Serial production of controlled periods of temporary heart block used to unmask and assess latent ventricular automaticity during experimental acute myocardial ischemia

Academic Article

Abstract

  • This study examined the onset, time course of development and response to overdrive stimulation of ventricular tachycardia in 10 dogs that underwent a Harris two-stage ligation of the left anterior descending coronary artery. Transient (12 ± 3 minutes) complete atrioventricular (AV) block was produced 2, 3, 4, 5, 8, 12, 16, 20 and 24 hours after onset of infarction through selective injection of physostigmine salicylate into the AV node artery. Seven of the 10 dogs had early transient arrhythmic episodes that occurred within 20 to 40 minutes after coronary occlusion but none of the dogs had any spontaneous ventricular tachycardia in the ensuing 2 hours. Two hours after left anterior descending coronary artery ligation, complete AV block unmasked in every dog a slow (37 ± 9 beats/min) AV junctional rhythm readily suppressed by overdrive. Three hours after coronary ligation, AV block revealed a monomorphic ventricular tachycardia (106 ± 10 beats/min) in 3 of the 10 dogs. Four and five hours after coronary ligation, five and eight dogs, respectively, had ventricular tachycardia during AV block and in three the tachycardia was polymorphic. The two remaining dogs did not develop ventricular tachycardia during the 24 hours of observation. Ventricular tachycardia always began abruptly, first with brief and then longer bursts. Soon after onset the rate of tachycardia began to increase to reach a plateau 2 to 3 hours later at frequencies 21 ± 9% greater than the initial tachycardia rate. Concomitant with this increase in rate there was a steady decline of overdrive suppressibility and during the plateau phase there was little or no overdrive suppression. In three dogs 12 to 20 hours after coronary ligation, overdrive stimulation caused intermittent biphasic responses characterized by a brief episode of overdrive acceleration followed by prolonged overdrive suppression. From these results it is concluded that abrupt onset of ventricular tachycardia 3 to 4 hours after infarction is probably due to partially depolarized ectopic pacemakers and that in some cases triggered activity is likely. © 1986, American College of Cardiology Foundation. All rights reserved.
  • Digital Object Identifier (doi)

    Author List

  • Rosenshtraukh LV; Urthaler F; Anjukhovsky EP; Beloshapko GG; Hageman GR; James TN
  • Start Page

  • 95A
  • End Page

  • 103A
  • Volume

  • 8
  • Issue

  • 1