Premium
Three‐Dimensional Mapping of Spontaneous Ventricular Arrhythmias in a Canine Thrombotic Coronary Occlusion Model
Author(s) -
ZHANG SHU,
SKINNER JONATHAN L.,
SIMS ANTHONY L.,
ROLLINS DENNIS L.,
WALCOTT GREGORY P.,
SMITH WILLIAM M.,
IDEKER RAYMOND E.
Publication year - 2000
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1111/j.1540-8167.2000.tb00048.x
Subject(s) - medicine , cardiology , ventricular tachycardia , occlusion , ventricular fibrillation , coronary occlusion , circumflex , sinus rhythm , anesthesia , artery , atrial fibrillation
Spontaneous Arrhythmias in Acute Ischemia. 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 deliver current to the proximal left circumflex artery (LCX). In nine doss, nonsustained VT (NSVT) anise from numerous focal sites. Sustained VT was initiated in six dogs (VT group) by a focus near or in the ischemic region. VT was maintained by a focus in the ischemic border in three dogs and by macroreentry 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 activation to traverse the ventricles, for a sinus heat when LCX current was first 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 before VT. Sinus VT 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 degenerated into VF (169 ± 29 msec) than in those that did not (81 ± 12 msec). Conclusion: Thrombotic LCX occlusion induced NSVT in 9%, VT in 60%, and VF in 50% of dogs, Focal mechanisms caused most NSVTs and VT initiation. VT was 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.