Mechanisms of triggered activity induction at the border zone of normal and abnormal cardiac tissue

Ionic mechanisms that may be involved in inducing triggered activations at the border zone (BZTAs) of normal and abnormal Purkinje fiber segments were investigated. In a two-chamber bath, fibers were divided into a normal segment and segment treated with ethylenediaminetetraacetic acid to stimulate electrophysiologic alterations 24 hours after infarct. Interventions to normal segments included 1.8 mM lidocaine (n = 10), 3 x 10(-4) mM tetrodotoxin (n = 5), 10(-3) mM aconitine (n = 4), 3 mM cesium chloride (n = 7), 10(-2) mM verapamil (n = 4), and 6-8 mM (n = 7) of K+. Ethylenediaminetetraacetic acid (3.3 mM) prolonged action potentials and induced low diastolic potentials in the normal segment border zone. Tetrodotoxin, lidocaine, and high K+ levels suppressed BZTAs; cesium chloride and aconitine increased BZTAs; and verapamil did not reduce BZTAs. The finding that BZTAs were not abolished by verapamil suggests that abnormal automaticity is not a mechanism. Apparently, BZTAs depend on the Na+ inward current activated by depolarization of the membrane secondary to depolarization of adjacent cells.