We keep the original whole-cell dynamics by reproducing the same characteristic action potential and calcium dynamics, whereas the Markov chain-based description of the L-type Calcium channels allows novel small spatial scale simulations of subcellular processes.

In summary, we have modified two cardiac models by proposing new Markov Chain models for the L-type Calcium. We discuss how model discrepancy, data availability, and parameter identifiability can influence the choice of the size of the collection. We show the importance of using an ensemble of a set of parameter values to obtain proper results when considering a second protocol that suppresses calcium inactivation and mimics a pathological condition. In addition, instead of presenting a single set of parameters, we present a collection of set of parameters employing Differential Evolution algorithms that can properly reproduce very different protocol data. In this paper, we develop Markov Chain models for the L-type Calcium current that can reproduce the electrophysiology of two established human models for the ventricular and Purkinje cells. In contrast to gate-based models, Markov Chain models are well suited to promote the integration of the subcellular level of the cardiomyocyte to the whole cell. The development of modeling structures at the channel level that can integrate subcellular and cell models and properly reproduce different experimental data is of utmost importance in cardiac electrophysiology.

Markov chain model