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This study intends to analyse the prevalence of viral or inflammatory aetiology, the course of disease in patients with clinical suspicion of cardiomyopathy and the effect of a causal therapy. The analysis is based on the data concerning all 1.710 patients that were treated at the university hospital in Marburg from 2000-2008. Therefore,information was collected from available heart catheter und echocardiographic examinations, the analysis of endomyocardial biopsy, the medical reports and other data in the data maintenance. The cardiac symptoms of more than 50% of the patients can be explained by analysing EMB. More than 27% of the patients suffer from viral genome and approximately 20% from intracardiac inflammation. However, there is no statistic association between the detection of viral genome or cardiac inflammation and clinical diagnosis. During the development of the illness patients with DCM show a significant improvement of their ejection fraction from an average of 28.2% to 39.0% (p-value < 0.01) after sixty months, regarding the EF as a surrogate parameter of the patients´ prognoses. Dividing the group of patients in 4 aetiologically distinguished subgroups, the improvement of EF is detectable in every one of these groups, but there are differences in the long-term outcome between those groups. Compared to the other groups the group of patients with detection neither of viral genome nor of inflammation shows the worst relative and absolute increase of the EF (relative increase +34% after 60 months). In contrast to that, patients with detection of intracardiac viral genome and/or inflammation show a significant higher increase of +51%, though most of these patients received a specific antiviral respectively antiinflammatoric therapy. The measurements of LVEDD also amplify these results, but with its fewer dynamics, comparisons between those groups did not show significant results. Comparing the three groups (DCMi, DCMi with detection of viral genome, DCM with detection of viral genome) with each other, there are no differences in the clinical outcome during long-term development. Furthermore, this study shows that the detection of viral genome in EMB counts as a negative prognostic factor for the patients, regardless of clinical diagnosis. Long-term results after 60 months indicate an increase of the EF of +2%, which is significantly lower than the group without viral genome in the myocardium with an increase of EF of +26% (p-value < 0,01). A specific antiviral therapy with Pentaglobin® accomplishes a significant improvement of the outcome. Patients with viral genome in the heart and antiviral therapy have a significant increase in the EF of +18% (p-value < 0,05) with is comparable with the course of patients without detection of viral genome. In addition to that, therapy supports patients for a significant higher possibility to improve EF during clinical course (p-value < 0,05). Furthermore, the elimination of viral genome out of the myocardium is 21% for patients with antiviral therapy compared to 0% for patients without antiviral therapy. The prognostic value of detection of a myocardial inflammation is negative. During the long-term course patients with myocardial inflammation show insignificantly less increase (+6,1% in comparison to 18,1% for patients without inflammation) of their EF. Additionally, elimination of inflammation out of the myocardium by the patientsdetermines an improvement regarding EF, LVEDD and NYHA-stage, whereas the persistence of the inflammation predicts a deterioration of these parameters. With an antiinflammatoric therapy, the patients exhibit a clearance of inflammation of 100% in comparison to patients without an antiinflammatoric therapy with a lower elimination rate of only 79%. Overall, this study shows that the analysis of the EMB concerning viral genome or an inflammation provides important information to the patients. It helps during differential diagnosis, provides information for the prognosis and opens the possibility for a specific antiviral respectively antiinflammatoric therapy.