Propagation velocity profile in a cross-section of a cardiac muscle bundle from PSpice simulation.

Background: The effect of depth on propagation velocity within a bundle of cardiac muscle fibers is likely to be an important factor in the genesis of some heart arrhythmias. MODEL AND METHODS: The velocity profile of simulated action potentials propagated down a bundle of parallel cardiac muscle fibers was examined in a cross-section of the bundle using a PSpice model. The model (20 x 10) consisted of 20 chains in parallel, each chain being 10 cells in length. All 20 chains were stimulated simultaneously at the left end of the bundle using rectangular current pulses (0.25 nA, 0.25 ms duration) applied intracellularly. The simulated bundle was symmetrical at the top and bottom (including two grounds), and voltage markers were placed intracellularly only in cells 1, 5 and 10 of each chain to limit the total number of traces to 60. All electrical parameters were standard values; the variables were (1) the number of longitudinal gap-junction (G-j) channels (0, 1, 10, 100), (2) the longitudinal resistance between the parallel chains (Rol2) (reflecting the closeness of the packing of the chains), and (3) the bundle termination resistance at the two ends of the bundle (RBT). The standard values for Rol2 and RBT were 200 KOmega.

Results: The velocity profile was bell-shaped when there was 0 or only 1 gj-channel. With standard Rol2 and RBT values, the velocity at the surface of the bundle (theta1 and theta20) was more than double (2.15 x) that at the core of the bundle (theta10, theta11). This surface:core ratio of velocities was dependent on the values of Rol2 and RBT. When Rol2 was lowered 10-fold, theta1 increased slightly and theta2decreased slightly. When there were 100 gj-channels, the velocity profile was flat, i.e. the velocity at the core was about the same as that at the surface. Both velocities were more than 10-fold higher than in the absence of gj-channels. Varying Rol2 and RBT had almost no effect. When there were 10 gj-channels, the cross-sectional velocity profile was bullet-shaped, but with a low surface/core ratio, with standard Rol2 and RBT values.

Conclusion: When there were no or few gj-channels (0 or 1), the profile was bell-shaped with the core velocity less than half that at the surface. In contrast, when there were many gj-channels (100), the profile was flat. Therefore, when some gj-channels close under pathophysiological conditions, this marked velocity profile could contribute to the genesis of arrhythmias.