| Project/Area Number |
12670705
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Osaka Medical College |
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Principal Investigator |
FUJIOKA Shigekazu Osaka Medical College, Faculty of Medicine Research Associate, 医学部, 助手 (20319528)
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| Co-Investigator(Kenkyū-buntansha) |
DEGUCHI Hirofumi Osaka Medical College, Faculty of Medicine Associate Professor, 医学部, 助教授 (90131341)
KITAURA Yasushi Osaka Medical College, Faculty of Medicine Professor, 医学部, 教授 (50084950)
SHIMIZU Akira Osaka Medical College, Faculty of Medicine Professor, 医学部, 教授 (00028581)
UKIMURA Akira Osaka Medical College, Faculty of Medicine Research Associate, 医学部, 助手 (50257862)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2001: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 2000: ¥3,200,000 (Direct Cost: ¥3,200,000)
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| Keywords | dilated cardiomyopathy / myocarditis / enterovirus / coxsackievirus / hepatitis C virus / adenovirus / viral replication / partial left ventriculectomy |
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| Research Abstract |
Idiopathic dilated cardiomyopathy (IDC) is a myocardial disease with a poor prognosis that can lead to severe heart failure and therapy-resistant arrhythmias. The demonstration of enteroviral genome and antigen in IDC hearts has reinforced the importance of enteroviruses in the pathogenesis of IDC. However, there remains uncertainty about the character and activity of enteroviruses detected in the myocardium.
In order to evaluate the viral etiology of lDC, myocardial specimens from 26 patients with IDC, 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. Plus-strand enteroviral RNA was detected in 9 (35 %) of the 26 patients. Minus-strand enteroviral RNA was demonstrated in 7 (78 %) of these 9 plus-strand RNA-positive patients. Sequence analysis revealed that the viruses detected were coxsackie B viruses, such as coxsackievirus B3 and B4. On light icroscopic in situ hybridization, viral signals were found in degenerating myocardial cells, interstitial inflammatory cells. Genomic material with other viruses, including hepatitis C virus and adenovirus was not detected. Six (86 %) of 7 minus-strand enteroviral RNA- positive patients died of cardiac insufficiency within the first 6 months after PLV.
Conclusions: Coxsackie B viruses were demonstrated in hearts with IDC. Active viral RNA replication appeared to be present in a significant proportion of these cases. Mlinus- strand coxsackieviral RNA in the myocardium can be a marker for poor clinical outcome after PLV. Therefore, specific therapies to coxsackie B viruses are implicated in the management of virus-positive IDC cases.
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