Abstract 2966: Detection of Viral Genome in the Myocardium: Lack of Prognostic and Functional Relevance in Patients with Dilated Cardiomyopathy
Background: The presence of viral genome in the myocardium of patients with dilated cardiomyopathy has been suggested as causative for the underlying cardiac disease. Nevertheless the results of present studies are conflicting regarding the natural course of heart diseases associated with detection of viral genome.
Methods and Results: In 216 patients admitted to the hospital with clinical signs of heart failure, left ventricular endomyocardial biopsies (EMB) were performed after exclusion of coronary artery disease. Analysis for viral genome, enteroviral replication and immunohistology was performed from EMBs. Patients with specific cardiomyopathies were excluded from the study, thus only patients with a diagnosis of dilated cardiomyopathy (DCM) were included into the study (n = 197). Adenovirus (ADV) genome was detected in 1.5%, enterovirus (EV) genome in 15.3%, parvovirus B19 (PVB19) genome in 31.8%, and a double infection of EV and PVB19 was detected in 12.9%. The increase of ejection fraction (EF) was 14.5 ± 12.4% in the EV-positve group compared to 11.1 ± 14.2 in the EV-negative group (p = NS) after a mean follow-up (FU) of 19.5 and 17.6 months. The increase of EF in the virus-positive group (positive for EV, ADV or PVB19) was 15.3 ± 13.3% compared to 12.3 ± 11.9% in the virus-negative group (p = NS) after a mean FU of 17.6 and 11.5 months. There was no significant difference in the change of EF between the EV-positive and the virus-negative group. Detection of enteroviral RNA replication (detection of EV minus-strand RNA) did not result in a deterioration of LV-function compared to the virus-negative group (p = NS) after mean FU of 11.2 and 12.0 months. The transplantation-free survival of the patients was not influenced by detection of viral genome.
Conclusion: The presence of viral genome in the myocardium of patients with left ventricular dysfunction is not associated with the course of the disease or the transplantation-free survival. In addition, EV replication did not deteriorate myocardial function either. The results favour the view that the mere detection of viral genome does not explain the underlying pathogenesis of DCM.