No detection of enteroviral genome in the myocardium of patients with arrhythmogenic right ventricular cardiomyopathy

Citation
F. Calabrese et al., No detection of enteroviral genome in the myocardium of patients with arrhythmogenic right ventricular cardiomyopathy, J CLIN PATH, 53(5), 2000, pp. 382-387
Citations number
45
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research Diagnosis & Treatment
Journal title
JOURNAL OF CLINICAL PATHOLOGY
ISSN journal
00219746 → ACNP
Volume
53
Issue
5
Year of publication
2000
Pages
382 - 387
Database
ISI
SICI code
0021-9746(200005)53:5<382:NDOEGI>2.0.ZU;2-0
Abstract
Aims-Despite the evidence of familial occurrence, chromosomal gene mapping, and apoptosis as a mechanism of myocyte death, the aetiopathogenesis of ar rhythmogenic right ventricular cardiomyopathy (ARVC) remains speculative. B ecause of the frequent histological finding of focal inflammatory infiltrat es, the hypothesis of an infective myocarditis aetiology has been put forwa rd. The aim of this investigation was to test this hypothesis. The presence of enteroviruses was investigated by a highly sensitive and specific molec ular technique. Methods-Endomyocardial tissue samples from 20 patients with ARVC (11 male, nine female; mean age, 40 years; SD, 16) and 20 control subjects with other cardiac diseases were analysed using reverse transcription and nested poly merase chain reaction (PCR). Myocardial samples obtained from four patients with enteroviral myocarditis and coxsackie B3 virus infected cells were us ed as positive controls. Results-Endomyocardial biopsy was diagnostic for ARVC in all patients: myoc ardial atrophy was seen, with less than 45% residual myocytes. Foci of infl ammatory infiltrates were seen in four biopsies, and the cells were identif ied by immunohistochemistry as mainly T cells. All samples, from both patie nts with ARVC and subjects with other cardiac diseases, were negative for e nteroviral genome by means of nested PCR. Conclusion-These findings indicate that enteroviruses are not involved in t he aetiopathogenesis of ARVC. Future molecular studies should investigate t he presence of other infective agents, as well as their possible role in tr iggering apoptosis.