Key result
Electrophysiologic, structural, and autonomic remodeling drive atrial, ventricular, and bradyarrhythmias in Takotsubo syndrome.
This review synthesizes how abnormal calcium handling, repolarization abnormalities, structural remodeling, and autonomic imbalance drive arrhythmogenesis in Takotsubo syndrome to guide diagnostic and therapeutic strategies.
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Should not yet alter arrhythmia management in Takotsubo syndrome; extends mechanistic synthesis but requires prospective validation.
Takotsubo syndrome (TTS), an acute stress‑induced heart failure, is frequently complicated by arrhythmias that significantly worsen prognosis. Despite advances in understanding its pathology, the electrophysiological basis of these arrhythmias remains incompletely elucidated. The present review synthesizes current evidence to explore the core electrophysiological mechanisms underlying arrhythmogenesis in TTS, including abnormal calcium handling, repolarization abnormalities, altered conduction and refractoriness due to structural remodelling, and autonomic nervous system imbalance. The corresponding clinical manifestations of ventricular arrhythmias, atrial arrhythmias and bradyarrhythmias were further delineated, and contemporary diagnostic and therapeutic strategies were discussed. By integrating clinical observations with experimental findings, the present review aims to bridge the knowledge gap between mechanistic insights and clinical practice. Finally, critical research gaps were highlighted and future directions were proposed, emphasizing the need for personalized medicine and novel therapeutic targets to improve arrhythmia management and patient outcomes in TTS.
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Xu et al. (2026) conducted a review in Takotsubo syndrome (TTS) complicated by arrhythmias. Abnormal calcium handling, repolarization abnormalities, structural remodeling, and autonomic imbalance drive ventricular, atrial, and bradyarrhythmias in Takotsubo syndrome.
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