Stress cardiomyopathy

A syndrome of catecholamine-mediated myocardial stunning?

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Pages (from-to)847-857
Number of pages11
JournalCellular and Molecular Neurobiology
Volume32
Issue number5
DOIs
StatePublished - Jul 2012

Fingerprint

Myocardial Stunning
Takotsubo Cardiomyopathy
Catecholamines
Left Ventricular Dysfunction
Nervous System Trauma
Coronary Thrombosis
Pheochromocytoma
Acute Coronary Syndrome
Cardiac Myocytes
Cyclic AMP
Muscle Cells
Infarction
Signs and Symptoms
Rupture
Central Nervous System
Animal Models
Heart Failure
Myocardial Infarction
Calcium
Wounds and Injuries

Keywords

  • Apical ballooning
  • Catecholamines
  • Myocardial stunning
  • Stress cardiomyopathy
  • Takotsubo cardiomyopathy

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Cell Biology

Cite this

Stress cardiomyopathy : A syndrome of catecholamine-mediated myocardial stunning? / Wittstein, Ilan S.

In: Cellular and Molecular Neurobiology, Vol. 32, No. 5, 07.2012, p. 847-857.

Research output: Contribution to journalArticle

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