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Hypertrophic cardiomyopathy (HCM) is defined as inappropriate ventricular hypertrophy without a cardiac or systemic cause. On the other hand, hepatitis C virus (HCV) causes extrahepatic manifestations as well as chronic persistent infection in hepatocytes. We studied the association of HCV infection with HCM, comparing the prevalence of HCV antibodies between HCM patients and age- and gender-matched controls with other cardiovascular diseases at a single institution, for reasons of exclusion of bias. We then described the clinical features and genotype analysis of HCV RNA in HCM. The diagnosis of HCM was established by echocardiographic demonstration of a hypertrophied (> or =15 mm), nondilated left ventricle in the absence of another systemic or cardiovascular disease capable of producing the magnitude of hypertrophy observed. The study population consisted of 80 patients with HCM, in whom HCV antibody was examined (55 men and 25 women; mean age 56.6 +/- 12.4 years; ranging from 19 to 80 years), compared with a total of 80 age- and gender-matched controls without HCM. The prevalence of HCV infection in patients with HCM (18/80) was significantly higher than in control subjects (5/80) (Chi(2) = 7.312, P = 0.007). Of the 12 patients in whom the genotype of HCV was analyzed, 7 had type 1b and 5 had type 2a. The prevalence of HCV infection was higher in patients with HCM than in age- and gender-matched control subjects with other cardiovascular diseases. The result suggests that HCV may play an important role in these HCV-positive HCM patients.

The pathogenesis of alcoholic cardiomyopathy (ACM) is not well understood. However, recent reports have shown that mutations in mitochondrial DNA (mtDNA) were associated with mitochondrial encephalomyopathy and cardiomyopathy. Our objective was to explore point mutations in mtDNA and the pathogenesis of ACM. We obtained heart biopsy specimens from ten male habitual drinkers with congestive heart failure. We amplified the total mtDNA obtained from these specimens using a two-step polymerase chain reaction method and analyzed the products using automated fluorescence-based direct sequencing. The sequences were compared with those of controls. MtDNA from the ACM patients contained multiple point mutations. Specifically, four of the ten patients carried five point mutations that had been detected previously in several other mitochondrial diseases. These point mutations were not observed in controls. These results suggest that mtDNA abnormalities are involved in the pathogenesis of ACM.

The purpose of this study was to examine the histopathological findings of right ventricular endomyocardial biopsies from ten patients less than 60 years of age (47 +/- 9.8 (mean +/- SD) years) with documented atrioventricular block but without apparent heart disease. They underwent electrophysiological testing, echocardiography, coronary angiography, and right ventricular endomyocardial biopsy. Biopsy specimens were assessed for morphologic changes in myocyte diameter, fibrosis, disarray, and degeneration. Electrophysiological testing demonstrated atrioventricular nodal block in 2, intra-His bundle block in 2, and infra-His bundle block in 6 patients. Histology revealed evidence of myocardial fibrosis with either myocyte hypertrophy or disarray in 7 of the 10 patients. The results of electrophysiological testing did not correlate with the histopathological findings or severity. In one patient, heart failure appeared during the follow-up period. We conclude that patients with atrioventricular block of unknown etiology have histological abnormalities of the ventricular endomyocardium in addition to the conduction system disturbances. We consider such cases as constituting one of the disease groups of cardiomyopathy, and suggest that it is necessary to follow up the clinical course in these patients.