Circulation, Vol 87, 126-134, Copyright © 1993 by American Heart Association
DJ Wilber, J Baerman, B Olshansky, J Kall and D Kopp
BACKGROUND. Sustained ventricular tachycardia in the absence of structural
heart disease may have diverse mechanisms. Termination of the tachycardia
by adenosine suggests triggered automaticity as the etiology in many of
these patients. We examined the clinical characteristics,
electrophysiological responses, and results of catheter ablation in this
patient subgroup. METHODS AND RESULTS. Intravenous adenosine terminated
sustained ventricular tachycardia in seven of 14 consecutive patients
without evidence of structural heart disease. In each of these patients,
the tachycardia had a left bundle branch block, inferior-axis QRS
configuration and occurred predominantly during stress or exertion. A
morphologically similar sustained tachycardia was induced in six of seven
patients during programmed ventricular stimulation, although day-to-day
reproducibility was poor. Signal-averaged ECGs were normal in all patients.
Imaging with 123I-metaiodobenzylguanidine did not reveal focal
abnormalities in any of five patients. A discrete site of origin was
identified in the free wall of the pulmonary infundibulum in all patients.
Limited application of direct current shocks (two patients) or
radiofrequency energy (five patients) resulted in long-term abolition of
spontaneous and inducible ventricular tachycardia in all patients.
CONCLUSIONS. Adenosine-sensitive ventricular tachycardia appears to arise
from relatively discrete sites predominantly located in the free wall of
the pulmonary infundibulum. The localized nature of this tachycardia
renders it amenable to long-term cure by catheter ablation techniques.
ARTICLES
Adenosine-sensitive ventricular tachycardia. Clinical characteristics and response to catheter ablation
Section of Cardiology, Loyola University Medical Center, Maywood, Ill 50153.
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