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European Heart Journal 1996 17(4):545-549;
Copyright © 1996 by the European Society of Cardiology.
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© 1996 The European Society of Cardiology

Enterovirus persistence and myocardial damage detected by 111In-monoclonal antimyosin antibodies in patients with dilated cardiomyopathy

V. Martí, P. Coll*, M. Ballester, D. Obrador, I. Carrió{dagger}, C. Moya, E. Lama, J. M. Augé and L. C. Archard{ddagger}

Cardiomyopathy and Transplantation Unit, Department of Cardiology
*Service of Microbiology, Hospital de la Santa Creu i Sant Pau Barcelona, Spain
{dagger}Unit of Nuclear Medicine, Hospital de la Santa Creu i Sant Pau Barcelona, Spain
{ddagger}Department of Biochemistry, Charing Cross and Westminster Medical School London, U.K.

Received 7 July 1995; accepted 7 August 1995.

Correspondence: Manel Ballester MD, Cardiomyopathy and Heart Transplantation Unit, Department of Cardiology, Hospital de la Santa Creu i Sant Pau, Avda. S. Antoni M. Claret 167, 08024 Barcelona, Spain. Fax: 34-3-291-93-04

Abstract

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 anti-bodies. 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 m 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.

Key Words: Dilated cardiomyopathy • monoclonal antimyosin antibodies • enterovirus • RNA


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