Role of Mechanics in Rhythm Disturbances in 1D Mathematical Model of Myocardial Tissue with Local Ca2+-Overload

Possible contribution of the mechanics to the arrhythmogenesis in Ca²⁺ overloaded cardiomyocytes has been under appreciated. Earlier developed mathematical model of cardiomyocyte electromechanical function predicted a significant role of intra- and extracellular mechanical factors in triggering rhythm abnormalities. We utilized the cellular model to study effects of the electromechanical coupling between cardiomyocytes in a 1D heterogeneous muscle strand comprised normal (N) and sub-critical (SC) cardiomyocytes with moderately decreased Na⁺-K⁺ pump activity. The single SC cardiomyocytes did not demonstrate spontaneous activity during isometric contractions at a reference length. In the tissue, excitation spreads via electro-diffusional cell coupling and activates cell contractions and force development. Mechanical interactions between Nand SC-cells in the tissue resulted in the spontaneous activity emerged in the SC zone between the regular stimuli. The results suggest that ectopic activity may emerge in a rather small SC-region and expand by capturing normal regions in myocardium due to the electromechanical coupling between cardiomyocytes.