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Atrial fibrillation (AF) is a widespread heart disease which prevalence increases essentially in the elderly. In this study, we combined age-related changes in cardiomyocytes electrophysiology with the effects of chronic atrial fibrillation on the population of human atrial cell models. Our age-dependent populations of models are able to reproduce experimentally observed effects of aging on action potential (AP) and calcium transient (CaT) morphology. Simulation of AF remodeling in aging models allowed us to reproduce specific shortening of AP duration on a 90% level, an increase in AP plateau, and a reduction in CaT amplitude. Our modeling results predict the increased risk of sustained arrhythmia in the elderly group of models. [ABSTRACT FROM AUTHOR]

The electrophysiological properties of cardiomyocytes change with age, affecting their arrhythmogenic activity and sensitivity to drugs. The literature on canine atriums has described changes in transmembrane currents and action potential that occur during aging. In this study, we attempt to reproduce these changes using three mathematical models of human atrial cardiomyocytes and one model of canine atrial cardiomyocytes. All models correctly reproduced the decrease in the action potential region between the spike and plateau. However, none of the models could reproduce the lengthening of the action potential at the 90% level observed in experiments with canines. This may be explained by age-related changes in transmembrane currents that have not been measured in experiments, or all observed models were built on experimental data from senior age peoples. [ABSTRACT FROM AUTHOR]