Circulation, Vol 89, 852-862, Copyright © 1994 by American Heart Association
L Boersma, J Brugada, C Kirchhof and M Allessie
BACKGROUND: Premature stimulation is used to characterize the reentrant
circuit during ventricular tachycardia (VT) in patients. The goal of this
study was to compare the effects of premature stimulation on functional and
anatomic reentrant VT. METHODS AND RESULTS: In 18 Langendorff-perfused
rabbit hearts, thin layers of anisotropic left ventricular subepicardium
were created by a cryoprocedure. In 8 hearts, rapid pacing induced reentry
around a line of functional conduction block; in 10 hearts, reentry
occurred around a fixed epicardial obstacle created by a cryoprobe. The
cycle lengths (CL) of functional and anatomic VT were 110 +/- 10 and 167
+/- 17 milliseconds, respectively. During anatomic VT, the excitable gap
measured 43% of the CL and premature stimuli could always reset VT (44 +/-
12 milliseconds). During early premature beats, conduction of the
orthodromic wave was slightly depressed, but anatomic VT was never
terminated. Reset curves at different sites in the ventricle revealed three
different response types, both determined by and characterizing the spatial
and temporal relation between pacing and recording sites. Premature
stimulation during functional VT revealed a local excitable gap at the
pacing site measuring 27% of the cycle length of VT. However, in only 3 of
8 hearts, premature stimuli could reset functional VT by 8%. In 5 VTs,
advancement of the paced activation was fully compensated by prolongation
of the return cycle, and VT was not reset. Due to slow conduction both
toward and inside the circuit, the paced orthodromic wave lost its
prematurity already within a distance of 6 to 10 mm from the pacing site.
CONCLUSIONS: Both during anatomic and functional reentry, an excitable gap
is present in the reentrant circuit. Three different response curves reveal
the localization of the pacing and recording sites in the circuit. Anatomic
VT can always be reset by premature stimuli, whereas in 5 of 8 hearts,
functional VT could not be reset. In the other 3 hearts, VT could only be
reset for less than 7% to 11% of the VT interval. Therefore, it seems very
unlikely that clinical VT based on functional reentry can be reset.
ARTICLES
Mapping of reset of anatomic and functional reentry in anisotropic rabbit ventricular myocardium
Department of Physiology, University of Limburg, Maastricht, The Netherlands.
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