Role of hepatitis C virus in cardiomyopathies.
Virus infection was conventionally considered to cause myocarditis, which resulted in development of dilated cardiomyopathy. Recent studies suggest that hepatitis C virus (HCV) is involved in the development of dilated cardiomyopathy, hypertrophic cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy in addition to myocarditis. Furthermore, left ventricular aneurysm represents the same morbid state not only after myocardial infarction but also after myocarditis. There were wide variations in the frequency of detection of HCV genomes in cardiomyopathies in different regions or in different populations. Major histocompatibility complex class II genes may play a role in the susceptibility to HCV infection, and may influence the development of different phenotypes of cardiomyopathies. If it is the fact that the myocardial damage is caused by HCV, it might be expected that interferon (IFN) treatment would be useful for its treatment. Patients receiving IFN treatment of hepatitis were screened by thallium myocardial scintigraphy, and an abnormality was discovered in half of patients. Treatment with IFN resulted in disappearance of the image abnormality. It has thus been suggested that mild myocarditis and myocardial damage may be cured with IFN. We have recently found that high concentrations of circulating cardiac troponin T are a specific marker of cardiac involvement in HCV infection. By measuring cardiac troponin T in patients with HCV infection, the prevalence of cardiac involvement in hepatitis C virus infection will be clarified. We are proposing a collaborative work on global network on myocarditis/cardiomyopathies due to HCV infection.
Matsumori
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Department of Cardiovascular Medicine, Kyoto University Graduate School of Medicine, Sakyo-ku, Japan. amat@kuhp.kyoto-u.ac.jp
D009202:Cardiomyopathies / Q000209:etiology / Q000503:physiopathology / Q000628:therapy / Q000821:virology; D004562:Electrocardiography; D005802:Genes, MHC Class II; D006680:HLA Antigens / Q000235:genetics / Q000378:metabolism; D006321:Heart / Q000821:virology; D016174:Hepacivirus / Q000235:genetics / Q000378:metabolism*; D006526:Hepatitis C / Q000150:complications* / Q000628:therapy; D006801:Humans; D007564:Japan; D015337:Multicenter Studies as Topic; D009206:Myocardium / Q000166:cytology / Q000378:metabolism / Q000473:pathology
D006680:HLA Antigens