Modeling the influence of high fibroblast level on arrhythmia development and obstructed depolarization spread

Aims: In the focus of this study stand the fibroblast cells that under physiological terms are providing structural support for the heart, but under pathophysiological conditions they can obstruct the pacemaker activity and the excitation spread function of the heart that may develop arrhythmia. Methods: We investigated the influence of high fibroblast level under several patho-physiological conditions. The simulation was performed on a 3D heart model, adopting a 0.25 mm spatial and 2 fJ.S temporal maximal resolution. In our simulation 25% volume of the normal cardiac tissue is occupied by fibroblast, and in presence of pathological cases or aging, the fibroblast cells accumulate up to 40%-95% volume. We employed the effect of cardio-myocyte death and laminar sheets. Results: In presence of 30%/35%/40%/45%/50% fibroblast in cardiac myocyte, the spread velocity of depolarization was obstructed by 3%/7%/JJ%/J5%/J9%, while regional inflammation and injures locally reduced the propagation speed of excitation by at least 20%. Tissue aging has reduced cardiac pacemaker activity and increased the possibility of irregular cardiac activity. Conclusion: High fibroblast levels not only detains significantly the spread of excitation, but it can obstruct the depolarization wave evolving cardiac arrhythmia.