In Figure 2, six individual frames of a networked simulation of a fibroblast-rich region, embedded within a grid of normal ventricular myocytes, are presented. The damaged tissue region measured 32 cells in diameter. Under mechanically stable, resting conditions cardiomyocytes are hardly affected by the attached fibroblasts: the fibroblast-rich region is electrophysiologically silent. Stretching of the fibroblasts in the model scar leads to their depolarization, which is partly transmitted to adjacent cardiomyocytes.This causes localized myocyte depolarization and, after reaching threshold, triggers action potentials in the cardiomyocytes within the damaged tissue. Subsequently, the ectopic focus generated in the scar spreads throughout the whole ventricular network.
Figure 2 Sequence ofsixframes taken from a networked simulation of the arrhythmogenic influence ofmechanosensitive fibroblasts in cardiac scar tissue. A model scar, 32 cells in diameter, consisting ofcardiomyocytes each connected to a single mechanosensitive fibroblast, is embedded in the centre of a 128×128 grid ofventricular myocyte models. Under mechanically stable conditions the fibroblast-rich region is electrophysio-logically silent (0 ms, top left). Stretch of the fibroblasts leads to local depolarization (40 ms, top centre) and localized generation ofaction potentials in myocytes of the damaged region (47 ms, top right), which subsequently cover the whole scar (50 ms, bottom left). Hereinafter, the excitation invades the adjacent healthy myocardium (60 ms, bottom centre) and spreads through the whole network (70 ms, bottom right). Cardiomyocytes are represented by one pixel each; the individual membrane potentials are colour- and altitude-coded
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