| Literature DB >> 34907620 |
Elmir Omerovic1, Rodolfo Citro2, Eduardo Bossone3, Bjorn Redfors1, Johannes Backs4,5, Bastian Bruns4,5,6, Michele Ciccarelli7, Liam S Couch8, Dana Dawson9, Guido Grassi10, Massimo Iacoviello11, Guido Parodi12, Birke Schneider13, Christian Templin14, Jelena R Ghadri14, Thomas Thum15, Ovidiu Chioncel16, C Gabriele Tocchetti17, Jolanda van der Velden18, Stephane Heymans19,20, Alexander R Lyon8,21.
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 β-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.Entities:
Keywords: Beta-adrenergic signalling; Catecholamine; Electrophysiology; G-protein coupled receptor kinase; Inflammation; Metabolism; Pathophysiology; Takotsubo syndrome
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Year: 2022 PMID: 34907620 DOI: 10.1002/ejhf.2400
Source DB: PubMed Journal: Eur J Heart Fail ISSN: 1388-9842 Impact factor: 17.349