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In summary, we hypothesize that stress cardiomyopathy is a form of myocardial stunning, but with cellular mechanisms different to those caused by transient episodes of ischemia secondary to coronary stenoses. High levels of circulating epinephrine trigger a switch in intracellular signal trafficking, from Gs protein to Gi protein signaling through the β2AR. This change in signaling is negatively inotropic, and the effect is greatest at the apical myocardium, in which the density of β-adrenoceptors is highest. This hypothesis has implications for the use of drugs or devices in the treatment of patients with stress cardiomyopathy.