Key Points
- Stress cardiomyopathy is the result of the direct effects of high levels of epinephrine on the ventricular myocardium
- High levels of epinephrine are negatively inotropic; they switch β2-adrenoceptor coupling in ventricular cardiomyocytes, from the Gs protein to the Gi protein signaling pathway
- The density of β-adrenoceptors is greatest at the apical myocardium of the mammalian heart, which explains the regional nature of the stunning in response to high levels of circulating epinephrine after stressful stimuli
- This effect is reversible after the epinephrine levels return to normal, which explains why left ventricular function and
apical wall motion return to normal within days to weeks of the acute insult
Reprint Address
Alexander R Lyon, Department of Cardiac Medicine, National Heart and Lung Institute, Dovehouse Street, London SW3 6LY, UK
[email protected]
Supplementary Information
Two movies are available on the Nature Clinical Practice Cardiovascular Medicine website.
Acknowledgment
Désirée Lie, University of California, Irvine, CA, is the author of and is solely responsible for the content of the learning objectives, questions and answers of the Medscape-accredited continuing medical education activity associated with this article.
