Signal transduction pathways initiated by catecholamines in takotsubo syndrome: focus on nitrosative stress and energetic impairment

Takotsubo syndrome reflects an ‘aberrant’ response to acute catecholamine stimulation, largely but not entirely as a manifestation of increased sensitivity to β‎2-adrenoceptor stimulation and signal transduction via Gi proteins, especially in ageing female hearts. It is now apparent that prolonged impairment of quality of life and slow recovery of echocardiographic parameters such as global longitudinal strain after episodes of takotsubo syndrome reflect ongoing myocardial inflammation and associated oedema, together with impairment of cardiac energetics on phosphorus magnetic resonance spectroscopy.