Examination of myocardial injury in patients with hepatitis C using myocardial scintigraphy and body surface signal-averaged ECG

Previous studies have reported an involvement of the hepatitis C virus (HCV) in hypertrophic or dilated cardiomyopathy. The presence or absence of myocardial injury associated with persistent HCV infection was examined using myocardial scintigraphy with 123I-beta-methyliodophenylpentadecanoic acid (BMIPP) and 99mTc-methoxyisobutylisonitrile (MIBI) and body surface signal-averaged electrocardiography (SAECG). For myocardial scintigraphy with 123I-BMIPP and SAECG, the subjects were 20 healthy adults (N-I group) and 20 HCV antibody-positive patients with liver cirrhosis (LC-I group). A time-domain analysis by SAECG to filtered QRS (f-QRS), the root mean square voltage of the terminal 40 msec of the f-QRS waveform (RMS40), and the amplitude over the last 40 msec under 40 μV duration (LAS40) were calculated. Using myocardial scintigraphy with 123I-BMIPP, the washout rate (%WR) on early and late images was calculated. For myocardial scintigraphy with 99mTc-MIBI, the subjects were 20 healthy adults (N-II group) and 20 HCV antibody-positive patients (LC-II group). The washout rate (%WR) from myocardial counts was calculated 1 and 3 hours after 99mTc-MIBI scintigraphy. In addition, the association between the HCV level and %WR were evaluated. The f-QRS and LAS40 in the N-I group were significantly higher than those in the LC-I group, and the RMS40 was significantly lower in the latter group. However, there were no marked differences between the Child A and C in LC-I groups. On myocardial scintigraphy with 123I-BMIPP, the %WR in the LC-I group was significantly higher than those in the N-I group. On myocardial scintigraphy with 99mTc-MIBI, the %WR of the left ventricular myocardium in the LC-II group was significantly more increased than those in the N-II group (p<0.05). No correlation between the HCV-RNA level and %WR was found in the LC-II group. There were no marked differences related to the stage of hepatitis C in the LC-II group. These results suggest that HCV continuously causes myocardial injury by releasing cytotoxic substances such as cytokines into myocardial cells, affecting SAECG parameters and %WR on myocardial scintigraphy. However, the onset of myocardial injury may not be associated with the stage of liver cirrhosis. (author)