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<p>Takotsubo syndrome (TTS) is a&#xa0;stress-associated acute heart failure mimicking the clinical features of acute myocardial infarction. Elevated catecholamine levels appear to play a&#xa0;pivotal role in the pathogenesis. Despite rapid recovery of systolic left ventricular function in most cases the acute and/or long-term prognosis is often limited depending mostly on the clinical risk profile. A&#xa0;pathophysiology-oriented treatment does not yet exist due to the lack of evidence-based strategies; however, basic research has identified several possible mechanisms beyond a&#xa0;purely catecholamine hypothesis. This includes, for example, an apical beta-2-adrenoceptor mediated myocardial inhibition, a microvascular, mitochondrial or metabolic dysfunction as well as myocardial inflammation. In a translational approach, based on experimental data, the inhibition of the calcineurin signalling pathway as the driver of TTS is currently being investigated in the acute setting in a&#xa0;randomized double-blind phase&#xa0;II clinical study. This article, for example, discusses how basic science can contribute to the identification of important aspects of the pathophysiology and translation of causal treatment strategies.</p>

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Takotsubo-Syndrom: Kann die Grundlagenwissenschaft helfen?

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年2月24日

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  • Bastian Bruns,
  • Norbert Frey,
  • Johannes Backs

摘要

Takotsubo syndrome (TTS) is a stress-associated acute heart failure mimicking the clinical features of acute myocardial infarction. Elevated catecholamine levels appear to play a pivotal role in the pathogenesis. Despite rapid recovery of systolic left ventricular function in most cases the acute and/or long-term prognosis is often limited depending mostly on the clinical risk profile. A pathophysiology-oriented treatment does not yet exist due to the lack of evidence-based strategies; however, basic research has identified several possible mechanisms beyond a purely catecholamine hypothesis. This includes, for example, an apical beta-2-adrenoceptor mediated myocardial inhibition, a microvascular, mitochondrial or metabolic dysfunction as well as myocardial inflammation. In a translational approach, based on experimental data, the inhibition of the calcineurin signalling pathway as the driver of TTS is currently being investigated in the acute setting in a randomized double-blind phase II clinical study. This article, for example, discusses how basic science can contribute to the identification of important aspects of the pathophysiology and translation of causal treatment strategies.