Hyperthermia as a trigger for Takotsubo syndrome in a rat model

Takotsubo syndrome is a well-characterized cause of acute yet reversible heart failure associated with periods of intense emotional stress, often mimicking on presentation an acute coronary syndrome. Animal models of Takotsubo syndrome have been developed, either through the application of a stresso...

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Published in:Frontiers in Cardiovascular Medicine
Main Authors: Matthew H. Tranter, Bjorn Redfors, Peter T. Wright, Liam S. Couch, Alexander R. Lyon, Elmir Omerovic, Sian E. Harding
Format: Article
Language:English
Published: Frontiers Media S.A. 2022-07-01
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Online Access:https://www.frontiersin.org/articles/10.3389/fcvm.2022.869585/full
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author Matthew H. Tranter
Matthew H. Tranter
Bjorn Redfors
Peter T. Wright
Peter T. Wright
Liam S. Couch
Alexander R. Lyon
Elmir Omerovic
Sian E. Harding
author_facet Matthew H. Tranter
Matthew H. Tranter
Bjorn Redfors
Peter T. Wright
Peter T. Wright
Liam S. Couch
Alexander R. Lyon
Elmir Omerovic
Sian E. Harding
author_sort Matthew H. Tranter
collection DOAJ
container_title Frontiers in Cardiovascular Medicine
description Takotsubo syndrome is a well-characterized cause of acute yet reversible heart failure associated with periods of intense emotional stress, often mimicking on presentation an acute coronary syndrome. Animal models of Takotsubo syndrome have been developed, either through the application of a stressor, or administration of exogenous catecholamine. We found that in a model of isoproterenol-induced Takotsubo syndrome in anesthetized rats hyperthermia (40–41°C) would occur after the administration of isoproterenol. Maintenance of this hyperthermia would result in an apical hypocontractility typical of the syndrome, whereas prevention of hyperthermia with active cooling to maintain a euthermic core body temperature prevented (but did not subsequently reverse) apical hypocontractility. In vitro experimentation with isolated cardiomyocytes showed no effect of hyperthermia on either baseline contractility or contractility change after beta-adrenoceptor stimulation. We suggest that the rise in body temperature that is characteristic of catecholamine storm may be a component in the development of Takotsubo syndrome.
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spelling doaj-art-832d9a42e1024e01ac9512c49e2013e42025-08-19T21:51:15ZengFrontiers Media S.A.Frontiers in Cardiovascular Medicine2297-055X2022-07-01910.3389/fcvm.2022.869585869585Hyperthermia as a trigger for Takotsubo syndrome in a rat modelMatthew H. Tranter0Matthew H. Tranter1Bjorn Redfors2Peter T. Wright3Peter T. Wright4Liam S. Couch5Alexander R. Lyon6Elmir Omerovic7Sian E. Harding8Faculty of Medicine, Imperial College London, Hammersmith Campus, National Heart and Lung Institute (NHLI), London, United KingdomOriel College, University of Oxford, Oxford, United KingdomDepartment of Molecular and Clinical Medicine/Cardiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, SwedenFaculty of Medicine, Imperial College London, Hammersmith Campus, National Heart and Lung Institute (NHLI), London, United KingdomSchool of Life and Health Sciences, University of Roehampton, London, United KingdomFaculty of Medicine, Imperial College London, Hammersmith Campus, National Heart and Lung Institute (NHLI), London, United KingdomFaculty of Medicine, Imperial College London, Hammersmith Campus, National Heart and Lung Institute (NHLI), London, United KingdomDepartment of Molecular and Clinical Medicine/Cardiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, SwedenFaculty of Medicine, Imperial College London, Hammersmith Campus, National Heart and Lung Institute (NHLI), London, United KingdomTakotsubo syndrome is a well-characterized cause of acute yet reversible heart failure associated with periods of intense emotional stress, often mimicking on presentation an acute coronary syndrome. Animal models of Takotsubo syndrome have been developed, either through the application of a stressor, or administration of exogenous catecholamine. We found that in a model of isoproterenol-induced Takotsubo syndrome in anesthetized rats hyperthermia (40–41°C) would occur after the administration of isoproterenol. Maintenance of this hyperthermia would result in an apical hypocontractility typical of the syndrome, whereas prevention of hyperthermia with active cooling to maintain a euthermic core body temperature prevented (but did not subsequently reverse) apical hypocontractility. In vitro experimentation with isolated cardiomyocytes showed no effect of hyperthermia on either baseline contractility or contractility change after beta-adrenoceptor stimulation. We suggest that the rise in body temperature that is characteristic of catecholamine storm may be a component in the development of Takotsubo syndrome.https://www.frontiersin.org/articles/10.3389/fcvm.2022.869585/fullTakotsubostresshyperthermiacatecholamineisoprenaline
spellingShingle Matthew H. Tranter
Matthew H. Tranter
Bjorn Redfors
Peter T. Wright
Peter T. Wright
Liam S. Couch
Alexander R. Lyon
Elmir Omerovic
Sian E. Harding
Hyperthermia as a trigger for Takotsubo syndrome in a rat model
Takotsubo
stress
hyperthermia
catecholamine
isoprenaline
title Hyperthermia as a trigger for Takotsubo syndrome in a rat model
title_full Hyperthermia as a trigger for Takotsubo syndrome in a rat model
title_fullStr Hyperthermia as a trigger for Takotsubo syndrome in a rat model
title_full_unstemmed Hyperthermia as a trigger for Takotsubo syndrome in a rat model
title_short Hyperthermia as a trigger for Takotsubo syndrome in a rat model
title_sort hyperthermia as a trigger for takotsubo syndrome in a rat model
topic Takotsubo
stress
hyperthermia
catecholamine
isoprenaline
url https://www.frontiersin.org/articles/10.3389/fcvm.2022.869585/full
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