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 Testing

Our hypothesis is readily testable in animal models by use of genetic tools to manipulate the density of β-adrenoceptors and assessment of the ventricular response to catecholamines. Measurement of the gradient of the density of β₂ARs in the human ventricle is more challenging. Direct measurement of the density of β₂ARs in tissue specimens taken from different regions of the human ventricle would be ideal, but obtaining left ventricular biopsies from 'normal' human hearts raises major ethical concerns, and 'normal' donor hearts unsuitable for transplantation have frequently been exposed to high catecholamine levels before explantation. An alternative is in vivo measurement with PET and labeled receptor ligands.^[61]In vivo or tissue measurements of β₁AR:β₂AR ratios in cardiomyocytes can also be confounded by β₂ARs on the coronary vasculature^[62] and on cardiac fibroblasts.^[63]