I've seen several references and videos showing isolated cardiomyocytes spontaneously beating in cell culture. This is surprising, since in the intact heart, these cells would never behave that way. Instead, they have a steady resting membrane potential. Only the pacemaker, AV node, and to some extent conducting cells should behave this way, not the cardiomyocytes. Is there an accepted explanation among those who work with these? Perhaps an ectopic expression of the f-channels?
Change in membrane potential, if set in the right solution will lead to contraction of the single isolated cell and/or the heart and vice versa(e.g. cardioplegia trough solution in heart transplant). Afib, SVES or VES might be an example for sponatneous membrane depletion in somewhat "normal" heart. A vicious circle does lead to different ionic expression through structural remodelling in Afib, as you figured.
My problem is not about the entire heart, but individual myotubes isolated in vitro. These should not beat because they do not (or should not) express the f channel, and so have a steady resting potential. In autorhythmic cells like in the SA node, the conducting cells have this channel, which produces the rising baseline that increases potential enough to initiate an action potential. But in the myocyte fraction, there should be none of this.
What do you exactly observe - in another words what you mean by "beating"? Fast twitch or slow propagating contraction? The second can be caused by spontaneous release of Ca from SR.
It isn't my observation, just literature and a video. However, I think I understand the situation a little better. It seems that the isolated heart cells that do beat are from embryonic states only. Heart cells from adult rats, for example, need to be stimulated to contract (e.g., Haworth, Circ. Res. 52:342 (1983)). That would seem to solve the dilemma. After all, if it were in fact beating in culture because of a leaky release from the SR through the RyR, the cell would not survive long at all, and the beats would not be uniform. That is a pathological situation; it would mean the Ca pump in the SR is overwhelmed by the leak.
The embryonic cell presumably has the f-channel and thus beats. Interestingly, it seems that after these cells are cultured and confluent, their beating becomes synchronized, indicating they may also form gap junctions.
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