The cell-based EMI model resolves micro-reentry and intricate dynamics near individual cardiomyocytes that standard averaged models cannot, albeit at a significantly increased computational cost.
Cell-based EMI modeling provides higher spatial resolution than standard bidomain models, enabling the simulation of micro-reentry in small clusters of myocytes, though it requires massive computational resources.
analysis of electrochemical wave dynamics in cardiac tissue is limited by the homogenization procedure (spatial averaging) intrinsic to standard continuum models of conduction. Averaged models cannot resolve the intricate dynamics in the vicinity of individual cardiomyocytes simply because the myocytes are not present in these models. Here we demonstrate how recently developed mathematical models based on representing every myocyte can significantly increase the accuracy, and thus the utility of modeling electrophysiological function and dysfunction in collections of coupled cardiomyocytes. The present gold standard of numerical simulation for cardiac electrophysiology is based on the bidomain model. In the bidomain model, the extracellular (E) space, the cell membrane (M) and the intracellular (I) space are all assumed to be present everywhere in the tissue. Consequently, it is impossible to study biophysical processes taking place close to individual myocytes. The bidomain model represents the tissue by averaging over several hundred myocytes and this inherently limits the accuracy of the model. In our alternative approach both E, M, and I are represented in the model which is therefore referred to as the EMI model. The EMI model approach allows for detailed analysis of the biophysical processes going on in functionally important spaces very close to individual myocytes, although at the cost of significantly increased CPU-requirements.
Jæger et al. (Wed,) conducted a other in Cardiac arrhythmias. EMI (Extracellular, Membrane, Intracellular) model vs. Bidomain/monodomain models was evaluated. The cell-based EMI model resolves micro-reentry and intricate dynamics near individual cardiomyocytes that standard averaged models cannot, albeit at a significantly increased computational cost.
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