Key result
Numerical studies demonstrate that the proarrhythmic effect of sodium channel blockers is a generic feature of slowed conduction, allowing channel kinetics to be ignored when exploring propagating wavefronts.
Computational modeling demonstrates that the proarrhythmic effect of sodium channel blockers is primarily due to slowed conduction rather than detailed channel kinetics, allowing for simplified 2-D and 3-D simulations.
Should not yet change sodium channel blocker use; hypothesis-generating for simplified conduction-based arrhythmia models.
Many drugs block the cardiac sodium channel including class I antiarrhythmics, tricyclic antidepressants, synthetic opiate analgesics, and cocaine. Under some conditions, these drugs promote initiation of reentrant arrhythmias that can lead to sudden cardiac death. Numerical studies of the interaction between these drugs and the cardiac sodium channel indicated that the proarrhythmic effect is not dependent on the detailed kinetics of the sodium channel but rather is a generic feature of slowed conduction secondary to sodium channel blockade. The authors present results demonstrating that when channel kinetics are rapid in comparison to drug-binding kinetics, the channel kinetics can be ignored, thus dramatically reducing the computational complexity necessary for exploring 2-D and 3-D propagating wavefronts.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">></ETX>
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Starmer et al. (2003) studied Reentrant arrhythmias. Sodium channel blockers was evaluated on Initiation of rotating vortices. Numerical studies demonstrate that the proarrhythmic effect of sodium channel blockers is a generic feature of slowed conduction, allowing channel kinetics to be ignored when exploring propagating wavefronts.
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