Prominent experts of the Nucleus of the WG “Myocardial and Pericardial Diseases” addressed the issues of Advances in Diagnosis and Therapy of Myocarditis.
H.D. Schultheiss underscored the fundamental diagnostic role of endomyocardial biopsy, with the employment of immunohistology, which reduces the risk of sampling error, and of molecular biology techniques, able to establish viral etiology. Viruses may be present either in the inflammatory or non-inflammatory stages. Etiological diagnosis is essential for therapy: virus positive patients should be treated with interferon, virus negative with immunosuppression or immune absorption. With viral persistence, prognosis is very poor in the absence of treatment.
E. Arbustini stressed again that viruses are detectable only with molecular tools and that the histopatological diagnosis based only on Dallas criteria is now something of the past, because this does not provide etiological diagnosis. Histological sensitivity is strictly dependent on number of samples (sampling error) and is poorly reliable due to interobserver variability. Quantitative PCR is mandatory to establish not only the presence but also the load of viruses.
A. Kerne focused his talk on therapy, underscoring why the Myocarditis Treatment Trial in 1995, which proved that immunosuppressive therapy was not effective, failed because endomyocardial biopsy was based only on Dallas Criteria. Treatment should be based on etiology.
There are specific types, like giant cell myocarditis, in which, without immunosuppression, death or cardiac transplantation occur in nearly 90% of cases by 6 months.
In cases of cardiogenic shock, left ventricular assistance device (LVAD) is indicated as a bridge to cardiac transplantation. In fulminant myocarditis LVAD may help the stunned myocardium to recover and to restore adequate ventricular contractility. Thus, LVAD is a life-saving device.
Interferon is indicated in viral inflammatory cardiomyopathy.
Finally, J.A. Marin Meto from Brazil reported the experience on treatment in the final stage of Chagas disease: mitral valve replacement and LV reconstruction in cases with aneurysms, LVAD, cardiac transplantation (with a disease recurrence in 29%), stem cell implantation, cardiac sincronization, implantable cardioverter defibrillator and amiodarone for life-threatening electrical instability. Since the main pathogenetic mechanism for progressive ventricular dysfunction is parasitic dependent inflammation, tripanocydal therapy with Benznidazole was accomplished with success.