Spontaneous Calcium Release in Cardiac Myocytes: Store Overload and Electrical Dynamics

Abstract

Heart disease is the leading cause of mortality in the United States. One cause of heart arrhythmia is calcium (Ca²⁺) mishandling in cardiac muscle cells. We adapt Izu's et al. mathematical reaction-diffusion model of calcium in cardiac muscle cells, or cardiomyocytes, [14], implemented by Gobbert [12], and analyzed in Coulibaly et al. [8] to include calcium being released from the sarcoplasmic reticulum (SR), the effects of buffers in the SR, particularly calsequestrin, and the effects of Ca²⁺ influx due to voltage across the cell membrane. Based on simulations of the model implemented in parallel using MPI, our findings aligned with known biological models and principles, giving us a thorough understanding of several factors that influence Ca²⁺ dynamics in cardiac myocytes. Speci cally, dynamic calcium store will cap previous calcium blow-up seen in the model. Calcium channels located in spatial opposition of calcium release units produce more predictable intracellular calcium propagation. And we used multi-parametric calcium dynamics tables, which act as a multidimensional bifurcation diagram, to visualize parameter boundaries between different biophysical dynamics.