Circulation, Vol 81, 267-280, Copyright © 1990 by American Heart Association
RC Bernstein and LH Frame
We studied an in vitro model of reentrant tachycardia in a ring of
ventricular endocardial tissue surrounding the canine mitral and aortic
valves to understand how the response of a reentrant tachycardia to
premature impulses can provide insight into the underlying tachycardia
mechanism, circuit characteristics, and nature of the central barrier.
Reproducible regular reentrant tachycardias (cycle length range, 177- 450
msec) were induced with programmed stimulation in 19 intact preparations
studied at 34-38 degrees C. Tachycardias were sustained and stable until
terminated by programmed stimulation in 95% of preparations. Reentry was
reliably reinitiated during experiments lasting 2-15 hours. Data supporting
reentry as the mechanism of these tachycardias included sequential
activation around the ring that spanned the cycle length of the
tachycardia, unidirectional block during initiation of the reentrant
rhythm, and termination of the tachycardia after interruption of the
circuit. Tachycardias in 13 preparations were systematically reset by
premature stimuli. During reentry, each of these preparations had full
recovery of excitability by the end of their excitable gap as evidenced by
a flat portion along their resetting response curve (eight of 13) or by
lack of faster conduction velocity during the second poststimulus beat
after premature impulses that produced a long return cycle (13 of 13). From
analysis of the conduction of premature impulses and their return cycles,
we reached several conclusions useful for interpreting resetting response
curves when the reentrant circuit is not fully accessible for study. The
duration of a flat portion of the resetting response curve indicated the
duration of the shortest fully recovered excitable gap in the reentrant
circuit. The window of reset of the tachycardia reflected only the local
excitable gap at the site of stimulation and did not define the shortest
excitable gap within the circuit. The extent of advancement of the
tachycardia provided a lower-limit estimate of the shortest excitable gap
in the reentrant circuit. Advancement of a tachycardia in time by premature
stimuli indicated advancement at each point in the circuit. Finally, for
tachycardias advanced by premature impulses, the length of the reentrant
path cannot be determined by the recovery of a refractory barrier.
ARTICLES
Ventricular reentry around a fixed barrier. Resetting with advancement in an in vitro model
Department of Internal Medicine, Hospital of the University of Pennsylvania, Philadelphia 19104.
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