Jae-Ok Shin

Myocardial injury occurs earlier than myocardial inflammation in acute experimental viral myocarditis

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.

Disruption of Dystrophin in Acute Fulminant Coxsackieviral B4 Infection

One mechanism that contributes to the pathogenesis of coxsackievirus B (CVB) viral heart disease is the direct cytopathic effect(s) on cardiomyocytes. It has been shown in mice that during CVB infection, the enteroviral protease 2A directly cleaves dystrophin in the hinge 3 region, leading to disruption of the dystrophin-glycoprotein complex and the loss of sarcolemmal integrity.1–3 We report for the first time a patient with fulminant myocarditis4 with CVB4 infection in which myocardial …