Marked action potential prolongation as a source of injury current leading to border zone arrhythmogenesis.

The objective of this study was to delineate electrophysiologic phenomena in a border zone adjacent to a zone of marked action potential prolongation. By means of a standard microelectrode technique, we studied sheep Purkinje fibers placed in a partitioned chamber and superfused with Tyrode's solution. Ethylenediamine tetraacetic acid (EDTA) was added to one chamber. Recordings were made in the abnormal segment (ABN) superfused with EDTA and at two sites in the normal segment (NL)--at the border within 0.5 mm (NL-B) and 3 to 4 mm from the partition (NL-D). Exposure of ABN to EDTA caused marked prolongation of the action potential duration (APD) and triggered activations (TAs), which were found to have the earliest recorded activation at NL-B (n = 20), at ABN (n = 8), or at both sites (n = 12). NL-B recordings displayed prolonged low-amplitude secondary plateaus, which were termed "border zone early afterdepolarizations." These were coincident with the plateaus of the prolonged action potentials in ABN and appeared to be due to electrotonic transmission of current from ABN to NL-B. Border zone TAs arose from these low-amplitude plateaus and were either eliminated by the addition of lidocaine to NL consistent with their presumed NL site of origin or occurred after localized withdrawal of EDTA from one segment in fibers rendered quiescent at the plateau by generalized superfusion with EDTA. In conclusion, APD and membrane potential inhomogeneities lead to electrotonic transmission of injury current to border zones adjacent to zones of abnormal APD prolongation. This injury current leads to TAs originating at the border zone. These findings may be relevant to the role of injury current in clinical arrhythmias.