4.5 Article

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

Journal

EUROPEAN JOURNAL OF HEART FAILURE
Volume 24, Issue 2, Pages 257-273

Publisher

WILEY
DOI: 10.1002/ejhf.2400

Keywords

Takotsubo syndrome; Pathophysiology; Catecholamine; Beta-adrenergic signalling; G-protein coupled receptor kinase; Electrophysiology; Inflammation; Metabolism

Funding

  1. Netherlands Cardiovascular Research Initiative
  2. Dutch Heart Foundation [2015-10, 2017-21]
  3. European Union Commission [305507, 602904]
  4. British Heart Foundation [PG/15/108/31928, FS/16/39/32174]
  5. Josephine Lansdell British Medical Association
  6. Tenovus Scotland [G13.10]
  7. Leducq Foundation Cardio-Oncology Network

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This scientific statement from the Heart Failure Association (HFA) of the European Society of Cardiology focuses on the pathophysiology of Takotsubo syndrome. It provides an overview of the disease and discusses the role of catecholamines and the sympathetic nervous system, as well as their direct effects on myocardial biology. The statement also explores the integrated effects on ventricular haemodynamics.
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.

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