ENTEROVIRUS PERSISTENCE AND MYOCARDIAL DAMAGE DETECTED BY IN-111-MONOCLONAL ANTIMYOSIN ANTIBODIES IN PATIENTS WITH DILATED CARDIOMYOPATHY

Citation
V. Marti et al., ENTEROVIRUS PERSISTENCE AND MYOCARDIAL DAMAGE DETECTED BY IN-111-MONOCLONAL ANTIMYOSIN ANTIBODIES IN PATIENTS WITH DILATED CARDIOMYOPATHY, European heart journal, 17(4), 1996, pp. 545-549
Citations number
43
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
0195668X
Volume
17
Issue
4
Year of publication
1996
Pages
545 - 549
Database
ISI
SICI code
0195-668X(1996)17:4<545:EPAMDD>2.0.ZU;2-J
Abstract
Background Patients with dilated cardiomyopathy in whom enteroviruses in the myocardium are detected are more likely to die than those in wh om no viruses have been demonstrated. The presence of enterovirus RNA in the myocardium at endomyocardial biopsy has been shown to be the st rongest predictor of reduced survival. These results raise the questio n as to whether persistent virus might be responsible for continuing m yocardial damage. Detection of myocardial cell damage is assessed usin g (111)Indium-labelled monoclonal antimyosin antibodies. The present s tudy was undertaken to address the question of whether the presence of myocardial cell damage by such antibodies in patients with dilated ca rdiomyopathy can be correlated with enterovirus persistence. Patients and methods A series of 19 consecutive patients diagnosed as having ch ronic dilated cardiomyopathy who were referred for evaluation for hear t transplantation were studied with (111)Indium labelled monoclonal an timyosin antibodies. These patients and 10 controls were screened for enterovirus RNA sequences in endomyocardial biopsy tissue by hybridiza tion with an enterovirus group-specific cDNA probe. Results Antimyosin uptake, indicative of myocardial cell damage, was observed in 16 of 1 9 patients (84%) with dilated cardiomyopathy, and enterovirus RNA sequ ences were detected in endomyocardial biopsies from four of these 16 p atients (25%), but not in myocardium from the remaining three patients with a negative antimyosin scan, nor from any of 10 controls. Conclus ions Although these data do not establish a causal relationship betwee n virus persistence in the myocardium and myocardial damage, the resul ts obtained in the preliminary study support the hypothesis that enter ovirus persistence is associated with continuing myocardial damage in patients with dilated cardiomyopathy.