Abstract
We have recently reported that spontaneous calcium oscillations (S-CaOs) triggering propagated membrane depolarizations can contribute to arrhythmogenesis in the setting of ischemia/reperfusion (I/R). In a perfused Langendorff guinea pig heart preparation subjected to global I/R, simultaneous optical mapping of intracellular calcium transient and membrane voltage showed, in a majority of experiments, that once S-CaOs developed they were either followed every basic beat resulting in a bigeminal rhythm or became sustained resulting in a tachyarrhythmia. In some experiments, S-CaOs seemed to occur sporadically following some but not all basic beats. To investigate the mechanism of synchronization of S-CaOs in the intact heart resulting in a localized dominant focal activity we developed a theoretical model of pacemaker cells coupled to excitable cells. An array of excitable cells coupled to a small number of oscillatory cells were modeled using modified FHN equations. Small changes in both the intrinsic period of the oscillatory cells and the diffusion coefficient resulted in transitions similar to those seen in experiments. The behavior of the model strongly suggests that intermittent synchronization of S-CaOs in the intact heart can result in sporadic focal propagated responses.
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