Computational modeling demonstrates that the initiation and termination of calcium-mediated triggered activity in cardiac myocytes are random events dictated by spontaneous Ca2+ release.
Significance A normal heart cell behaves dynamically as an excitable element that generates a nonlinear electrical impulse in response to a suprathreshold current stimulus. However, under pathological conditions, cardiac myocytes can self-generate their own impulses after a normal excitation. This rogue behavior, known as triggered activity, can cause arrhythmias. However, how it is initiated and terminated is not fundamentally understood. We demonstrate computationally that initiation and termination are random events. Moreover, we elucidate the statistical properties of spontaneous Ca 2+ release from intracellular stores that dictate the probability of those events and link fundamentally stochasticity at the ion channel and whole-cell levels. Our results provide mechanistic insights into cardiac arrhythmogenesis and highlight important differences between Ca 2+ dynamics in cardiac myocytes and other eukaryotic cells.
Song et al. (Tue,) conducted a other in Cardiac arrhythmias. Computational modeling was evaluated on Initiation and termination of triggered activity. Computational modeling demonstrates that the initiation and termination of calcium-mediated triggered activity in cardiac myocytes are random events dictated by spontaneous Ca2+ release.