Circulation, Vol 84, 1915-1923, Copyright © 1991 by American Heart Association
W Shimizu, T Ohe, T Kurita, H Takaki, N Aihara, S Kamakura, M Matsuhisa and K Shimomura
BACKGROUND. Several recent experimental and clinical studies have shown
that early afterdepolarizations (EADs) are important in the genesis of QTU
prolongation and ventricular tachyarrhythmias (VTs) in patients with long
QT syndrome. On the other hand, sympathetic stimulation is well known to
contribute to the genesis of QTU prolongation and VTs in patients with
congenital long QT syndrome. The present study was performed to examine the
influence of isoproterenol on the genesis of EADs and on the action
potential durations and QTU intervals in patients with congenital long QT
syndrome. METHODS AND RESULTS. We recorded monophasic action potentials
(MAPs) with a contact electrode during right atrial pacing at a constant
cycle length of 500 msec before and after continuous isoproterenol infusion
(1 microgram/min). MAPs were obtained from the right and left ventricular
endocardium in six patients with congenital long QT syndrome (LQT group, 18
recording sites) and in eight control patients (control group, 19 recording
sites). Although no EADs were recorded from either group during the control
state, MAP duration at 90% repolarization (MAPD90) was significantly longer
in the LQT group (n = 18) than in the control group (n = 19) (275 +/- 36
versus 231 +/- 22 msec; p less than 0.0005). Isoproterenol induced EADs in
four of the six LQT patients (five of 18 recording sites) but not in the
eight control patients (zero of 19 recording sites). The appearance of EADs
in the LQT group was associated with an increased amplitude of the late
component of the TU complex, and the corrected QT (QTc) interval was
prolonged by isoproterenol from 543 +/- 53 to 600 +/- 30 msec 1/2 (n = 6; p
less than 0.05). Isoproterenol also prolonged the MAPD90 from 275 +/- 36 to
304 +/- 50 msec in the LQT group (n = 18; p less than 0.005), whereas it
shortened the MAPD90 from 231 +/- 22 to 224 +/- 25 msec in the control
group (n = 19; p less than 0.05). Moreover, isoproterenol increased the
dispersion of MAPD90 (difference between the longest MAPD90 and the
shortest MAPD90 in each patient) from 30 +/- 5 to 62 +/- 35 msec in the LQT
group (n = 6; p = 0.08), whereas it did not change the dispersion of MAPD90
in the control group (n = 8; 25 +/- 14 versus 27 +/- 14 msec). CONCLUSIONS.
These results suggest that patients with congenital long QT syndrome have
primary repolarization abnormalities and that EADs induced by isoproterenol
play an important role in the exaggeration of these repolarization
abnormalities.
ARTICLES
Early afterdepolarizations induced by isoproterenol in patients with congenital long QT syndrome
Cardiology Division of Medicine, National Cardiovascular Center, Osaka, Japan.
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