epatitis C virus (HCV) has been associated with cryoglobulinemia, Sjögren's syndrome, membranoproliferative glomerulonephritis, sporadic porphyria cutanea tarda, leukocytoclastic vasculitis, and idiopathic pulmonary fibrosis. 1 We found an association of HCV infection with dilated cardiomyopathy, 2,3 and a more recent report supports our findings. 4 Hypertrophic cardiomyopathy (HCM) is characterized by inappropriate myocardial hypertrophy and a variety of clinical manifestations, including sudden death, which can strike both symptomatic and asymptomatic individuals. Pathologic findings consist of increased myocardial mass and myofiber disarray. Familial HCM has been found to be caused by mutations in the genes for -cardiac myosin heavy chain, 5 -tropomyosin, and cardiac troponin T. 6 However, in over 50% of familial cases, and in most cases of non-familial HCM, the cause remains unknown. The etiology of HCM may be heterogeneous; for instance, a recent study reported that Fabry's disease was also associated with left ventricular hypertrophy. 7 Myocarditis has been reported to lead to asymmetrical septal hypertrophy, which is one of the characteristic clinical features of HCM. [8][9][10] We have shown, in a preliminary study, that the anti-HCVantibody was more prevalent in patients with HCM than in those with ischemic heart disease 11 or dilated cardiomyopathy. 12 The present study shows an association of HCV infec-
Methods
Patient PopulationThe study protocol was approved by the Human Research Committee of the Kyoto University Hospital. The patient population consisted of 65 consecutive patients admitted to the Kyoto University Hospital with the diagnosis of HCM. The age of these 39 men and 26 women ranged from 16 to 80 years (mean =57.9±9.8 years, mean ± SD). All patients underwent detailed clinical, electrocardiographic, and echocardiographic evaluations as well as right and left heart catheterization, and selective coronary artery cineangiography by the Judkins technique.
EvaluationsThe maximal echocardiographic thickness of the left ventricular wall was measured in diastole in the region of greatest hypertrophy, and the diagnosis of HCM was based on a maximal left-ventricular wall thickness of at least 13 mm in the absence of other cause of ventricular hypertrophy. 5,6 Careful detailed family histories were taken for each patient to determine whether or not a familial form HCM was present.Endomyocardial biopsy of the right ventricle was performed with a Stanford or Cordis bioptome by the internal jugular approach, and left ventricular biopsy was done by the long-sheath method. Five samples were usually obtained from each patient, 3 of which were fixed in 10% formalin, embedded in paraffin, and cut into 6-m sections; the other 2 samples were immediately frozen in liquid Jpn Circ J 1999; 63: 433 -438 (Received January 5, 1999; accepted February 18, 1999 The familial form of hypertrophic cardiomyopathy (HCM) is attributed to mutations in the genes for contractile proteins, but the etiology of non-familial for...