A newly developed iterated map model unifies two previously contradictory mechanisms of calcium alternans into a single cohesive mathematical framework, showing they work synergistically.
A unified mathematical model demonstrates that fractional SR Ca2+ release/uptake and Ca2+ spark refractoriness work synergistically to promote calcium alternans in ventricular myocytes.
Abstract Intracellular calcium (Ca 2+ ) alternans is a dynamical phenomenon in ventricular myocytes, which is linked to the genesis of lethal arrhythmias. Iterated map models of intracellular Ca 2+ cycling dynamics in ventricular myocytes under periodic pacing have been developed to study the mechanisms of Ca 2+ alternans. Two mechanisms of Ca 2+ alternans have been demonstrated in these models: one relies mainly on fractional sarcoplasmic reticulum Ca 2+ release and uptake, and the other on refractoriness and other properties of Ca 2+ sparks. Each of the two mechanisms can partially explain the experimental observations, but both have their inconsistencies with the experimental results. Here we developed an iterated map model that is composed of two coupled iterated maps, which unifies the two mechanisms into a single cohesive mathematical framework. The unified theory can consistently explain the seemingly contradictory experimental observations and shows that the two mechanisms work synergistically to promote Ca 2+ alternans. Predictions of the theory were examined in a physiologically-detailed spatial Ca 2+ cycling model of ventricular myocytes.
Qu et al. (Thu,) conducted a other in Calcium alternans in ventricular myocytes. Iterated map model of intracellular Ca2+ cycling dynamics was evaluated. A newly developed iterated map model unifies two previously contradictory mechanisms of calcium alternans into a single cohesive mathematical framework, showing they work synergistically.
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