Lone hepatitis C virus myocarditis responsive to immunosuppressive therapy

This study analyzes the causal role of hepatitis C virus (HCV) in patients with lone myocarditis, and its susceptibility to immunosuppression.

Prevalence of HCV in lone myocarditis, its mechanism of damage, and possible treatment are still unknown.

Among 48 consecutive patients with myocarditis serologically screened for HCV and other cardiotropic viruses, 3 patients had anti-HCV antibodies. Clinical manifestation was heart failure in two cases, and left bundle-branch block with moderate cardiac dysfunction was present in patient 3. The three patients underwent two-dimensional echocardiography, coronary angiography, and endomyocardial biopsy. Nested polymerase chain reaction (PCR) for positive and negative strands of HCV on sera and myocardial samples, and PCR for the most common cardiotropic viruses were performed. HCV in the myocardium was detected by TORDJI-22 antibody.

At histology, a lymphocytic myocarditis associated with myocytes positively stained by TORDJI-22 was shown in all. Cardiac autoantibodies were detected in all cases. Nested PCR showed both positive and negative strands of HCV RNA in serum and myocardium; other viral genomes were absent. Patients were treated with prednisone and azathioprine for 6 months, with recovery of cardiac volumes and function. At 4-week control biopsy, myocarditis progressed to a healed phase, though HCV RNA was still detectable in the serum and myocardium. Cardiac improvement was maintained at the 12-month overall follow-up.

HCV can be detected in the myocardium of as many as 6% of patients with lone myocarditis; HCV myocarditis can benefit from immunosuppression despite persistence of viral genome, suggesting an immunomediated mechanism of damage.