Background: Patients with dilated cardiomyopathy in whom enteroviruses in the myocardium are detected are more likely to die than those in whom no viruses have been demonstrated. The presence of enterovirus RNA in the myocardium at endomyocardial biopsy has been shown to be the strongest predictor of reduced survival. These results raise the question as to whether persistent virus might be responsible for continuing myocardial damage. Detection of myocardial cell damage is assessed using 111Indium-labelled monoclonal antimyosin antibodies. The present study was undertaken to address the question of whether the presence of myocardial cell damage by such antibodies in patients with dilated cardiomyopathy can be correlated with enterovirus persistence.
Patients and methods: A series of 19 consecutive patients diagnosed as having chronic dilated cardiomyopathy who were referred for evaluation for heart transplantation were studied with 111Indium labelled monoclonal antimyosin antibodies. These patients and 10 controls were screened for enterovirus RNA sequences in endomyocardial biopsy tissue by hybridization with an enterovirus group-specific cDNA probe.
Results: Antimyosin uptake, indicative of myocardial cell damage, was observed in 16 of 19 patients (84%), with dilated cardiomyopathy, and enterovirus RNA sequences were detected in endomyocardial biopsies from four of these 16 patients (25%), but not in myocardium from the remaining three patients with a negative antimyosin scan, nor from any of 10 controls.
Conclusions: Although these data do not establish a causal relationship between virus persistence in the myocardium and myocardial damage, the results obtained in the preliminary study support the hypothesis that enterovirus persistence is associated with continuing myocardial damage in patients with dilated cardiomyopathy.