Circulation, Vol 86, 1872-1887, Copyright © 1992 by American Heart Association
SM Pogwizd, RH Hoyt, JE Saffitz, PB Corr, JL Cox and ME Cain
BACKGROUND. To determine the mechanisms of ventricular tachycardia (VT) in
humans, three-dimensional intraoperative mapping of up to 156 intramural
sites was performed in 13 patients with healed myocardial infarction and
refractory VT. METHODS AND RESULTS. Mapping was of sufficient density to
define the mechanism of 10 VTs in eight patients. In five of 10 cases,
sustained VT was initiated in the subendocardium or epicardium by
intramural reentry with marked conduction delay as well as functional and
anatomic block most prominent in the subendocardium and midmyocardium. The
initiating beats of reentrant VT induced by programmed electrical
stimulation arose in the endocardium or midmyocardium by progressive
slowing of conduction leading to unidirectional block. Multiple
simultaneous reentrant circuits can be present. In contrast, five of the 10
sustained VTs were initiated by a focal mechanism as defined by the absence
of electrical activity between the termination of one beat and the
initiation of the next despite the presence of multiple intervening
intramural electrode recording sites. Comparisons of the mapping data with
results of histopathological analysis of tissue demonstrated that the
location of infarction as well as that of adjacent fibrotic muscle
determined sites of both fixed and functional conduction block during
macroreentrant VT and that slowing of conduction occurred in a direction
transverse rather than longitudinal to fiber orientation. CONCLUSIONS. Both
intramural reentry and a focal mechanism underlie sustained VT in patients
with healed myocardial infarction.
ARTICLES
Reentrant and focal mechanisms underlying ventricular tachycardia in the human heart
Cardiovascular Division, Washington University School of Medicine, St. Louis, MO 63110.
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