Influence of collateral flow reduction on electrophysiologic properties of preexisting ischemic area and inducibility of ventricular arrhythmias in the dog

Jpn Heart J. 1987 Nov;28(6):899-911. doi: 10.1536/ihj.28.899.

Abstract

Electrophysiologic properties of the left ventricle, vulnerability to ventricular arrhythmias and regional myocardial blood flow (RMBF) of the left ventricle were examined during superposition of acute ischemia on a healed myocardial infarction. The left circumflex coronary artery (LCX) was ligated in 13 dogs with a 28-day-old anteroapical infarction. Six (46%) of 13 dogs had reproducible ventricular tachycardia in response to programmed ventricular stimulation before LCX ligation. Ventricular fibrillation could be induced in 2 of these 6 dogs. After LCX ligation, 11 (85%) of 13 dogs had ventricular arrhythmias induced by ventricular stimulation. Nine of 13 dogs had ventricular tachycardia and 7 of 13 dogs had ventricular fibrillation. The heterogeneity of the effective refractory period (delta ERP) and the local intraventricular conduction time (LIVCT) in the border and the infarct zones of the left ventricle increased significantly after LCX ligation. RMBF in the border and the infarct zones were markedly decreased by LCX ligation. The magnitude of reduction of RMBF was correlated significantly with the prolongation of LIVCT. In conclusion, acute critical reduction of the collateral blood supply causes a more heterogeneous refractory period and conduction delay in the preexisting ischemic area of the heart, increasing the vulnerability to lethal ventricular arrhythmias.

MeSH terms

  • Animals
  • Arrhythmias, Cardiac / etiology*
  • Arrhythmias, Cardiac / physiopathology
  • Collateral Circulation*
  • Coronary Circulation*
  • Coronary Disease / complications
  • Coronary Disease / physiopathology*
  • Dogs
  • Electric Stimulation
  • Electrocardiography
  • Female
  • Heart Conduction System / physiopathology
  • Heart Ventricles
  • Male
  • Myocardial Infarction / complications
  • Myocardial Infarction / physiopathology*