The same gene may produce both the trouble in development and increased susceptibility to cardiotropic viruses in ARVD extended to cardiomyopathies

International Conference and Exhibition on Molecular Medicine and Diagnostics

August 24-26, 2015 London, UK

Fontaine G H

Posters-Accepted Abstracts: J Mol Genet Med

Abstract :

ARVD is the most frequent presentation of ARVCs which includes Brugada syndrome, RVOT VT etc. A recent report has
demonstrated for the first time that two mutations (one is new) the other is desmoplakine (a desmosomal protein) seems
responsible for both the induction of the trouble in development but also biologic signs of inflammation probably due to an increased
susceptibility to cardiotropic viruses (not yet identified). This concept is in agreement with a decrease in LVEF observed sometimes
abruptly during the time course of ARVD leading in the most severe cases to irreversible CHF. It seems possible to extrapolate
this phenomenon to other forms of cardiomyopathies known to show the spectrum of multiple aspect of myocarditis going from
the fulminant form leading to hyper acute heart failure to complete healing without sequel including chronic, chronic active and
completely healed myocarditis. The problem is therefore to identify the inflammatory agent which can be performed nowadays by the
recent technic of time of flight viral RNA identification by mass spectroscopy. This approach needs endomyocardial biopsy which is a
safe procedure if properly performed by a trained personnel following a strict protocol. In particular IDCM and HCM are well known
to exhibit the same clinical patterns which can explain the wide spectrum of prognosis observed in these conditions. The abolition of
the phenotype by small molecule in ARVD Zebra fish and mouse also open a completely new formidable area of resarch for the future.