Three-dimensional mapping of spontaneous ventricular arrhythmias in a canine thrombotic coronary occlusion model

Introduction: Ventricular tachycardia (VT) and ventricular fibrillation (VF ) induced by thrombotic coronary occlusion were mapped in three dimensions in ten dogs. Methods and Results: Thrombotic occlusion was induced using a wire to deliv er current to the proximal left circumflex artery (LCX). In nine dogs, nons ustained VT (NSVT) arose from numerous focal sites. Sustained VT was initia ted in six dogs (VT group) by a focus near or in the ischemic region. VT wa s maintained by a focus in the ischemic border in three dogs and by macrore entry that involved both the ischemic and nonischemic regions in the other three dogs. In five dogs, VT degenerated into VF due to intramural reentry in different locations. Mean total activation time (AT), the time for activ ation to traverse the ventricles, for a sinus beat when LCX current was fir st applied was 40 +/- 4 msec, In the four dogs in which VT occurred 3 to 7 minutes after total occlusion, sinus AT increased to 98 to 146 msec just be fore VT. Sinus AT in the four dogs without VT was always <98 msec, Mean AT of the first ten cycles of VT was significantly longer in those VTs that de generated into VF (169 +/- 29 msec) than in those that did not (81 +/- 12 m sec), Conclusion: Thrombotic LCX occlusion induced NSVT in 90%, VT in 60%, and VF in 50% of dogs. Focal mechanisms caused most NSVTs and VT initiation. VT w as maintained by a focus near or in the ischemic region or by macroreentry involving both the ischemic and nonischemic regions. AT identified animals in which VT occurred soon after LCX occlusion and in which VT progressed to VF.