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Figure 3.8. AP propagation during reduced intercellular gap junction coupling. Conduction ve-
locity (solid line) decreases monotonically as coupling is reduced. In contrast, SF first increases to
a maximum and then decreases sharply to the point of conduction block (horizontal bar at SF=1).
Conduction reaches very slow velocity (0.26 cm/sec) before block occurs. From Shaw and Rudy
[174], with permission from Wolters Kluwer Health, Inc.
underlie slow conduction with very different properties. Reduced excitability is associated with
reduced SF; it cannot support very slow conduction and favors conduction failure. Reduced
coupling is associated with increased SF and can support very slow conduction that is robust.
This property is made use of in the atrio-ventricular node, where slow, safe excitation is required
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to provide the delay between atrial and ventricular contraction needed for effective pumping
action of the heart. Reduced cell-to-cell coupling in the direction transverse to the main fiber axis
contributes to anisotropic conduction in atrial and ventricular myocardium. 181,186,212 Pathologically,
gap junction decoupling occurs after the first 15 minutes of acute ischemia, 209,213 in heart failure
and in the hypertrophied ventricle, 214,215,216 and in the border zone of infracted myocardium. Very
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slow velocities (< 1 cm/sec) were measured in the infarct border zone, indicating the possibility of
micro-reentrant circuits forming there.
The ionic mechanism of slow conduction in decoupled tissue is explored in Figure 3.9
through simulations in the 1-dimensional strand. The upstroke and early plateau of the
propagating action potential are shown in a given cell (cell 1). The time of its excitation (indicated
by dV /dt max ) is set to 0 msec, and the delay to excitation of its downstream neighbor (cell 2) is
m
indicated by the horizontal shaded bar above the action potential. Two simulated action