Abstract

The article by Stiermaier et al. published in this journal recently1 describing mortality, predictors, cause, and clinical consequences of takotsubo cardiomyopathy (TTC) presented interesting data. The pathogenesis of TTC, to date, is still not fully understood. A popular hypothesis suggests the involvement of a catecholamine-mediated mechanism. However, the role of an inflammatory and energetic–metabolic pathway in the pathophysiological evolution of TTC has also been subsequently proposed and discussed in detail.2 Consensus has dictated a favourable prognosis for patients with TTC. However, recently published studies have elevated the impact of TTC as a disease mimicking an acute coronary syndrome (ACS) and compared its associated complications, such as arrhythmias, cardiogenic shock, right ventricular involvement, and thrombo-embolic events, with CAD, highlighting the similar mortality rates in each scenario.3, 4 The outcome of ACS patients with diabetes mellitus is worse when compared with that of the general ACS population.5 However, in the case of TTC, there are some data pointing to a protective effect of diabetes mellitus on clinical outcome.6 The findings of Ali et al. regarding the contribution of baroreceptor dysfunction and the review by Madias in 2016 demonstrating a low prevalence of diabetes mellitus in patients with TTC, might support the hypothesis that diabetes mellitus has a protective effect in TTC.6, 7 An analysis of the 114 patients diagnosed with TTC in our institution between January 2003 and September 2015 indicated the prevalence of diabetes mellitus in patients with TTC at ∼22.8%. This retrospective observation demonstrated a better clinical outcome for patients suffering from TTC with co-existent diabetes mellitus. The incidence rate of thrombo-embolic events, life-threatening arrhythmias, all-cause mortality, re-hospitalization due to heart failure, stroke, and recurrent TTC was significantly lower in diabetic patients with TTC than in those with TTC alone. Only 4 diabetic patients (15%) with TTC suffered from a major clinical event (1 case of a thrombo-embolic event, 2 cases of life-threatening arrhythmias, and 1 case of death) vs. 31 (35%) recorded events among those with TTC alone (10 cases of thrombo-embolic events, 11 cases of life-threatening arrhythmias, 9 cases of death, and 1 case of stroke). Another interesting data point observed in our TTC study (cohort of 114 patients) was related to long-term mortality and gender bias. Our analysis highlighted a significantly poorer clinical outcome among male patients when compared with female patients [8/19 (42%) vs. 21/95 (22%)]. Our data suggest that diabetes mellitus may have protective effects for TTC as shown by a lower prevalence of diabetic patients and by the better outcomes of the diabetic patients with TTC. These data, however, should be confirmed in larger patient groups. Ibrahim El-Battrawy First Department of Medicine Faculty of Medicine University Medical Centre Mannheim (UMM) Theodor-Kutzer-Ufer 1-3 D-68167 Mannheim Germany Tel: +49 621 383 1447 Fax: +49 621 383 1474 E-mail: [email protected] DZHK (German Center for Cardiovascular Research), Partner Site Heidelberg-Mannheim Germany Martin Borggrefe First Department of Medicine Faculty of Medicine University Medical Centre Mannheim (UMM) University of Heidelberg Mannheim Germany DZHK (German Center for Cardiovascular Research), Partner Site Heidelberg-Mannheim Germany Ibrahim Akin First Department of Medicine Faculty of Medicine University Medical Centre Mannheim (UMM) University of Heidelberg Mannheim Germany DZHK (German Center for Cardiovascular Research), Partner Site Heidelberg-Mannheim Germany

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