PROTRACTED VENTRICULAR TACHYCARDIA INDUCED BY PREMATURE STIMULATION OF THE CANINE HEART AFTER CORONARY-ARTERY OCCLUSION AND REPERFUSION

The effects of premature ventricular stimuli were studied in 2 groups of dogs with infarcts, one group subjected to permanent occlusion of the left anterior descending coronary artery and the other to temporary occlusion for 2 hr. In dogs with permanent occlusion, spontaneous ventricular arrhythmias occurred after 3-6 hr. In 13 dogs with temporary occlusion, ventricular arrhythmias occurred immediately after reperfusion and then persisted. In 5 dogs with temporary occlusion, ventricular arrhythmias did not occur spontaneously until 13-15 hr after occlusion. On days 2-9 after surgery, after sinus rhythm had returned, the ventricles of each awake dog were stimulated. After permanent occlusion, premature stimuli occurring on the T wave usually induced from 1 to 10 repetitive responses on days 2-4. Protracted ventricular tachycardia (lasting >10 sec) was induced in only 2 of 10 dogs. The response to premature stimuli was similar after temporary occlusion when ventricular arrhythmias did not occur spontaneously until 13-15 hr after occlusion. Protracted tachycardia was not induced. In the dogs with temporary occlusion, which initially had continuous arrhythmias, premature stimuli occurring on the T wave on days 3-5 after surgery induced both repetitive responses and protracted ventricular tachycardia. Stimuli applied to the ventricles during tachycardia terminated it. Histological studies on all infarcts showed that, after permanent occlusion, necrosis was uniform; after temporary occlusion, viable myocardium survived in the necrotic region. These salvaged myocardial fibers may provide reentrant pathways, causing long-lasting tachycardia.