Arrhythmogenic mechanism of an LQT-3 mutation of the human heart Na(+) channel alpha-subunit: A computational analysis.

@article{Wehrens2000ArrhythmogenicMO,
  title={Arrhythmogenic mechanism of an LQT-3 mutation of the human heart Na(+) channel alpha-subunit: A computational analysis.},
  author={Xander H T Wehrens and H. Abriel and Candido Cabo and Jesaia Benhorin and Robert S. Kass},
  journal={Circulation},
  year={2000},
  volume={102 5},
  pages={584-90}
}
BACKGROUND D1790G, a mutation of SCN5A, the gene that encodes the human Na(+) channel alpha-subunit, is linked to 1 form of the congenital long-QT syndrome (LQT-3). In contrast to other LQT-3-linked SCN5A mutations, D1790G does not promote sustained Na(+) channel activity but instead alters the kinetics and voltage-dependence of the inactivated state. METHODS AND RESULTS We modeled the cardiac ventricular action potential (AP) using parameters and techniques described by Luo and Rudy as our… CONTINUE READING