Ventricular fibrillation resulting from ischemia at a site remote from previous myocardial infarction : A conscious canine model of sudden coronary death

Abstract

In anesthetized dogs, a 30 gauge silver wire was inserted into the lumen of the left circumflex (LC) coronary artery and myocardial ischemic injury was produced by subsequent occlusion of the left anterior descending (LAD) coronary artery for 90 minutes followed by reperfusion through a critical stenosis. Four days after acute myocardial infarction, with the dog ambulatory, the intimai surface of the LC coronary artery was injured by applying a 150 [mu]A anodal current. Coronary artery thrombosis and subsequent reduction in coronary artery blood flow were accompanied by S-T segment changes at 132 +/- 65 minutes (mean +/- standard deviation [SD]) with ventricular fibrillation (VF) occurring in 29 of 30 dogs (97% ) at 141 +/- 60 minutes. Infarct mass in the LAD distribution was 15 +/- 8% of total left ventricular mass with no histochemical evidence of irreversible ischemic injury in the LC coronary artery distribution. VF was preceded by the development of delayed electrical activity within the LC coronary artery distribution, and the development of ventricular arrhythmias accompanied by continuous local electrical activity within the subepicardial region of the distribution of the LC coronary artery. In 10 dogs with placement of a critical stenosis around the LAD coronary artery without earlier occlusion and reperfusion, LC intimal injury and subsequent thrombus formation resulted in only 2 deaths (20% ) from VF. Thus, acute myocardial ischemia at a site distant to a previous myocardial infarction enhances the likelihood of primary VF in the conscious dog. This model of sudden coronary death may simulate the clinical state in man and might serve as an appropriate model for the study of electrophysiologic mechanisms associated with the development of VF and for the evaluation of potential antifibrillatory drugs.