Role of Intracellular Ca2+ Dynamics in Supporting Spiral Wave Propagation

The intracellular Ca2+ dynamics play a key role in the transition from ventricular tachycardia to ventricular fibrillation through their influence on Ca-sensitive membrane currents. That was shown in our previous publication which deals with modified Luo and Rudy cardiac cell model. Here using the same model we study the effect of increasing sensitivity of non-specific calcium current, Ins(Ca), to [Ca2+]i on wave propagation in two dimensional tissue model under conditions of ventricular tachycardia. Under these conditions some of the tissue cells come across high rates of stimulation with subsequent calcium overload and release from the Junctional Sarcoplasmic Reticulum. Our results show that increasing sensitivity of Ins(Ca) to [Ca]i leads to progressive prolongation of the action potential duration in some of the tissue cells. That causes a non-uniform increase in the length of the propagated spiral wave to such an extent that the size of the tissue becomes insufficient for further propagation. The temporary block of propagation causes the appearance of cells with single and multiple early after depolarization (EAD), which formed in a portion of space with retarding repolarization. This area is the source of consequent initiation of direct or backward spiral waves, when the surrounding tissue goes out of excitation.