We thank Del Buono et al. (1) for their interest in our study about diabetes in Takotsubo syndrome (TTS) (2), and we are pleased that our work was inspiring for their analysis.
The potential causal association between diabetes and the occurrence of TTS is obviously an extremely controversially discussed issue. Previously, the observation of a low diabetes prevalence in some TTS populations led to the assumption that diabetes is protective for the emergence of the disease (3). Diabetic cardiovascular autonomic neuropathy leading to catecholamine hyposecretion and amelioration of adrenergic effects to the heart was postulated as a possible mechanism. In contrast, Del Buono et al. (1) present a retrospective analysis that showed a significantly higher diabetes prevalence in TTS (30%) compared with non–ST-segment elevation myocardial infarction (19%). The authors interpret these results as indicating a greater susceptibility to TTS in patients with diabetes, possibly related to an upregulation of vasoactive neuropeptides.
Our study in a large, international population of prospectively identified TTS patients showed a diabetes prevalence of 21.1%, which was slightly higher than the expected sex- and age-adjusted rates in the general population of the participating countries (2). Therefore, both our findings and the analysis of Del Buono et al. consistently rebut the previously suggested low diabetes prevalence among patients with TTS. However, we do not think that these results provide a reasonable basis to postulate an increased risk for TTS in patients with diabetes. Assessment and interpretation of diabetes prevalence rates are highly dependent on the method of evaluation regarding the presence of diabetes (e.g., prospective examination of each individual patient versus retrospective analysis of hospital discharge letters) and the selection of the control group (e.g., healthy subjects versus populations with other disease such as myocardial infarction). Furthermore, it seems generally insufficient to draw etiological conclusions solely from prevalence rates. The establishment of a causal connection between TTS and diabetes requires a comprehensive scientific approach including experimental models. Likewise, we would attribute the increased mortality in TTS patients with diabetes in our study to the long-term deleterious effects of diabetes rather than to a more severe course of TTS itself.
In conclusion, currently available data do not provide sufficient evidence to assume a causal connection between diabetes and the occurrence or course of TTS, neither as a positive nor as a negative effect. Nevertheless, a potential interaction between diabetes and TTS is definitely a fascinating field of research that deserves further scientific efforts.
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Duality of Interest. No potential conflicts of interest relevant to this article were reported.
