Copyright © 1993 by the European Society of Cardiology.
© 1993 The Europen Society of Cardiology
Induction and the possible mechanism of ventricular tachycardia after catheter ablation with direct current shocks in dogs
The Cardiovascular Institute 7-3-10, Roppongi, Minato-ku, Tokyo 106, Japan
accepted 24 March 1993.
Correspondence: Hiroshi Ishibashi, MD. The Cardiovasacular Institute, 7-3-10, Roppongi, Minato-ku, Tokyo 106, Japan
Abstract
Cathodal DC shocks (150-J) were administered via the His bundle to 20 closed-chest dogs, and in a further three dogs 25-J cathodal shocks were given via the left ventricular endocardium. In 18 dogs, including three that underwent left ventricular ablation, Holter electrocardiograms were recorded from 1 to 7 days after ablation, and 4 weeks after ablation. There were frequent episodes of sustained ventricular tachycardia (VT) from the first few hours after ablation to 4 days after ablation in all dogs, but both the rate and the coupling interval of VT were variable. In five conscious dogs stimulated 1 day after ablation, it was difficult to induce and terminate VT repeatedly. There was a direct relationship between the paced cycle length and the interval of the last paced beat to the initiating VT beat in three out of four dogs. In the fourth dog there was an inverse relationship. There was no transient entrainment with ventricular burst pacing during VT in any of the four dogs tested. The effects of lidocaine (2–3 mg.kg–1), verapamil (0.2–0.4 mg.kg–1), and propranolol (0.2 mg.kg–1) on VT were tested within 2 days of ablation in 10 conscious dogs. In general, both lidocaine and verapamil terminated VT, and propranolol slowed VT. In conclusion, VT soon after ablation possibly results from triggered activity, although abnormal automaticity cannot be ruled out.
Key Words: Catheter ablation • ventricular tachycardia • triggered activity