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

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• 作者：Shigekazu Fujioka ; Yasushi Kitaura ; Akira Ukimura ; Hirofumi Deguchi ; Keishiro Kawamura ; Tadashi Isomura ; Hisayoshi Suma ; Akira Shimizu
• 刊名：Journal of the American College of Cardiology
• 出版年：2000
• 出版时间：15 November 2000
• 年：2000
• 卷：36
• 期：6
• 页码：1920-1926
• 全文大小：226 K

文摘

OBJECTIVES

The aim of this study was to evaluate the viral etiology of idiopathic dilated cardiomyopathy (DCM).

BACKGROUND

The demonstration of enteroviral genome in hearts with DCM has reinforced the importance of enteroviruses in the pathogenesis of DCM. However, 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 were obtained at partial left ventriculectomy (PLV), were examined virologically. Strand-specific detection of enteroviral RNA was performed to differentiate active viral replication from latent persistence. Polymerase chain reaction was used to detect genomic sequences of hepatitis C virus, adenovirus, cytomegalovirus, influenza viruses, mumps virus, herpes simplex viruses, varicella-zoster virus and Epstein-Barr virus.

RESULTS

Plus-strand enteroviral RNA was detected in 9 (35 % ) of the 26 patients. Minus-strand enteroviral RNA was determined in seven (78 % ) of these nine plus-strand RNA-positive patients. Sequence analysis revealed that the enteroviruses detected were coxsackie B viruses, such as coxsackievirus B3 and B4. However, genetic material from other viruses was not detected. Six (86 % ) of seven minus-strand enteroviral RNA-positive patients died of cardiac insufficiency within the first six months after PLV.

CONCLUSIONS

Coxsackie B viruses were seen in hearts with idiopathic DCM. Active viral RNA replication appeared to be present in a significant proportion 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 persistent infection by other viruses in hearts with DCM.