From the Cardiology Divisions, Veterans National Administration and
Georgetown University Medical Centers, Washington, DC (P.F.K., C.L.F., M.R.F.)
and the University of Münster, Germany (P.F.K., C.L.F.).
Correspondence to Michael R. Franz, MD, PhD, Veterans Administration Medical Center, 50 Irving St, NW, Washington, DC 20422.
Background—Conduction block may be
both antiarrhythmic and proarrhythmic. Drug-induced postrepolarization
refractoriness (PRR) may prevent premature excitation and
tachyarrhythmia induction. The effects of propafenone
and procainamide on these parameters, and their
antiarrhythmic or proarrhythmic consequences, were
investigated.
Methods and Results—In 11 isolated Langendorff-perfused rabbit
hearts, monophasic action potentials (MAPs) were recorded
simultaneously from six to seven different right and left
ventricular sites, along with a volume-conducted ECG. All
recordings were used to discern ventricular
tachycardia (VT) or ventricular fibrillation
(VF) induced by repetitive extrastimulation (S2-S5) or 10-second burst
stimulation at 25 to 200 Hz at baseline and after addition of
procainamide (20 µmol/L) or propafenone (1
µmol/L) to the perfusate. MAPs were analyzed for
action potential duration at 90% repolarization (APD90),
conduction times (CT) between the pacing site and the other MAPs, and
PRR (effective refractory period-APD90=PRR) and related to
the induction of VT or VF. During steady-state pacing,
procainamide and propafenone prolonged APD90 by
12% and 14%, respectively. Procainamide slowed mean CT by
40% during S2-S5 pacing, whereas propafenone slowed mean CT by up to
400% (P<0.001 versus baseline and
procainamide). Wavelength was not changed significantly by
procainamide but was shortened fourfold by propafenone at S5.
Both drugs produced PRR, which was associated with a 70% decrease in
VF inducibility with procainamide and elimination of VF with
propafenone. Despite this protection from VF, monomorphic VT was
induced with propafenone in 57% of burst stimulations.
Conclusions—Drug-induced PRR protects against VF induction.
Propafenone promotes slow monomorphic VT, probably by use-dependent
conduction slowing and wavelength shortening.
© 1998 American Heart Association, Inc.
Basic Science Reports
Postrepolarization Refractoriness Versus Conduction Slowing Caused by Class I Antiarrhythmic Drugs
Antiarrhythmic and Proarrhythmic Effects
Key Words: fibrillation • conduction • propafenone • procainamide
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