This preclinical study elucidates the mechanisms of impulse conduction during cardiac repolarization, highlighting that apparent supernormal conduction is an artifact of the action potential origin site.
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Hypothesis-generating for repolarization conduction; prospective human studies needed before clinical adoption.
The propagation of impulses in partially depolarized cardiac fibers has been studied by stimulating isolated preparations of mammalian Purkinje fibers or ventricular muscle at selected intervals during and after repolarization. Electrical activity has been recorded simultaneously through multiple intracellular microelectrodes located at various distances from the stimulus site. Three possibilities appear to exist for conduction during the latter part of repolarization in cardiac fibers which contrast with conduction occurring after the completion of repolarization: 1) Slow conduction. This has been observed when the action potential propagates into fibers in which repolarization is less advanced. This may be associated with a decrease in the rate of rise and the voltage of the action potential and corresponds more or less to decremental conduction. When entering more fully repolarized fibers, the action potential may show reverse changes. 2) Conduction at normal velocity. This has been observed when impulses propagate in fibers which are more or less in the same stage of repolarization even though the transmembrane potential may not be of normal magnitude. 3) Fast conduction. The present study offers no clear evidence for this type, which should correspond to the so-called supernormality of conduction. In contrast, apparent supernormal conduction was shown to be caused by a shift of the site of origin of the action potential when stimuli were applied during the relative refractory period.
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Dam et al. (1963) studied this question.
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