The interruption of collateral blood flow to the ischemic canine myocardium by embolization of a coronary artery with latex: effects on conduction delay and ventricular arrhythmias.

We studied the importance of collateral blood flow in the genesis of epicardial conduction delay and ventricular arrhythmias by creating a model of myocardial ischemia in which coronary collateral channels were embolized with a rapidly hardening vinyl latex. In 33 open-chest anesthetized dogs, heart rate was held constant (18O-200/min) and the proximal left anterior descending coronary artery (LAD) was occluded for 10 minutes, followed by 30 minutes of reperfusion. The LAD then was ligated and latex was injected just below the ligature. The latex filled coronary vessels branching from the LAD down to a diameter of 20-30 jun and produced transmural infarcts averaging 42% of the left ventricular mass (range 35-58%). The amount of epicardial conduction delay was measured during atrial rhythm at multiple electrode sites within the ischemic zone. The maximal delay following coronary occlusion was 97 48 msec (mean SD), whereas latex embolization increased the delay to 203 51 msec (P < 0.001). In response to coronary occlusion, 8% of the electrograme demonstrated Wenckebach-like alternation, whereas 58% showed alternation following latex embolization (P < 0.001). Compared to coronary occlusion, coronary embolization with latex significantly increased the number of dogs that developed ectopic beats during the first 10 minutes of ischemia (66% vs. 94%; P = 0.02). However, coronary occlusion evoked ventricular fibrillation in 21% of the dogs, whereas no animal developed fibrillation at any time following coronary embolization (P = 0.002). Ventricular fibrillation also was absent in an additional 18 animals in which the LAD was embolized without an earlier period of occlusion. The results indicate that embolization of the LAD with vinyl latex increases the severity of local conduction abnormalities while reducing the incidence of lethal arrhythmias. The interruption of collateral blood flow to the ischemic myocardium may depress conduction in a homogeneous manner such that the ischemic zone may be unable to support a sufficient number of reentrant circuits to initiate fibrillation.