Proarrhythmic response to sodium channel blockade. Theoretical model and numerical experiments.

@article{Starmer1991ProarrhythmicRT,
  title={Proarrhythmic response to sodium channel blockade. Theoretical model and numerical experiments.},
  author={C. Frank Starmer and Anselmo Lastra and Vladislav V. Nesterenko and Augustus O. Grant},
  journal={Circulation},
  year={1991},
  volume={84 3},
  pages={1364-77}
}
BACKGROUND The use of flecainide and encainide was terminated in the Cardiac Arrhythmia Suppression Trial because of an excess of sudden cardiac deaths in the active treatment group. Such events might arise from reentrant rhythms initiated by premature stimulation in the presence of anisotropic sodium channel availability. Drugs that bind to sodium channels increase the functional dispersion of refractoriness by slowing (a result of the drug-unbinding process) the transition from an inexcitable… CONTINUE READING

Citations

Publications citing this paper.
Showing 1-10 of 47 extracted citations

References

Publications referenced by this paper.
Showing 1-10 of 37 references

Cellular mechanisms of delayed recovery of excitability in ventricular tissue

  • Lesh, M Pring, JF Spear
  • Am J Physiol
  • 1991

Lidocaine blockade of a transiently accessible site in cardiac sodium channels

  • R Gruber, E Carmeliet
  • J Mol Cell Cardiol
  • 1991

Amplifica - tion of flecainideinduced ventricular conduction slowing by exercise : A potentially significant clinical consequence of usedependent sodium channel blockade

  • J Weirich, H Antoni
  • Circulation
  • 1989

Similar Papers

Loading similar papers…