Circulation, Vol 87, 783-792, Copyright © 1993 by American Heart Association
ML Markel, WM Miles, JC Luck, LS Klein and EN Prystowsky
BACKGROUND. Autonomic modulation, especially increased sympathetic activity
may play a role in the genesis of ventricular arrhythmias. The purpose of
this study was to determine whether beta-sympathetic stimulation with
isoproterenol would alter sustained ventricular tachycardia (VT) circuits
similarly during the drug-free and antiarrhythmic drug-treated states.
METHODS AND RESULTS. Twenty-five patients with repeatedly inducible,
hemodynamically stable, sustained VT were evaluated by programmed
ventricular stimulation. In the antiarrhythmic drug-free state,
isoproterenol (0.03 microgram/kg per minute) shortened the following
intervals (in milliseconds; mean +/- SEM; 25 patients; paired t test):
sinus cycle length (792 +/- 37 to 568 +/- 18; (p < 0.001), ventricular
paced QT interval (386 +/- 8 to 348 +/- 6; p < 0.001), ventricular paced
QRS duration (185 +/- 4 to 182 +/- 4; p = 0.014), ventricular effective
(238 +/- 5 to 208 +/- 4; p < 0.001) and functional (261 +/- 6 to 227 +/-
5; p < 0.001) refractory periods, and the VT cycle length (VTCL) (311
+/- 9 to 291 +/- 9; p < 0.001). Isoproterenol (0.03 microgram/kg per
minute) was administered during 31 antiarrhythmic drug trials
(procainamide, n = 18; quinidine, n = 13) in 22 patients. Isoproterenol
shortened the sinus cycle length, QT interval during ventricular pacing,
and ventricular effective and functional refractory periods before and
during procainamide and quinidine therapy (ANOVA; isoproterenol effect, p
< or = 0.0002 for all). The amount of decrease in these intervals with
isoproterenol was the same before and during procainamide and quinidine
therapy (ANOVA interaction, p = NS for all). The QRS duration during
ventricular pacing and VTCL were also shortened by isoproterenol before and
during procainamide (baseline, n = 17; QRS, 182 +/- 4 to 178 +/- 4 msec;
VTCL, n = 18, 314 +/- 11 to 291 +/- 11 msec; during procainamide, QRS, 218
+/- 7 to 197 +/- 6 msec; VTCL, 422 +/- 15 to 359 +/- 11 msec) and quinidine
(baseline, n = 13; QRS, 190 +/- 6 to 185 +/- 5 msec; VTCL, n = 12, 298 +/-
10 to 280 +/- 9 msec; during quinidine, QRS, 223 +/- 9 to 208 +/- 8 msec;
VTCL, 415 +/- 14 to 355 +/- 10 msec) (isoproterenol effect p < or =
0.0003 for all). However, the amount of decrease in QRS duration and VTCL
with isoproterenol was greater during procainamide and quinidine than in
the drug-free state (ANOVA interaction, p < or = 0.02 for all). These
changes continued to be significant when normalized for the initial QRS
duration and VTCL (p < or = 0.03 for all). CONCLUSIONS. Isoproterenol
affects presumed reentrant sustained VT circuits less in the absence of
antiarrhythmic drugs but markedly attenuates the antiarrhythmic
drug-induced slowing of sustained VT. To the extent that the change in QRS
duration reflects a change in conduction within the VT circuit, these data
imply that the attenuation of drug-induced slowing of VT by isoproterenol
is due to a greater change in conduction rather than refractoriness.
ARTICLES
Differential effects of isoproterenol on sustained ventricular tachycardia before and during procainamide and quinidine antiarrhythmic drug therapy
Krannert Institute of Cardiology, Indianapolis, Ind.
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