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Circulation. 1995;92:3481-3489

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(Circulation. 1995;92:3481-3489.)
© 1995 American Heart Association, Inc.


Articles

Catheter Ablation of the Mitral Isthmus for Ventricular Tachycardia Associated With Inferior Infarction

David J. Wilber, MD; Douglas E. Kopp, MD; Dennis N. Glascock DO; Charles A. Kinder, MD; John G. Kall, MD

From the University of Chicago Hospitals, Chicago, Ill.

Correspondence to David J. Wilber, MD, Section of Cardiology, MC2080, University of Chicago Hospitals, 5841 S Maryland Ave, Chicago, IL 60637. E-mail dwilber@medicine.bsd.uchicago.edu.

Background Intraoperative mapping studies suggest that an isthmus of myocardium between the mitral valve annulus and the border of inferior myocardial infarction may play a role in the genesis of ventricular tachycardia. We examined the frequency with which a slow conduction zone within the mitral isthmus was critical to the maintenance of ventricular tachycardia associated with remote inferior infarction in patients undergoing catheter ablation.

Methods and Results In 4 of 12 patients, a critical zone of slow conduction was identified within the mitral isthmus. In each of these patients, two characteristic and morphologically distinct tachycardias were induced: a left bundle (rS in V1, R in V6), left superior axis morphology and a right bundle (R in V1, QS in V6), right superior axis morphology (cycle length, 610 to 320 ms). In each patient, a zone of slow conduction, shared by both morphologies, was characterized by diastolic potentials with electrogram-QRS intervals of 85 to 161 ms (21% to 47% of tachycardia cycle length) and entrainment with concealed fusion during pacing associated with stimulus-QRS intervals of 81 to 400 ms (20% to 91% of tachycardia cycle length). In each patient, a single radiofrequency energy application at the shared site of slow conduction eliminated inducibility of both morphologies. During follow-up of 1 to 11 months, no patient had recurrent tachycardia.

Conclusions The mitral isthmus contains a critical region of slow conduction in some patients with ventricular tachycardia after inferior myocardial infarction, providing a vulnerable and anatomically localized target for catheter ablation. Characteristic tachycardia morphologies may provide clinical markers for this underlying mechanism.


Key Words: tachycardia • ablation • myocardial infarction




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