Action potential changes due to Y1795H mutation in Brugada syndrome patients: A simulation study

Stefano Severi, S. Vecchietti, I. Rivolta, C. Napolitano, S. G. Priori, S. Cavalcanti

Research output: Chapter in Book/Report/Conference proceedingConference contribution

Abstract

Several mutations of the gene encoding for the cardiac sodium channel (SCN5A) are associated with Congenital Brugada syndrome (BrS), but the assessment of their functional consequences with the experimental models is biased by technical limitations. To overcome such limitations we used a novel approach combining in vitro data and computer modeling. The Y1795H mutation of SCN5A was evaluated. A Markovian model capable to reproduce the kinetics of both wild type (WT) and mutant channels was incorporated into the Luo-Rudy comprehensive model of ventricular cells. Here presented results highlight the high sensitivity of simulated AP of virtual transgenic cells to the maximum conductance assigned to the sodium current in mutant channel model. A value of about 10000 S/F allows the reproduction of coherent action potentials in WT and mutant cells.

Original languageEnglish
Title of host publicationComputers in Cardiology
EditorsA. Murray
Pages437-440
Number of pages4
Volume30
Publication statusPublished - 2003
EventComputers in Cardiology 2003 - Thessaloniki Chalkidiki, Greece
Duration: Sep 21 2003Sep 24 2003

Other

OtherComputers in Cardiology 2003
CountryGreece
CityThessaloniki Chalkidiki
Period9/21/039/24/03

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Software

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