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No detection of enteroviral genome in the myocardium of patients with arrhythmogenic right ventricular cardiomyopathy
  1. Fiorella Calabrese1,
  2. Annalisa Angelini1,
  3. Gaetano Thiene1,
  4. Cristina Basso1,
  5. Andrea Nava2,
  6. Marialuisa Valente1
  1. 1Institute of Pathological Anatomy, University of Padua, 61-35121 Padova, Italy
  2. 2Institute of Cardiology, University of Padua
  1. Dr Thiene, Istituto di Anatomia Patologica, Via A Gabelli, 61-35121 Padova, Italy email: cardpath{at}


Aims—Despite the evidence of familial occurrence, chromosomal gene mapping, and apoptosis as a mechanism of myocyte death, the aetiopathogenesis of arrhythmogenic right ventricular cardiomyopathy (ARVC) remains speculative. Because of the frequent histological finding of focal inflammatory infiltrates, the hypothesis of an infective myocarditis aetiology has been put forward. The aim of this investigation was to test this hypothesis. The presence of enteroviruses was investigated by a highly sensitive and specific molecular 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 polymerase chain reaction (PCR). Myocardial samples obtained from four patients with enteroviral myocarditis and coxsackie B3 virus infected cells were used as positive controls.

Results—Endomyocardial biopsy was diagnostic for ARVC in all patients: myocardial atrophy was seen, with less than 45% residual myocytes. Foci of inflammatory infiltrates were seen in four biopsies, and the cells were identified by immunohistochemistry as mainly T cells. All samples, from both patients with ARVC and subjects with other cardiac diseases, were negative for enteroviral genome by means of nested PCR.

Conclusion—These findings indicate that enteroviruses are not involved in the aetiopathogenesis of ARVC. Future molecular studies should investigate the presence of other infective agents, as well as their possible role in triggering apoptosis.

  • arrhythmogenic right ventricular cardiomyopathy
  • myocarditis
  • enterovirus
  • molecular biology

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