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Histologically proven myocarditis has a polymorphic clinical presentation with variable modality of onset ranging from fulminant to acute, subacute or chronic arrhythmia or heart failure signs or symptoms, to asymptomatic biventricular dysfunction. Prognosis is related to aetiology, pathogenic mechanisms, and severity of biventricular dysfunction at presentation. However, studies on risk stratification and prognosis have provided no uniform conclusions, often due to a lack of diagnostic confirmation by endomyocardial biopsy (EMB). A high incidence of myocarditis has been reported in autopsy series among sudden cardiac death victims but these are not representative of thewhole disease spectrum. A complex interplay of environmental and genetic factors is likely to be responsible formyocarditis. Physical, chemical, andmicrobiological agents may directly damage themyocardium, inducing an inflammatory reaction, e.g. toxic or infectious myocarditis (Table 1). Endogenous biochemical substances may also damage the cardiomyocytes, activating danger-related inflammatory pathways, such as in catecholamine-induced or in thyrotoxicosis-associated myocarditis. Genetic and epigenetic factors have also been implicated by modulating the immune response and cardiac susceptibility to damaging agents. The inflammatory response may become inappropriate to the initial myocardial damage, because of hypersensitivity reactions or loss of self-tolerance (autoimmune post-injury reactions). Autoimmune myocarditismay be isolated, e.g. organ-specific, or occur in the context of systemic immune-mediated diseases (SIDs). In autoimmune myocarditis forms, specific auto-reactive clones are directed against cardiac self-antigens or neoantigens with development of heart-specific autoantibodies (AHA). Conversely, the myocardium may be passively infiltrated and damaged by the proliferation of immunocompetent cells during systemic hyper-inflammatory reactions, such as in hypereosinophilia syndromes, auto-inflammatory diseases, septic shock, or macrophage activation syndrome. Some functional autoantibodies or toxic compoundsmay also directly impair metabolic and mechanical functions of the cardiomyocytes. Regardless of the eliciting mechanisms, myocardial inflammationmay evolve through healing and recovery with or without residual scar, persistent cardiac damage and cardiomyocytes necrosis, metabolic stunning or apoptosis, and finally, interstitial or substitutive fibrosis. According to the 1986 Dallas Criteria, myocarditis is defined by the presence of an inflammatory infiltrate in the myocardium accompanied by degenerative and/or necrotic changes of adjacent cardio myocytes not typical of ischaemic damage associated with myocardial infarction (Table 2). Although the Dallas criteria are still part of the pathological diagnosis on EMB, they are nowadays insufficient to describemyocarditis. The immunohistochemical and virological techniques improve sensitivity and specificity of EMB analysis and allow the differential diagnosis of infectious, and immune-mediated or autoimmune forms, which are infectious negative (Table 2). Aetiology-specific recommendations have been included in the 2013 European Society of Cardiology (ESC) expert consensus document onmyocarditis (Table 2). Myocarditis presentation is heterogeneous ranging from pseudo-infarction with normal coronary arteries, to

How to improve therapy in myocarditis: role of cardiovascular magnetic resonance and of endomyocardial biopsy