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Endocardial mapping of ventricular tachycardia in one-day-old myocardial infarction
Endocardial mapping of ventricular tachycardia (VT) was performed in one-day-old myocardial infarction using a matrix electrode (6 X 7 = 42) placed on the endocardial surface of the perfused isolated canine heart. Spontaneous focal VT was observed in all 7 dogs. It was neither affected nor terminated by electrical stimulation. Focal VT was induced in 5 dogs by constant pacing or premature programmed stimulation of the main left bundle. It was terminated by electrical stimulation and induction of the VT was suppressed by verapamil (5 X 10(-7)). Endocardial mapping of the spontaneous focal VT and induced focal VT showed initiation of activation from the surviving Purkinje fiber in the infarcted or border zone with subsequent circular expansion of excitation. Reentrant VT was induced in 3 dogs by bursts of rapid pacing and deteriorated into ventricular fibrillation. Endocardial mapping showed a continuous arc of functional conduction block and slowly circulating activation front around the block. It is suggested that in experimental one-day-old myocardial infarction VT resulted from abnormal automaticity and triggered activity in the surviving Purkinje fiber and reentry in the subendocardial muscle layer.
Endocardial mapping of ventricular tachycardia (VT) was performed in one-day-old myocardial infarction using a matrix electrode (6 X 7 = 42) placed on the endocardial surface of the perfused isolated canine heart. Spontaneous focal VT was observed in all 7 dogs. It was neither affected nor terminated by electrical stimulation. Focal VT was induced in 5 dogs by constant pacing or premature programmed stimulation of the main left bundle. It was terminated by electrical stimulation and induction of the VT was suppressed by verapamil (5 X 10(-7)). Endocardial mapping of the spontaneous focal VT and induced focal VT showed initiation of activation from the surviving Purkinje fiber in the infarcted or border zone with subsequent circular expansion of excitation. Reentrant VT was induced in 3 dogs by bursts of rapid pacing and deteriorated into ventricular fibrillation. Endocardial mapping showed a continuous arc of functional conduction block and slowly circulating activation front around the block. It is suggested that in experimental one-day-old myocardial infarction VT resulted from abnormal automaticity and triggered activity in the surviving Purkinje fiber and reentry in the subendocardial muscle layer.