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Apical hypertrophic cardiomyopathy and hepatitis C virus infection
A Matsumori1, N Ohashi, R Nishio
1Department of Cardiovascular Medicine, Kyoto University Graduate School of Medicine, Japan. amat@kuhp.kyoto-u.ac.jp
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.
Abstract:
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 5.5x10(3)-8.6x10(5) 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.