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Response to: Correspondence on ‘Beta-blockers are associated with better long-term survival in patients with Takotsubo syndrome’ by Chang et al
  1. Angelo Silverio1,
  2. Michele Bellino1,
  3. Gennaro Galasso1,
  4. Eduardo Bossone2,
  5. Rodolfo Citro3,4
  1. 1Department of Medicine, Surgery and Dentistry, University of Salerno, Baronissi, Salerno, Italy
  2. 2Division of Cardiology, Ospedale Cardarelli, Napoli, Campania, Italy
  3. 3Cardiovascular and Thoracic Department, San Giovanni di Dio e Ruggi d’Aragona University Hospital, Salerno, Italy
  4. 4Vascular Physiopathology Unit, IRCCS Neuromed, Pozzilli, Italy
  1. Correspondence to Dr Rodolfo Citro, Cardiovascular, University Hospital “San Giovanni di Dio e Ruggi d’Aragona”, Salerno, Italy; rodolfocitro{at}

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The Authors’ reply We appreciate the interest of Dr Chang and Dr Liu in our study.1 Cardiogenic shock (CS) complicates the in-hospital course of patients with takotsubo syndrome (TTS) in 6%–20% of cases and is the main cause of in-hospital mortality.2

Treatment of CS in TTS is a clinical challenge and, due to the complexity of investigating this subject in dedicated randomised controlled trials, current evidence is limited to case reports or retrospective observational studies.

The use of catecholamines in TTS complicated by CS is still debated since the administration of exogenous catecholamines might re-exacerbate the acute phase and increase the risk of in-hospital adverse events. In this scenario, previous case series have suggested the use of the Ca2+ sensitiser levosimendan as a safe and feasible non-adrenergic alternative to common inotropic agents in TTS.3

Owing to the key role of catecholamine overstimulation in TTS pathophysiology, the use of beta-blockers has been proposed to mitigate the sympathetic drive and the effects of further catecholamine surges during the acute phase. In a monkey model of epinephrine-induced TTS, metoprolol improved left ventricular dysfunction, diminished the catecholamine-induced …

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  • Contributors All authors have contributed substantially to the content of this manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Provenance and peer review Commissioned; internally peer reviewed.

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