Circulation, Vol 83, 268-278, Copyright © 1991 by American Heart Association
N el-Sherif, WB Gough and M Restivo
The electrophysiological mechanism by which a short-long-short stimulated
cardiac sequence facilitates the induction of ventricular tachyarrhythmia
was investigated in dogs 4 days after ligation of the left anterior
descending coronary artery. In these dogs, reentry develops in the
surviving electrophysiologically abnormal epicardial layer that overlies
the infarct zone when premature stimulation results in a critically long
arc of functional conduction block. The activation wavefront circulates
around both ends of the arc, coalesces, and conducts slowly distal to the
arc before reactivating sites proximal to the arc to initiate a
figure-eight reentrant circuit. Epicardial isochronal activation maps and
effective refractory periods (ERPs) were determined during three different
stimulation protocols: A, a basic train of eight beats at a cycle length of
300 msec followed by a single premature stimulus (S2); B, a basic train of
eight beats at a cycle length of 300 msec with abrupt lengthening of the
last cycle of the train before S2 to 600 msec; C, a basic train of eight
beats at a cycle length of 600 msec followed by S2. Protocol B was found to
result in a differential lengthening of ERP at adjacent sites within the
border of the epicardial ischemic zone, whereas protocols A and C induced,
respectively, comparable shortening and lengthening of ERPs at the same
sites. The differential lengthening of ERPs at adjacent sites resulted in
an increased dispersion of refractoriness so that a premature stimulus
induced functional conduction block between those sites. The development of
a longer arc of conduction block and, hence, a longer reentrant pathway as
well as slower conduction of the circulating wavefront during protocol B
allowed more time for refractoriness to expire proximal to the arc and for
the circulating wavefront to reexcite those sites to initiate reentry. The
lengthening of ERP, associated with a single long cycle (protocol B),
ranged from 44% to 79% of the total increase in ERP after a series of eight
long cycles (protocol C). Epicardial sites with longer ERPs located close
to the center of the ischemic zone showed more lengthening of
refractoriness during protocol B compared with more normal sites near the
border of the ischemic zone. This strongly suggests that the increased
dispersion of refractoriness during protocol B is caused by the shorter
memory of ischemic myocardium to the cumulative effects of preceding cycle
lengths.
ARTICLES
Reentrant ventricular arrhythmias in the late myocardial infarction period: mechanism by which a short-long-short cardiac sequence facilitates the induction of reentry
Department of Medicine, State University of New York Health Science Center, Brooklyn 11203.
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