Evaluating Propagation Pattern During Reentry-like Activity of Cultured Cardiomyocytes

Abstract

Heart failure is one of frequent diseases for the elderly, and it is required to unveil the pathogenic mechanism of reentry, a type of lethal arrhythmia. Although fibrosis can cause arrythmia, little is known about how fibrosis disrupts normal cardiac function, and then causes arrythmia. In this study, we aimed to model reentry-like activity in vitro for elucidating the mechanism of reentry. First, rat cardiomyocytes were purified with a glucose-free medium, and cultured on microelectrode arrays. Extracellular potential was measured with or without lidocaine, a proarrhythmic reagent, on day 6-7. Reentry-like activities were observed from three out of five samples in presence and absence of lidocaine. We evaluated transitions between reentry and normal propagation. Activity pattern gradually changed from normal propagation to reentry, but that did rapidly from reentry to normal propagation, suggesting different mechanisms between start and end of reentry. Furthermore, changes in propagation pattern during reentry suggested that delay prolongation in partial area can terminate reentry-like activity in vitro. Overall, our system is suitable for elucidating pathogenic mechanisms of reentry.