Abstract

The mechanisms of ventricular fibrillation (VF) are unknown. Reentrant wavefronts have been shown to underlie the onset (Wiggers’ stage I) of electrically induced VF in intact canine ventricles. These reentrant wavefronts, however, have a limited lifespan (1–2 s) while VF persists. Using computerized mapping techniques, we studied the mechanism by which VF is maintained beyond the initial few seconds (Wiggers’ stage II), both in normal and subendocardium-ablated canine ventricles. Eleven open-chest dogs were studied. In 6 of the dogs, the RV subendocardium was ablated with lugol's solution. A plaque electrode array with 317–509 bipolar recording electrodes was sutured on the RV epicardium. VF was induced by a strong premature stimulus (S 2 ). Starting 2.5 s after the onset of VF, 2–5 s of data were analyzed. The activation patterns were visualized via dynamic display. Conventional isochronal maps were also constructed. Of the 15 runs of VF in dogs with intact ventricles, 3 episodes of reentrant wavefronts were detected. The mean lifespan was 4.5 ± 2.1 rotations. The mean cycle length was 102.5 ± 5.5 msec. The incidence of reentry was 0.018 ± 0.048 rotations/sec-cm 2 . Of the 18 runs of VF in dogs with ablated ventricles, 8 episodes of reentry were detected. The mean lifespan was 3.6 ± 1.1 rotations (p = 0.39 compared with intact ventricles). The mean cycle length was 107.2 ± 9.6 msec (p = 0.16). The incidence of reentry was 0.075 ± 0.097 rotations/sec-cm 2 (p = 0.048). In both groups of dogs, dynamic displays of the activation patterns demonstrate that the reentrant wavefronts spiral rather than follow a simple circular pathway. (a) reentrant wavefronts are consistently present during Wiggers’ stage II VF, (b) ablation of the subendocardium and Purkinje fibers results in an increased incidence of reentrant wavefronts on the epicardium, and (c) the reentrant wavefronts are compatible with spiral waves of excitation.

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