Phase 1B ventricular arrhythmia in the dog: localized reentry within the mid-myocardium.

Intramural and epicardial composite electrograms, signal-averaged orthogonal bipolar electrograms across the ischemic zone, and closely-spaced bipolar electrograms from subendocardium, mid-myocardium, and subepicardium were utilized to determine if phase 1B reentry resulted from localized reentry within ischemic mid-myocardium. During the first 10 minutes following coronary ligation, activation delays were largest in ischemic subepicardium, with continuous electrical activity in ischemic epicardium linking a ventricular extrasystole to the preceding beat. During the 15-30 minute period, activation delay observed in ischemic mid-myocardium exceeded activation delay on the epicardial surface. Ventricular extrasystoles were associated with mid-myocardial delays > 130 msec. With short-coupled extrasystoles (< 300 msec), electrical activity in ischemic mid-myocardium linked an extrasystole with the preceding beat. Although single extrasystoles with coupling intervals > 300 msec were also associated with mid-myocardial delays > 130 msec, most extrasystoles (68%) demonstrated an isoelectric gap > 20 msec. The data demonstrate an association between delayed activation within ischemic mid-myocardium and phase 1B arrhythmia resulting from (1) localized reentry in ischemic mid-myocardium and (2) a delay-dependent "non-reentrant" mechanism.