Experimental acute myocardial infarction. Characterization and treatment of the malignant premature ventricular contraction

The majority of deaths from acute myocardial infarction (AMI) occur prior to the arrival of medical aid and appear to be due to ventricular fibrillation (VF). Since the premature ventricular contraction and bradycardia are believed to predispose to VF, it has been suggested that administration of atropine or lidocaine during the prehospital phase of AMI may effectively reduce mortality in AMI. To test the efficacy of these drugs in treating arrhythmias during the acute phase of AMI we studied 72 closed-chest conscious dogs in which AMI was produced by inflating a balloon cuff previously implanted around the left anterior descending coronary artery. Ventricular arrhythmias developed in 52 dogs either during occlusion or within 2 min of release of occlusion. Arrhythmias were treated by (1) atropine, (2) atrial pacing, (3) lidocaine, or (4) atropine plus lidocaine. Of the 18 dogs that developed VF, all had ectopic ventricular beats that followed a preceding beat (R-R PVC interval) by ≤0.43 sec; no dog with a ventricular arrhythmia that exhibited only R-R PVC intervals >0.43 sec developed VF. On this basis arrhythmias were defined as "benign" (R-R PVC >0.43 sec) or "malignant" (R-R PVC ≤0.43 sec). Using this classification, we found that benign arrhythmias were successfully suppressed by atropine (10 of 13 arrhythmias), pacing (nine of 11), and lidocaine (three of five); however, atropine suppressed only two of 18, pacing two of 14, and lidocaine none of six malignant arrhythmias. We conclude that (1) not all ventricular arrhythmias are potentially lethal and (2) while atropine, pacing, and lidocaine successfully suppress most benign arrhythmias, they appear considerably less effective in suppressing those faster arrhythmias that frequently lead to the precipitation of VF.