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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Clinical Implications

This pathophysiological hypothesis might enable improved management of patients in the acute phase of stress cardiomyopathy. Whereas some patients require only supportive therapy, others can present with acute cardiogenic shock, necessitating admission to intensive care for hemodynamic support. Epinephrine has a causative role in stress cardiomyopathy and the deterioration of myocardial function, and additional 'therapeutic' epinephrine might drive further β₂AR–G_i-protein-mediated negative inotropism. The use of inotropic agents, particularly dobutamine, in patients with stress cardiomyopathy and cardiogenic shock, therefore, seems counterintuitive. Some β-blockers can also cause stimulus trafficking of β₂ARs to G_i protein coupling,^[64] which suggests that use of these agents in patients with stress cardiomyopathy might be inappropriate, despite the high catecholamine levels. Aortic balloon pump counterpulsation might be the best first-line hemodynamic support, with intravenous calcium or levosimendan, the calcium- sensitizing agent, as second-line pharmacological support. In cases of life-threatening acute left ventricular failure, temporary mechanical support with a left ventricular assist device can be indicated. Ventricular support could provide time for the ventricular myocardium to recover, as observed in the natural history of stress cardiomyopathy. We must highlight, however, that these proposals are founded on a hypothesis and require a clinical study for validation.