Actions of lidocaine on reentrant ventricular rhythms in the
subacute myocardial infarction period in dogs.
Yin, Hong, Nabil El-Sherif, Edward B. Caref, Gjin Ndrepepa, Richard
Levin, Nidal Isber, Kathleen Stergiopolus, Mahshid A. Assadi, William
B. Gough, Mark Restivo.
State University of New York Health Sciences Center at Brooklyn and
Veterans Administration Medical Center, Brooklyn, NY
APStracts 3:0292H, 1996.
The actions of lidocaine were studied in 18 dogs, 4 days after
ligation of the left anterior descending artery, by computerized
mapping. Lidocaine only occasionally suppressed the induction of
reentry. At fast heart rates, lidocaine actually facilitated the
induction of reentry. The effects on conduction and refractoriness of
normal and ischemic myocardium were measured using high resolution
techniques. Lidocaine promoted reentry by a rate-dependent increase
in refractory gradient, resulting in additional block, and a
selective decrease in conduction velocity in ischemic tissue,
resulting in additional conduction delay. Lidocaine could prevent
reentry through a rate-independent differential increase in
refractory period gradient at the entrance to the common pathway of
the circuit, causing block of the reentrant impulse. Conclusion. The
proarrhythmic effect of lidocaine is due to increased conduction
delay and block while the antiarrhythmic effect is due to block of
the reentrant impulse by prolonged refractoriness in the common
pathway.
Received 15 March 1996; accepted in final form 2 July 1996.
APS Manuscript Number H251-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 25 July 1996