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Circulation, Vol 83, 1577-1591, Copyright © 1991 by American Heart Association
L Littmann, RH Svenson, JJ Gallagher, JG Selle, SH Zimmern, JM Fedor and PG Colavita
BACKGROUND. Conventionally, monomorphic sustained ventricular tachycardia
in patients with remote myocardial infarction is believed to originate from
the subendocardium. In a previous study, we demonstrated that electrical
activation patterns during ventricular tachycardia occasionally suggest a
subepicardial rather than subendocardial reentry. METHODS AND RESULTS. This
study prospectively evaluated the functional role of the epicardium in
postinfarction ventricular tachycardia with complex intraoperative
techniques including computerized electrical activation mapping,
entrainment, observation of changes in activation pattern during successful
epicardial laser photoblation, and histological study. Five of 10
consecutive patients undergoing intraoperative computerized activation
mapping had 10 ventricular tachycardia morphologies displaying epicardial
diastolic activation These 10 "epicardial" ventricular tachycardias
revealed the following global activation patterns: monoregional spread
(two), figure-eight activation (five), and circular macroreentry (three).
Entrainment of ventricular tachycardia using epicardial stimulation was
successfully performed from an area of slow diastolic conduction in four
tachycardia morphologies. During entrainment, global activation remained
undisturbed with recordings showing a long stimulus to QRS interval,
unchanged QRS morphology, and pacing capture of all components of the
reentry circuit. Neodymium:yttrium aluminum garnet laser photocoagulation
was delivered during ventricular tachycardia to epicardial sites of
presumed reentry. Epicardial photoablation terminated five of five
figure-eight tachycardias, two of three circular macroreentry tachycardias
but not the monoregional tachycardias. Electrophysiological recordings
during epicardial laser photocoagulation demonstrated progressive
prolongation of ventricular tachycardia cycle length and apparent
interruption of the presumed reentrant circuit. Histological evaluation of
the reentrant region (three patients) showed a rim of surviving myocardium
under the epicardial surface. CONCLUSIONS. This study suggests that 1)
chronic postinfarction ventricular tachycardia may result from
subepicardial macroreentry, 2) slow conduction within the reentry circuit
can be localized by computerized mapping and epicardial entrainment, and 3)
ventricular tachycardia interruption by laser photocoagulation results from
conduction delay and block within critical elements of the reentrant
pathway. Viable subepicardial muscle fibers may constitute the underlying
pathology.
ARTICLES
Functional role of the epicardium in postinfarction ventricular tachycardia. Observations derived from computerized epicardial activation mapping, entrainment, and epicardial laser photoablation
Sanger Clinic, Charlotte, N.C.
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