Evaluation of viral infection in the myocardium of patients with idiopathic dilated cardiomyopathy

Citation
S. Fujioka et al., Evaluation of viral infection in the myocardium of patients with idiopathic dilated cardiomyopathy, J AM COL C, 36(6), 2000, pp. 1920-1926
Citations number
48
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
ISSN journal
07351097 → ACNP
Volume
36
Issue
6
Year of publication
2000
Pages
1920 - 1926
Database
ISI
SICI code
0735-1097(20001115)36:6<1920:EOVIIT>2.0.ZU;2-U
Abstract
OBJECTIVES The aim of this study was to evaluate the viral etiology of idio pathic dilated cardiomyopathy (DCM). BACKGROUND The demonstration of enteroviral genome in hearts with DCM has r einforced the importance of enteroviruses in the pathogenesis of DCM. Howev er, there is uncertainty about the character and activity of enteroviruses detected in the myocardium. Recently, the association of hepatitis C virus or adenovirus with DCM has been reported. METHODS Myocardial specimens from 26 patients with idiopathic DCM, which we re obtained at partial left ventriculectomy (PLV), were examined virologica lly. Strand-specific detection of enteroviral RNA was performed to differen tiate active viral replication from latent persistence. Polymerase chain re action was used to detect genomic sequences of hepatitis C virus, adenoviru s, cytomegalovirus, influenza viruses, mumps virus, herpes simplex viruses, varicellazoster virus and Epstein-Barr virus. RESULTS Plus-strand enteroviral RNA was detected in 9 (35%) of the 26 patie nts. Minus-strand enteroviral RNA was determined in seven (78%) of these ni ne plus-strand RNA-positive patients. Sequence analysis revealed that the e nteroviruses detected were coxsackie B viruses, such as coxsackievirus B3 a nd B4. However, genetic material from other viruses was not detected. Six ( 86%) of seven minus-strand enteroviral RNA-positive patients died of cardia c insufficiency within the first six months after PLV. CONCLUSIONS Coxsackie B viruses were seen in hearts with idiopathic DCM. Ac tive viral RNA replication appeared to be present in a significant proporti on of these cases. Minus-strand coxsackieviral RNA in the myocardium can be a marker for poor clinical outcome after PLV. There was no evidence of per sistent infection by other viruses in hearts with DCM. (C) 2000 by the Amer ican College of Cardiology.