takotsubo Syndrome Study Group and Myocardial Function Working Group of the European Society of Cardiology - Part 1: overview and the central role for catecholamines and sympathetic nervous system

Elmir Omerovic* (Corresponding Author), Rodolfo Citro, Eduardo Bossone, Bjorn Redfors, Johannes Backs, Bastian Bruns, Michele Ciccarelli, Liam S. Couch, Dana Dawson, Guido Grassi, Massimo Iacoviello, Guido Parodi, Birke Schneider, Christian Templin, Jelena R. Ghadri, Thomas Thum, Ovidiu Chioncel, C. Gabriele Tocchetti, Jolanda van der Velden, Stephane HeymansAlexander R. Lyon

*Corresponding author for this work

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Abstract

This is the first part of a scientific statement from the Heart Failure Association (HFA) of the European Society of Cardiology focused upon the pathophysiology of Takotsubo syndrome and is complimentary to the previous HFA position statement on Takotsubo syndrome which focused upon clinical management. In part 1 we provide an overview of the pathophysiology of Takotsubo syndrome and fundamental questions to consider. We then review and discuss the central role of catecholamines and the sympathetic nervous system in the pathophysiology, and the direct effects of high surges in catecholamines upon myocardial biology including beta-adrenergic receptor signalling, G-protein coupled receptor kinases, cardiomyocyte calcium physiology, myofilament physiology, cardiomyocyte gene expression, myocardial electrophysiology and arrhythmogenicity, myocardial inflammation, metabolism and energetics. The integrated effects upon ventricular haemodynamics are discussed and integrated into the pathophysiological model.

Original languageEnglish
Pages (from-to)257-273
Number of pages17
JournalEuropean Journal of Heart Failure
Volume24
Issue number2
Early online date16 Feb 2022
DOIs
Publication statusPublished - 23 Feb 2022

Bibliographical note

Acknowledgements
S.H. acknowledges the support from the Netherlands Cardiovascular Research Initiative, an initiative with support of the Dutch Heart Foundation, CVON2016-Early HFPEF, 2015-10, and CVON She-PREDICTS, grant 2017-21, CVON-Arena-PRIME, European Union Commission’s Seventh Framework programme under grant agreement n. 305507 (HOMAGE) and n. 602904 (FIBROTAR-GETS). D.D. acknowledges support from the British Heart Foundation grants PG/15/108/31928 and FS/16/39/32174, the Josephine Lansdell British Medical Association 2015Award and Tenovus Scotland, G13.10. A.R.L. is supported by the Leducq Foundation Cardio-Oncology Network. Conflict of interest: none declared

Keywords

  • Takotsubo syndrome
  • Pathophysiology
  • Catecholamine
  • Beta-adrenergic signalling
  • G-protein coupled receptor kinase
  • Electrophysiology
  • Inflammation
  • Metabolism
  • TAKO-TSUBO CARDIOMYOPATHY
  • COUPLED-RECEPTOR KINASE-5
  • STRESS-INDUCED CARDIOMYOPATHY
  • LIFE-THREATENING ARRHYTHMIAS
  • QT INTERVAL PROLONGATION
  • BALLOONING SYNDROME
  • CLINICAL-FEATURES
  • VENTRICULAR DYSFUNCTION
  • NATRIURETIC PEPTIDE
  • DIAGNOSTIC-CRITERIA

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