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Takotsubo Syndrome: Impact of endothelial dysfunction and oxidative stress


Münzel, Thomas; Templin, Christian; Cammann, Victoria Lucia; Hahad, Omar (2021). Takotsubo Syndrome: Impact of endothelial dysfunction and oxidative stress. Free Radical Biology & Medicine, 169:216-223.

Abstract

Takotsubo Syndrome (TTS) is characterized by a transient left ventricular dysfunction recovering spontaneously within days or weeks. Although the pathophysiology of TTS remains obscure, there is growing evidence suggesting TTS to be associated with increased production of reactive oxygen species (ROS), which may be involved in causing transient coronary and peripheral endothelial dysfunction leading to a transient impairment of myocardial contraction due to stunning (apical ballooning). Endothelial dysfunction is mainly caused by decreased vascular and myocardial nitric oxide bioavailability in response to increased ROS production. Accordingly, studies in humans and animal models demonstrated increased myocardial dihydroethidium staining of the myocardium in endomyocardial biopsy specimens, increased levels of hydrogen peroxide and malondialdehyde as well as reduced glutathione levels compatible with increased oxidative stress. As significant superoxide sources the mitochondria and the NADPH oxidase isoform NOX-4 and the NOX-2 regulating cytosolic subunit p67phox have been identified. Treatment with antioxidants such as sodium hydrosulfide reduced superoxide production in mitochondria and reduced expression of NOX-4 and p67phox, respectively. The presence of superoxide and nitric oxide also provides the basis for the concept of nitro-oxidative as well as nitrosative stress in TTS.

Abstract

Takotsubo Syndrome (TTS) is characterized by a transient left ventricular dysfunction recovering spontaneously within days or weeks. Although the pathophysiology of TTS remains obscure, there is growing evidence suggesting TTS to be associated with increased production of reactive oxygen species (ROS), which may be involved in causing transient coronary and peripheral endothelial dysfunction leading to a transient impairment of myocardial contraction due to stunning (apical ballooning). Endothelial dysfunction is mainly caused by decreased vascular and myocardial nitric oxide bioavailability in response to increased ROS production. Accordingly, studies in humans and animal models demonstrated increased myocardial dihydroethidium staining of the myocardium in endomyocardial biopsy specimens, increased levels of hydrogen peroxide and malondialdehyde as well as reduced glutathione levels compatible with increased oxidative stress. As significant superoxide sources the mitochondria and the NADPH oxidase isoform NOX-4 and the NOX-2 regulating cytosolic subunit p67phox have been identified. Treatment with antioxidants such as sodium hydrosulfide reduced superoxide production in mitochondria and reduced expression of NOX-4 and p67phox, respectively. The presence of superoxide and nitric oxide also provides the basis for the concept of nitro-oxidative as well as nitrosative stress in TTS.

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Item Type:Journal Article, refereed, further contribution
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Clinic for Cardiology
Dewey Decimal Classification:610 Medicine & health
Scopus Subject Areas:Life Sciences > Biochemistry
Health Sciences > Physiology (medical)
Language:English
Date:June 2021
Deposited On:17 Feb 2022 15:04
Last Modified:27 Jun 2024 01:36
Publisher:Elsevier
ISSN:0891-5849
OA Status:Hybrid
Free access at:Publisher DOI. An embargo period may apply.
Publisher DOI:https://doi.org/10.1016/j.freeradbiomed.2021.03.033
PubMed ID:33864955
  • Content: Published Version
  • Licence: Creative Commons: Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)