We read with great interest the letter from Eitel et al. We would like to reemphasize that in the reported case of Takotsubo cardiomyopathy (TTC), endomyocardial biopsy (EMB), the diagnostic gold standard for myocarditis, had not been systematically performed, in spite of the fact that Mayo Criteria specify that myocarditis should be excluded in all cases of suspected TTC.1,2 As mentioned by Eitel, there are case reports of TTC that appear to be caused by myocarditis, in keeping with our findings.1 Our patient was virus-negative, thus the issue of virus pathogenicity is not relevant.3–5 In relation to Eitel's provocative proposal that our case may be a TTC with secondary inflammation, we think this is highly unlikely. Active myocarditis is not simply characterized by sparse mononuclear cell infiltrates, as suggested by Eitel et al., but is defined (Dallas criteria), as an inflammatory infiltrate of the myocardium with necrosis and/or degenerative changes of adjacent myocytes not typical of infarction.6 Our case fulfils state-of-the-art WHO histological (active myocarditis by the Dallas criteria), immunological (serum anti-heart autoantibodies), immunohistochemical (infiltrating activated lymphocytes and macrophages), and molecular (absence of viral genomes) diagnostic criteria of a virus-negative, immune-mediated form of acute myocarditis masquerading as TTC.3–6 Further, in our case the ‘stressful event’ dated back 3 months, thus the onset was not strictly time-related with clinical presentation; autoimmune myocarditis is more likely to occur in females, as other autoimmune diseases; the rapid resolution of cardiac dysfunction is a clinical hallmark of myocarditis.3,5 Last but not least, lymphocytic myocarditis can occur in relation to hypercatecholaminergic states, but it is not a feature known to be associated with microvascular ischaemia.5 Thus, a proportion of TTC patients with sympathetic overdrive may have an underlying virus-negative toxic myocarditis, explaining the reversible systolic dysfunction, chest pain and non-ischaemic troponin release. We propose1 in agreement with Eitel et al. that the role of inflammation in the pathogenesis of TTC merits further study, to differentiate myocarditis mimicking TTC from ‘idiopathic’ TTC, and/or to have a better understanding of the frequency of (viral, immune-mediated, or toxic) myocarditis in TTC. Takotsubo cardiomyopathy may be a syndrome, rather than a distinct pathological entity. Regarding Eitel's proposal that EMB is not an adequate method for the diagnosis of myocarditis, we disagree. First, EMB sensitivity is higher using immunohistochemistry.3–5,7 Secondly, EMB is safe with a complication rate that is similar to that of standard coronary angiography,3,7,8 which is always performed in TTC. Thirdly, myocarditis is challenging to identify clinically,3–5,7,8 and current validation studies of cardiac magnetic resonance imaging (CMR) are mainly based upon clinical presentation.9 Finally, CMR is unable to differentiate viral from non-viral myocarditis.9 Viral genome10 and chronic inflammation may have independent prognostic value in distinct subsets of patients.7 EMB, with adjunct immunohistology and molecular detection of the viral genome is the mainstay to achieve confirmation or exclusion of myocarditis3,5,9,10 as well as identify its aetiopathogenetic forms and aetiology-based therapies.3,5