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Stress Cardiomyopathy: A Syndrome of Catecholamine-Mediated Myocardial Stunning?
Open accessAbstract
During the past few years, a novel syndrome of heart failure and transient left ventricular systolic dysfunction precipitated by acute emotional or physical stress has been described. While patients with "stress cardiomyopathy"(SCM) typically present with signs and symptoms that resemble an acute coronary syndrome, it has become clear that this syndrome has unique clinical features that can readily be distinguished from acute infarction.In particular, in contrast to the irreversible myocardial injury seen with infarction, the myocardial dysfunction of SCM is completely reversible and occurs in the absence of plaque rupture and coronary thrombosis. There is increasing evidence that exaggerated sympathetic stimulation may play a pathogenic role in the development of SCM. Plasma catecholamine levels have been found to be markedly elevated in some patients with SCM, and the syndrome has been observed in other clinical states of catecholamine excess such as central neurologic injury and pheochromocytoma.Further, intravenous catecholamines can precipitate SCM in humans and can reproduce the syndrome in animal models. The precise mechanism in which excessive sympathetic stimulation may result in transient left ventricular dysfunction remains controversial. Abnormal myocardial blood flow due to sympathetically mediated microvascular dysfunction has been suggested and is supported by decreased coronary flow reserve during the acute phase of this syndrome. An alternative explanation is the direct effect of catecholamines on cardiac myocytes, possibly through cyclic AMP-mediated calcium overload. This manuscript will review the clinical and diagnostic features of SCM and will summarize the evidence supporting a sympathetically mediated pathogenesis. Clinical risk factors that appear to increase susceptibility to SCM, possibly by modulating myocyte and microvascular sensitivity to catecholamines, will also be highlighted.
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“Acute instances of distress can lead to immediate changes and even dramatic elevations in catecholamines. 102-107”
From Psychological Health, Well-Being, and the Mind-Heart-Body Connection: A Scientific Statement From the American Heart Association (2021) · cites this paper as [107]
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Metadata
- Authors
- Wittstein, I. S.
- Affiliations
- Johns Hopkins University (US)
- Corresponding author
- Wittstein, Ilan S.
- ORCID
- Wittstein, Ilan S.
- Venue
- Cellular and Molecular Neurobiology
- Published
- 2012-02-02
- Volume
- 32
- Issue
- 5
- Pages
- 847-857
- ISSN
- 0272-4340 (ISSN-L)
- 1573-6830
- PMC
- PMC11498407
- OpenAlex
- W2088380166
- Cited by
- 183
- References
- 74
- Citations by year
- 2026: 12 · 2025: 9 · 2024: 12 · 2023: 10 · 2022: 9 · 2021: 14 · 2020: 5 · 2019: 9 · 2018: 13 · 2017: 17 · 2016: 13 · 2015: 12 · 2014: 26 · 2013: 15 · 2012: 7
- FWCI
- 3.15
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Cellular and Molecular Neurobiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Takotsubo Cardiomyopathy and Associated Phenomena
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Cardiac Imaging and Diagnostics
- Health Sciences › Medicine › Infectious Diseases › Viral Infections and Immunology Research
- Keywords
- takotsubo cardiomyopathy, catecholamines, sympathetic stimulation, myocardial stunning, left ventricular dysfunction, heart failure, coronary flow reserve, microvascular dysfunction, cyclic AMP, calcium overload, pheochromocytoma, risk factors
- MeSH terms
- Animals, Catecholamines, Humans, Models, Cardiovascular, Syndrome, Myocardial Stunning, Genetic Predisposition to Disease, Takotsubo Cardiomyopathy
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