Apical Hypertrophic Cardiomyopathy and Hepatitis C Virus Infection

  • Matsumori Akira
    Department of Cardiovascular Medicine, Kyoto University Graduate School of Medicine
  • Ohashi Naohiro
    Department of Cardiovascular Medicine, Kyoto University Graduate School of Medicine
  • Nishio Ryosuke
    Department of Cardiovascular Medicine, Kyoto University Graduate School of Medicine
  • Kakio Tadashi
    Department of Cardiovascular Medicine, Kyoto University Graduate School of Medicine
  • Hara Masatake
    Department of Cardiovascular Medicine, Kyoto University Graduate School of Medicine
  • Furukawa Yutaka
    Department of Cardiovascular Medicine, Kyoto University Graduate School of Medicine
  • Ono Koh
    Department of Cardiovascular Medicine, Kyoto University Graduate School of Medicine
  • Shioi Tetsuo
    Department of Cardiovascular Medicine, Kyoto University Graduate School of Medicine
  • Hasegawa Koji
    Department of Cardiovascular Medicine, Kyoto University Graduate School of Medicine
  • Sasayama Shigetake
    Department of Cardiovascular Medicine, Kyoto University Graduate School of Medicine

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The familial form of hypertrophic cardiomyopathy (HCM) is attributed to mutations in the genes for contractile proteins, but the etiology of non-familial form remains unknown. This study was designed to examine the clinical features, histopathologic changes, and hepatitis C virus (HCV) genomes in patients with HCM associated with HCV infection. Anti-HCV antibody was present in the sera of 9 of 65 patients (13.8%) with HCM versus 2.41% in a control population of voluntary blood donors in Japan, a statistically significant difference (p<0.0001). Among these 9 patients, 6 had ace-of-spades-shaped deformities of the left ventricle with apical hypertrophy. Myocardial fibrosis was found in all patients, and mild cellular infiltration was observed in 5 patients. Type 1b HCV RNA was present in the sera of 5 of the 9 patients. The copy number of HCV was 5.5×10 3-8.6×105 genomes/ml serum, and multiple clones of HCV were detected in the sera of each patient by an analysis of the hypervariable regions using fluorescent single-strand conformation polymorphism. Positive strands of HCV were found in the hearts of 5 patients, and negative strands in the hearts of 2 patients. A high prevalence of HCV infection was found in patients with HCM, particularly of the apical variety, suggesting that HCV is an important causal agent in the pathogenesis of the disease. (Jpn Circ J 1999; 63: 433 - 438)

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