Abstract
The antiarrhythmic efficacy of ventriculotomy without further resection or ablation was evaluated in 15 dogs with reliably inducible ventricular tachycardia after experimental myocardial infarction. The dogs were placed on cardiopulmonary bypass and assigned to one of two treatment groups: (1) cardiopulmonary bypass only (control) — 5 dogs, (2) ventriculotomy through the infarct scar — 10 dogs. The effects on induction of ventricular tachycardia were evaluated 2 and 4 weeks postoperatively and infarct histology was examined at the termination of the experiment. All of the control dogs maintained inducible ventricular tachycardia postoperatively. In contrast, ventriculotomy abolished arrhythmia induction in 6 of 10 dogs ( p<0.05). Ventriculotomy resulted in destruction of the surviving subepicardial myocardium overlying the infarct, which is a feature of arrhythmogenic areas in this model of postinfarction ventricular tachycardia. In conclusion, inducibility of ventricular tachycardia in this canine model of myocardial infarction is unaffected by thoracotomy and cardiopulmonary bypass, and is therefore well suited to investigation of surgical antiarrhythmic interventions. Ventriculotomy results in subepicardial scarring and is significantly antiarrhythmic. This effect should be taken into account when evaluating any adjunctive procedure in this model.
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