Autoantibodies against cardiac troponin I in patients presenting with myocarditis

Abstract

Background

Autoantibodies against cardiac troponin I (cTnI) play an important role in the pathogenesis of experimental cardiomyopathy. We developed a new method to measure anti-cardiac troponin I autoantibody (Anti-cTnIAAB) in patients with myocarditis with or without HCV infection.

Methods

Patients with heart failure for up to 2 years, without a distinct cause, were enrolled in the Myocarditis Treatment Trial between 1986 and 1990. Frozen blood samples were available from 1315 to 2233 enrolled patients. Anti-cTnIAAB was determined by a two-step immunoassay.

Results

The mean (±SEM) value of serum Anti-cTnIAAB titer in the 1315 patients was 0.067 ± 0.003 arbitrary unit (AU), significantly higher than in 1115 healthy volunteers (0.053 ± 0.002 AU, P < 0.01). The mean Anti-cTnIAAB titer in 88 patients whose endomyocardial biopsies (EMB) satisfied the diagnostic Dallas criteria was 0.086 ± 0.010 AU, versus 0.066 ± 0.004 AU in 1227 patients whose EMB did not satisfy these criteria. The mean Anti-cTnIAAB in both groups was significantly higher than that measured in the healthy volunteers (P < 0.01). The mean Anti-cTnIAAB titer in the 88 patients with Dallas criteria-confirmed myocarditis tended to be higher than in the other 1227 patients. Among the 88 patients with Dallas criteria-confirmed myocarditis, the mean Anti-cTnIAAB titer in 5 patients infected with the hepatitis C virus infection (HCV) was significantly higher (0.146 ± 0.047 AU) than in 83 patients without HCV infection (0.082 ± 0.010 AU, P < 0.05).

Conclusions

Elevated autoantibody titers against cTnI were detected in patients with myocarditis, and were higher in HCV-infected patients. The presence of Anti-cTnIAAB might correlate with inflammation and viral infection of the heart.