Abstract
Endomyocardial biopsy often fails to show myocardial inflammation for patients with clinically suspected myocarditis. The serum isoforms of troponin T (cTnT) level is a very sensitive marker of myocardial injury and it is elevated even in the absence of myocardial inflammation. We investigated the correlations for myocardial injury, virus titers and inflammation in acute viral infection. Using the murine coxsackievirus group B3 (CVB3) myocarditis model, the histopathologic findings and virus titers in mouse hearts were compared with the serum cTnT levels measured by ELISA at various time points. Viable virus titers in the hearts peaked at 3 days after infection (8.22 +/- 0.13 log10 PFU/100 mg of heart); they decreased at day 7 and no viable virus was detected from day 14. Myocardial inflammation was minimal at day 3, peaked at day 7 and markedly decreased at day 14. The individual serum TnT levels were significantly increased at day 3 (7.37 +/- 1.46 ng/ml), persisted to day 7 (0.73 +/- 0.08 ng/ml), and normalized at day 14. Serum cTnT levels were correlatable with virus titers in the heart (r = 0.744, P <0.01), but the serum cTnT levels were not correlated with the degrees of inflammation. Using the less myocarditic strain of CVB3, similar relationships were observed between the changes for the serum cTnT levels and the heart virus titers. During the course of viral infection, myocardial injury precedes the pathologic evidence of inflammation, and the elevated cTnT levels provide evidence of myocardial injury even in the absence of any histologic findings of myocarditis.
Highlights
Viral myocarditis is the result of a viral infection that produces myocardial necrosis, and this triggers an immune response for eliminating the viral agent (Kawai et al, 1999; Knowlton et al, 1999; Feldman et al, 2000)
Using the m urine coxsackievirus group B3 (CVB3) m yocarditis m odel, the histopathologic findings and virus titers in m ouse hearts were com pared with the serum cardiac isoforms of troponin T (cTnT) levels m easured by ELISA at various tim e points
Viable virus titers in the hearts peaked at 3 days after infection (8.22 ± 0.13 log[10] plaque forming unit (PFU)/100 m g of heart); they decreased at day 7 and no viable virus was detected from day 14
Summary
Viral myocarditis is the result of a viral infection that produces myocardial necrosis, and this triggers an immune response for eliminating the viral agent (Kawai et al, 1999; Knowlton et al, 1999; Feldman et al, 2000). Cardiac isoforms of troponin T or I (cTnT, cTnI) are only expressed in cardiac muscle and their serum levels have been proved to be more sensitive than the CK levels to detect myocardial injury in many clinical situations including unstable angina pectoris (Hamm et al, 1992; Bachmaier et al, 1995; Lauer et al, 1997; Smith et al, 1997). The serum TnT level is elevated even in the absence of any histologic signs of myocarditis (Lauer et al, 1997; Smith et al, 1997). To investigate the correlations among myocardial injury, virus titers and inflammation during the course of acute viral infection, we measured the serum cTnT levels and the viral titers, and examined the histologic findings in mouse hearts at various time points during the experimental course of a murine coxsackieviral B3 (CVB3) myocarditis
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