Apical hypertrophic cardiomyopathy and hepatitis C virus infection

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A Matsumori1, N Ohashi, R Nishio

  • 1Department of Cardiovascular Medicine, Kyoto University Graduate School of Medicine, Japan. amat@kuhp.kyoto-u.ac.jp

Japanese Circulation Journal
|July 16, 1999
PubMed

Insights

Hepatitis C virus (HCV) infection is linked to non-familial hypertrophic cardiomyopathy (HCM). This study found a high prevalence of HCV in HCM patients, suggesting it may cause the disease, especially apical HCM.

Area of Science:

  • Cardiology
  • Virology
  • Pathology

Background:

  • Familial hypertrophic cardiomyopathy (HCM) is linked to genetic mutations.
  • The cause of non-familial HCM remains largely unknown.
  • Hepatitis C virus (HCV) infection is a potential etiological factor.

Purpose of the Study:

  • To investigate the association between HCV infection and non-familial HCM.
  • To analyze clinical features, histopathology, and HCV genomes in HCM patients.
  • To determine HCV's role in HCM pathogenesis.

Main Methods:

  • Serological testing for anti-HCV antibodies in HCM patients and controls.
  • Analysis of left ventricular morphology, myocardial fibrosis, and cellular infiltration.
  • Detection and quantification of HCV RNA in serum and heart tissue.
  • Genotyping of HCV using fluorescent single-strand conformation polymorphism.

Main Results:

  • A significantly higher prevalence of anti-HCV antibodies was observed in HCM patients (13.8%) compared to controls (2.41%).
  • Six of nine HCV-positive HCM patients exhibited ace-of-spades-shaped left ventricular deformities with apical hypertrophy.
  • Myocardial fibrosis was present in all HCM patients; HCV RNA was detected in serum and heart tissue.
  • Multiple HCV clones were identified, with both positive and negative strands found in heart tissue.

Conclusions:

  • HCV infection is highly prevalent in patients with hypertrophic cardiomyopathy, particularly the apical form.
  • HCV is suggested as a significant causal agent in the pathogenesis of HCM.
  • Further research is warranted to elucidate the mechanisms of HCV-induced cardiac damage.

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