Takotsubo syndrome (TTS), also known as stress-induced cardiomyopathy or broken heart syndrome, represents approximately 1-3% of all acute coronary syndrome (ACS) presentations and up to 6% of ACS
presentations in women (1,2,3). Its in-hospital mortality is comparable to that of acute STelevation myocardial infarction, and the risk does not end with the initial event (1,4,5,6). Long-term follow-up studies report all-cause mortality rates of approximately 5.6% per patient-year and major adverse cardiac and cerebrovascular event rates approaching 10% per patient-year (1), with recurrence occurring in 11–14% of patients within five years of the index event (7,8).

The exact mechanisms underpinning TTS are not completely understood. Although traditionally attributed to catecholamine-mediated myocardial stunning, emerging evidence points to a far more complex pathophysiology involving oestrogen deficiency, altered β₂-adrenergic receptor signalling, genetic predisposition, neuropsychiatric elements, nitrosative stress, disrupted myocardial energetics, inflammation and microvascular dysfunction (9). This expanding mechanistic framework has stimulated growing interest in long-term pharmacotherapies to improve outcomes beyond the acute phase of the syndrome.