Mechanisms of phase 1a and 1b early ventricular arrhythmias during acute myocardial ischemia in the dog.
Two phases of ventricular arrhythmia occur within the first 30 minutes of experimental myocardial ischemia. Possible differences in their mechanisms of pathogenesis were investigated in anesthetized dogs by detailed mapping of patterns of epicardial activation and regional myocardial blood flow during phase 1a and phase 1b early ventricular arrhythmias induced by high ligation of the left anterior descending coronary artery. Data were derived from 80 sites in a 4 by 5 cm area of left ventricular anterior free wall and displayed using computer graphics. Regional myocardial blood flow and the relation of regional flow to epicardial delay did not differ significantly during the 2 phases of arrhythmia in central ischemic or nonischemic areas, although epicardial flow in border region segments was increased during phase 1b. Significantly greater mean epicardial delays and spatial heterogeneity of epicardial delay (assessed by intersite variance within the ischemic area) occurred during phase 1a arrhythmias. Serial studies show striking increases in spatial heterogeneity of delays during phase 1a, but not during phase 1b, relating to temporal dispersion of a phenomenon of transient prolongation of activation delay at individual electrode sites. These data are consistent with the concept that phase 1a and 1b arrhythmias arise through different electrophysiologic mechanisms independent of flow-dependent effects.
D000208:Acute Disease; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology / Q000503:physiopathology*; D003201:Computers; D003326:Coronary Circulation; D003327:Coronary Disease / Q000150:complications / Q000503:physiopathology*; D004285:Dogs; D005260:Female; D006352:Heart Ventricles / Q000503:physiopathology; D008297:Male; D013997:Time Factors