Transseptal catheter ablation using 30-100 J discharges in dogs caused acute ventricular fibrillation in 60% of shocks but no inducible ventricular tachycardia after ablation.
Does transseptal catheter electrode discharge cause arrhythmogenicity and histologic changes in a canine model?
Transseptal catheter ablation using lower energy discharges creates transmural septal lesions without perforation and without inducing sustained ventricular arrhythmias in a canine model.
Ventricular tachycardia commonly arises within the intraventricular septum and successful catheter ablation of septal tachycardia might be enhanced by transseptal electrode placement. We have evaluated the safety of a transseptal ablation procedure. Arrhythmogenicity and histology were examined after high-energy capacitor discharges were delivered to an intracavitary cathode-anode pair placed on opposite sides of the interventricular septum in pentobarbital-anesthetized dogs. After two discharges of 200 or 100 J proved lethal, paired discharges of 30 or 50 J (10 dogs) or a single discharge of 100 J (four dogs) was used to induce 28 lesions. Acute rhythm changes and risk of induction of ventricular tachycardia by programmed stimulation were measures of arrhythmogenicity. Gross and histologic examination of the hearts after 20 min to 28 days allowed characterization of the evolution of lesions. The conduction system in nearby and remote locations was extensively examined in four dogs. Refractory ventricular fibrillation developed with paired shocks at 200 or 100 J. At lower energy levels, acute ventricular fibrillation occurred with 12 of 20 shocks (60%), but defibrillation was consistently achieved. After ablation, no dog had ventricular tachycardia or fibrillation induced with programmed stimulation. Matching anodal and cathodal lesions spanned the septum without perforation in 10 of 16 dogs, and the lesions were of similar histology. Each contained central areas of hemorrhage surrounded by a region of coagulation necrosis merging with normal myocytes peripherally. There was necrosis and edema without inflammation at 20 min, acute inflammatory cell infiltration at 1 to 2 days, and myocyte replacement by granulation tissue after 6 days.(ABSTRACT TRUNCATED AT 250 WORDS)
Davis et al. (Mon,) conducted a other in Ventricular tachycardia (ablation model) (n=16). Transseptal catheter electrode ablation (high-energy capacitor discharges) was evaluated on Acute rhythm changes, risk of induction of ventricular tachycardia, and histologic evolution of lesions. Transseptal catheter ablation using 30-100 J discharges in dogs caused acute ventricular fibrillation in 60% of shocks but no inducible ventricular tachycardia after ablation.