Stress (Takotsubo) Cardiomyopathy

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Author(s)

Alexander R Lyon, MB, MRCP

Cardiology Specialist Registrar, MRC Clinical Research Training Fellow, National Heart and Lung Institute, Imperial College London, London, United Kingdom

Disclosures

Disclosure: Alexander R. Lyon, MB, MRCP, has disclosed no relevant financial relationships.

Paul SC Rees, MD

Royal Navy Specialist Registrar in Cardiology, Wessex Cardiothoracic Centre, Southampton, United Kingdom

Disclosures

Disclosure: Paul S.C. Rees, MD, has disclosed no relevant financial relationships.

Sanjay Prasad, MD, MRCP

Consultant in Cardiology, Cardiovascular Magnetic Resonance (CMR) Unit, Royal Brompton Hospital, London, United Kingdom

Disclosures

Disclosure: Sanjay Prasad, MD, MRCP, has disclosed no relevant financial relationships.

Philip A Poole-Wilson, MD, FRCP

British Heart Foundation Simon Marks Professor of Cardiology, National Heart and Lung Institute, Imperial College London, London, United Kingdom

Disclosures

Disclosure: Philip A. Poole-Wilson, MD, FRCP, has disclosed no relevant financial relationships.

Sian E Harding, PhD

Professor of Cardiac Pharmacology, Department of Cardiac Medicine, National Heart and Lung Institute, Imperial College London, London, United Kingdom

Disclosures

Disclosure: Sian E. Harding, PhD, has disclosed no relevant financial relationships.

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Conclusions

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 G_s protein to G_i 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.