Background We used a mathematical model of a sinoatrial nodal cell (SA
N model) electrically coupled to real ventricular cells (VCs) to inves
tigate action potential conduction from an automatic focus. Methods an
d Results Since input resistance of a VC is less than that of an SAN c
ell, coupling of the SAN model, with a size factor of 1, to a VC produ
ced either (1) spontaneous pacing at the slower rate of the SAN model
but without driving (activation) of the VC for lower values of couplin
g conductance (G(i)) or (2) inhibition of pacing of the SAN model by e
lectrical coupling to the VC for higher values of G(j). When the SAN m
odel was adjusted in size to be 3 to 5 times larger than a sinoatrial
nodal cell, thus making effective SAN model capacitance 3 to 5 times l
arger and input resistance 3 to 5 times smaller, the SAN model propaga
ted activity to the coupled VC for G(j) above a critical value. When t
he VC was paced at 1 Hz, the coupled cell pair demonstrated a stable r
hythm of alternating cycle lengths and alternating conduction directio
ns. By increasing pacing frequency to 2 Hz, we converted this rhythm t
o a regular 2-Hz frequency in which each action potential originated i
n the VC. More complex periodic interactions were observed at intermed
iate cycle lengths and lower or higher values of G(j). Conclusions The
phenomena we observed demonstrate the critical role of the size of an
automatic focus as well as the coupling in the propagation of activit
y from the focus into surrounding myocardium.