(RT), we studied li epended on intraveno (2-g/ug/min). ltn all Pts. AV RT used inde system for antegrade and anomalous Seven pts
f&znavenous suppressed
;opranolol
i&zing AV RT in 4/j pis; depressed AV node conduction but exerted no In contrast, ~roD~a~olo1 comvletelv abolished i~d~c~b~~~ty of AV RT in lO/lO (106%) g&p II ~ote~e~o~-~~d~~ed facilitation bf cQnduct~om in atrium. AV node. ventricPe an amil
sl&ed ventricular IX pts with inducible atrial fibrillation w~t~-ve~t~icu~a~ Dreexcitation. Thus. in catec~o~~~~e-ae~s~t~ve AV M’, propranolol is
~o~~~~t~orn
in- 2/10
kar more specific
bout effects
TERMINATION
and effective
then ver&&niP
OF AYRlAL
FLUTTER
BY PROCAlNA rio
rry JGM Crijns MD, 3
Clinical Pharmacology The Netherlands
in
ility of AV RT, and b’lockade should be considered treatment of choice for chronic prophylaxis.
use-dependent in man.
D, Harry Wesseling M and Cardiology, University
randjean MD, eparlments of of Groningcn,
Procairramide (P, n=6) or flecainide (F, n=lO) were used to terminate atrial flutter (AF) in a reentry model with a partially refractory excitable gap. Plunge wire electrodes were introduced around a Y-shape.i incision in the right atrium in 16 pigs (body weight approx. 32 kg), and 59 sustained AT’s (mean cycle length 171215 ms) were induced by programmed stimulation in 14 pigs. Strength-interval curves were obtained with 2 ms stimuli to assess excitability. P or F were administered until the termination of AF. Flutter cycle length increased gradually to 269574 ms after F and to 281233 ms afkr P (not different, P versus F). Current thresholds, refractory periods (RP) and conducrion velocity al baseline and at termination were: flecaiaide baseline prbcaiaamide baseline 12~0.6~ 0.7IO.4 1.4~0.4 Thresh. (mA) 1.3-cO.8 205zX? 201+24 228116~ Effec. RP(ms) 198215 164-c?2 158221 184t16* Absol. RP(ms) 155z18 282 4. 302 4’ 452 2 Cond. (cm/s) 502 7 ean values 2 SD: + = ~~0.05 versus corresponding baseline value. In conclusion, both drugs terminate this subtype of reentry by a comparable reduction of the conduction velocity, procainamide by its effect on atria1 refractoriness and flecainide by an increase of the current threshold and hence by its inhibition of the source of propagation. Therefore, this model differentiates class la (procainamide) from class Ic (flecainide) antiarrhythmic actSties.
I.
itz,
Sztern,
ugh) plasma theophyl6.0 and 9.3 mg L”. added on days 6 and 9,