A novel mechanism for arrhythmia formation.

I. M. IRURZUN; D. S. ANDRES; M. M. DEFEO; E. E. MOLA

Arica, Chile

Workshop; LAWNP2007; 2007

In both numerical simulations in cellular models and experiments, polymorphic patterns appear in the ECG related either to the potassium channel blockade, which produces a prolonged refractoriness, or to the sodium channel blockade, that produces a prolongation of the recovery of excitability.             More recently experimental studies of three members of the conexin family of the gap junction channel proteins (conexin43, conexin40 and conexin45) produced ventricular outflow tract defects, slowed conduction, spontaneous ventricular tachycardia and sudden cardiac death, prolonged P-R intervals and bundle branch block, and lethal embryonic cardiac cushion developmental defects, respectively.             Myocardial gap junctions couple adjacent cells both electrically and metabolically by facilitating the intercellular exchange and participating in a number of biological functions such as embryogenesis and cellular growth. In the heart, the current flow trough the gap junctions synchronizes the pacing activity.             In the extended cellular models used to simulate the propagation of the electrical wave fronts on the heart muscle so far, the gap junction coupling was introduced as a conductance in the so-called cable model. However recent experimental information indicates that this picture must be improved; junctional current exponentially decays when a constant voltage difference is applied across the junction.             In the present work, we generalizes the cable model to introduce the above-mentioned finding and show that modulating the gap junction characteristics it is possible either suppress or produce meandering spiral waves associated to cardiac arrhythmia.