Journal of Cardiac Failure
Volume 12, Issue 4 , Pages 293-298, May 2006

Myocarditis and Heart Failure Associated With Hepatitis C Virus Infection

  • Akira Matsumori, MD, PhD

      Affiliations

    • From the Department of Cardiovascular Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan
    • Corresponding Author InformationReprint requests: Akira Matsumori, MD, PhD, Department of Cardiovascular Medicine, Kyoto University Graduate School of Medicine, 54 Kawahara-cho Shogoin, Sakyo-ku, Kyoto 606-8507, Japan.
  • ,
  • Toshio Shimada, MD, PhD

      Affiliations

    • Division of Cardiovascular Medicine, Shimane University School of Medicine, Izumo, Japan
  • ,
  • Nora M. Chapman, PhD

      Affiliations

    • Department of Pathology and Microbiology, University of Nebraska, Omaha
  • ,
  • Steven M. Tracy, PhD

      Affiliations

    • Department of Pathology and Microbiology, University of Nebraska, Omaha
  • ,
  • Jay W. Mason, MD

      Affiliations

    • Covance Central Diagnostics Inc., Reno, Nevada

Received 12 August 2005; received in revised form 8 November 2005; accepted 8 November 2005.

Kyoto, Japan; Izumo, Japan; Omaha, Nebraska; Reno, Nevada

Abstract 

Background

The aim of study is to determine the prevalence of hepatitis C virus (HCV) infection and myocardial injury among patients enrolled in the Myocarditis Treatment Trial. HCV infection has recently been noted in patients with cardiomyopathies and myocarditis. However, prevalence of HCV infection in myocarditis and heart failure remains to be clarified.

Methods and Results

Patients with heart failure up to 2 years in duration without a distinct cause were enrolled in the trial between 1986 and 1990. Frozen blood samples were available from 1355 among 2233 patients enrolled and examined for presence of anti-HCV antibodies, circulating cardiac troponins I and T, and N-terminal pro-brain natriuretic peptide (NT-proBNP). Anti-HCV antibodies were identified in 59 of 1355 patients (4.4%). This higher prevalence of HCV infection than that observed in the general US population (1.8%), varied widely (0–15%) among the different medical centers and regions. The concentrations of circulating cardiac troponin (cTn) I were elevated in 17 of 56 patients (30%), and cTnT was detectable in 28 of 59 patients (48%) with HCV antibodies, suggesting the persistence of ongoing myocardial injury. The concentrations of NT-proBNP were elevated in 42 of 42 patients (100%) with HCV antibodies, (10,000 ± 5860 pg/mL), a mean value significantly greater than in 1276 patients without HCV antibody (2508 ± 160 pg/mL, P < .0001).

Conclusion

Anti-HCV antibodies were identifiable in sera stored for 13 to 17 years and were more prevalent in patients with myocarditis and HF than in the general population. In regions where its prevalence is high, HCV infection may be an important cause of myocarditis and HF. NT-proBNP is a more sensitive marker of myocardial injury than cardiac troponins in patients with heart failure from HCV myocarditis.

Key Words: Myocarditis, Heart failure, Hepatitis C virus, Troponin, proBNP

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 Supported in part by a Research Grant from the Japanese Ministry of Health, Labour and Welfare and a Grant for Scientific Research from the Japanese Ministry of Education, Culture, Sports, Science, and Technology.

PII: S1071-9164(05)01339-4

doi:10.1016/j.cardfail.2005.11.004

Journal of Cardiac Failure
Volume 12, Issue 4 , Pages 293-298, May 2006