Ventricular fibrillation during and after coronary artery occlusion: Incidence and protection afforded by various drugs ∗

Abstract

The incidence of ventricular fibrillation during and after temporary experimental occlusion of the left anterior descending coronary artery or its branches was studied in 351 dogs. A standardized procedure of thirty-minute temporary occlusion of this artery was employed in 330. There is usually a critical period after twelve and up to fifteen minutes of ischemia which is characterized by a tendency to arrhythmia: extrasystoles, singly or in runs, ventricular tachycardia, or both extrasystoles and tachycardia if not a fatal ventricular fibrillation. Several instances of transient ventricular fibrillation were observed. Of 239 animals surviving thirty minutes of occlusion, 71 per cent developed ventricular fibrillation immediately after release of the artery, while only 28 per cent of 330 animals developed fibrillation during the occlusion. The re-establishment of blood flow to an area of the myocardium made ischemic for thirty minutes by occlusion of the anterior descending coronary artery is more likely to precipitate ventricular fibrillation than is the period of ischemia itself. Various drugs were evaluated in 324 dogs. Quinidine was the most effective drug in affording protection from ventricular arrhythmia during (7 per cent) and following (47 per cent) occlusion. Procaine, procaine amide and Apresoline offered good protection during the ischemic period. Apresoline and Regitine also reduced the incidence (44 and 37 per cent) of ventricular fibrillation upon reopening the ligature. Of the other drugs tested, only one, pendiomide, showed significant protection (52 per cent incidence). Systemic arterial pressures did not predict the onset of ventricular arrhythmia. Electrical countershock accomplished cardiac resuscitation in 75 per cent of the fibrillating dogs. From these experiments, quinidine appears to be the drug of choice in the prophylaxis of fatal ventricular arrhythmias.