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According to the WHO/ISFC classification of cardiomyo-pathies,
“myocarditis is an inflammatory heart muscle disease associated with cardiac dysfunction and is diagnosed
by established histological, immunological and immunohistochemical criteria”1. Classification may be based
on etiological criteria (infective or non infective myocarditis, whether isolated or in the setting of systemic
inflammation), temporal (acute, fulminant, rapidly progressive, chronic or persistent)2,3 clinical (active,
borderline, ongoing, resolving, resolved) or histological (lymphocitic, eosinophilic, polymorphous,
granulomatous, giant cell)4. It is obvious the superiority of an etiological
classification as far as therapeutic implications are concerned.
Many open questions still exist in regards to myocarditis. Clinical criteria of diagnosis are aspecific, since
myocarditis may have disparate clinical presentations including chest-pain, infarct-like necrosis, arrhythmias,
congestive heart failure, cardiogenic shock or even sudden, unexpected cardiac arrest. Titers of antiviral
antibodies lack of significance and are not of help; cultures also are not reliable. The diagnosis is based
on histology of the myocardium, which is now feasible also in vivo thanks to the introduction of endomyocardial
biopsy in the clinical practice5. The diagnostic criteria based on the observation of inflammatory infiltrates in
association with myocyte degeneration-necrosis at routine stains, are nowadays reinforced by the use of
the immunohistochemistry, which allows a precise identification and quantitation of leucocytes-macrophages,
not only in the acute but also in chronic phases6. The natural history of myocarditis is frequently
characterized by the evolution in dilated cardiomyopathy7,8; however, it is not clear whether progression
towards dilated cardiomyopathy is related to viral genome persistence within the myocytes, to the onset
of antibody or cell mediated immune mechanisms, or to the triggering of programmed cell death
(apoptosis)9. Identification of organ specific cardiac autoantibodies (antimyosin) in some cases suggested
the occurrence of autoimmune mechanisms, although whether they are a consequence of viral infection
is uncertain10. Unfortunately, the microscopic observation of inflammatory infiltrates does not allow to
establish the infectious, immune or idiopathic nature of myocarditis. Thanks to the advent of molecular
biology techniques, like polymerase chain reaction (PCR) and in situ hybridization, it is now possible to
systematically investigate the presence of viral genome in the myocardium in order to establish the precise
etiology of the disease, set up targeted therapeutic strategies and make prediction of the course or recurrence
of the inflammatory disease11-13. The recently published American Multicenter Treatment Trial on
immunosoppressive therapy of myocarditis14 failed because of the absence of any etiological background.
The viral myocarditis, indeed, should be approached from the therapeutic stand point with antiviral drugs,
leaving immunosuppressive therapy to idiopathic or immune forms. Thus, employment of molecular diagnosis
should be not only the gold standard for the diagnosis but also for a proper therapy.
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