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(Circulation Research. 2005;96:144.)
© 2005 American Heart Association, Inc.

Editorials

Hepatitis C Virus Infection and Cardiomyopathies

Akira Matsumori

From the Department of Cardiovascular Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan.

Correspondence to Akira Matsumori, MD, PhD, Department of Cardiovascular Medicine, Kyoto University Graduate School of Medicine, 54 Kawahara-cho Shogoin, Sakyo-ku, Kyoto 606-8507, Japan. E-mail amat@kuhp.kyoto-u.ac.jp

See related article, pages 148–150

Key Words: hepatitis C virus • cardiomyopathy • myocarditis • heart failure • interferon

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Cardiomyopathies may present as idiopathic dilated, hypertrophic, or restrictive disease, arrhythmogenic right ventricular cardiomyopathy (ARVC), and various other distinct disorders of the heart muscle.¹ They constitute a heterogeneous group of myocardial diseases of multifactorial etiologies, including genetic anomalies and acquired immune factors, such as viral infections. The myocardium may be infected by a wide variety of viruses, although most commonly by enteroviruses, coxsackievirus B in particular. However, in many cases, when myocarditis has been diagnosed on the basis of clinical manifestations, a viral origin cannot be confirmed, despite extensive laboratory investigations.

The clinical presentation of viral myocarditis is variable. When myocardial necrosis is diffuse, congestive heart failure develops, and growing evidence now links viral myocarditis with dilated cardiomyopathy.^2,3 Localized myocardial lesions may result in thinning or aneurysms of the ventricular wall which, in the case of ARVC, are complicated by arrhythmias.⁴ When myocardial necrosis is limited to the subendocardium, restrictive cardiomyopathy may develop. Finally, although it has not been established that hypertrophic cardiomyopathy is a complication of viral myocarditis, asymmetrical septal hypertrophy has been observed in some patients with myocarditis.⁵

A high prevalence of hepatitis C virus (HCV) infection has recently been noted in patients with hypertrophic cardiomyopathy, dilated cardiomyopathy, and myocarditis (Figure 1).^6–15 In this issue of Circulation Research, Omura et al¹⁶ report that mice transgenic for the HCV-core gene develop ventricular dilatation, cardiac dysfunction, and myocardial fibrosis at 12 months, similar to the pathological manifestations observed in human dilated cardiomyopathy. Although HCV infection may be . . . [Full Text of this Article]

Related Article:

Core Protein of Hepatitis C Virus Induces Cardiomyopathy

Takashi Omura, Minoru Yoshiyama, Tetsuya Hayashi, Shuhei Nishiguchi, Masahiko Kaito, Shinichiro Horiike, Katsuhiko Fukuda, Sakiko Inamoto, Yasushi Kitaura, Yasuhiro Nakamura, Masakazu Teragaki, Takeshi Tokuhisa, Hiroshi Iwao, Kazuhide Takeuchi, and Junichi Yoshikawa
Circ. Res. 2005 96: 148-150. [Abstract] [Full Text] [PDF]

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