Stress (Takotsubo) cardiomyopathy—a novel pathophysiological hypothesis to explain catecholamine-induced acute myocardial stunning View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2008-01

AUTHORS

Alexander R Lyon, Paul SC Rees, Sanjay Prasad, Philip A Poole-Wilson, Sian E Harding

ABSTRACT

Stress cardiomyopathy, also referred to as Takotsubo cardiomyopathy, is an increasingly recognized clinical syndrome characterized by acute reversible apical ventricular dysfunction. We hypothesize that stress cardiomyopathy is a form of myocardial stunning, but with different cellular mechanisms to those seen during transient episodes of ischemia secondary to coronary stenoses. In this syndrome, we believe that high levels of circulating epinephrine trigger a switch in intracellular signal trafficking in ventricular cardiomyocytes, from G(s) protein to G(i) protein signaling via the beta(2)-adrenoceptor. Although this switch to beta(2)-adrenoceptor-G(i) protein signaling protects against the proapoptotic effects of intense activation of beta(1)-adrenoceptors, it is also negatively inotropic. This effect is greatest at the apical myocardium, in which the beta-adrenoceptor density is greatest. Our hypothesis has implications for the use of drugs or devices in the treatment of patients with stress cardiomyopathy. More... »

PAGES

22-29

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ncpcardio1066

DOI

http://dx.doi.org/10.1038/ncpcardio1066

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1033401452

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/18094670


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