Role of channel blockade in promoting the initiation of rotating vortices in cardiac muscle

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