Circulation, Vol 72, 344-352, Copyright © 1985 by American Heart Association
KA Ellenbogen, LD German, WG O'Callaghan, PG Colavita, AC Marchese, MR Gilbert and HC Strauss
We sought to determine if verapamil induces frequency-dependent
prolongation of atrioventricular nodal conduction in 10 consecutive
patients studied in the electrophysiology laboratory. We used a maintenance
infusion of verapamil designed to produce plasma concentrations of
verapamil in the "therapeutic" range and that did not alter heart rate or
blood pressure significantly. Frequency-dependent prolongation of
atrioventricular nodal conduction (AH interval) was demonstrated in all 10
patients (p less than .001), and no change in HV conduction time with
decreasing cycle length was noted in any patients while receiving
verapamil. Two patterns of use-dependent response were seen. In four
patients frequency-dependent prolongation of the delta(AH) interval
[delta(AH) = AHverapamil - AHcontrol at a given cycle length] was seen with
each decrement in pacing cycle length. In six patients frequency-dependent
prolongation of the delta(AH) interval was not manifest until the fifth to
eighth pacing cycle length tested. There was no association between the
pattern observed and the initial heart rate or AH interval. After an abrupt
change in pacing cycle length, the kinetics of delta (AH) interval
prolongation were rapid; equilibrium was achieved by five to eight pulses
in all patients. There was no correlation between the magnitude of
prolongation of the AH interval noted at a particular cycle length and the
concentration of verapamil during the maintenance infusion. These results
indicate that verapamil causes use-dependent prolongation of
atrioventricular nodal conduction in man.
ARTICLES
Frequency-dependent effects of verapamil on atrioventricular nodal conduction in man
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