Heart 1998;79:56-58 ( January )
Relation between bradycardia dependent long QT syndrome and QT prolongation by disopyramide in humans
The First
Department of Internal Medicine, Niigata University School of Medicine,
Niigata, 1-754 Asahi-machi, Niigata, 951 Japan
Correspondence to: Dr Furushima.
Accepted for publication 31 July 1997
Background
Recent molecular biological
investigations have identified abnormal genes in familial forms of long
QT syndrome, but in bradycardia dependent acquired long QT syndrome, no
such genetic abnormality has yet been identified.
Objective
To investigate the relation between the
responses of QT interval to pacing change and to disopyramide.
Methods
This study included 13 patients with
bradyarrhythmia who had undergone pacemaker implantation. The patients
were divided into two groups: group I (n = 8), patients with QT
prolongation (QT interval
500 ms) during bradycardia; group II
(n = 5), patients without QT prolongation (QT interval < 500 ms)
during bradycardia. The responses of QT interval caused by the change
of pacing rate were determined and compared with the changes of the QT
interval after disopyramide administration.
Results
The QT interval in group I was
significantly longer than that in group II when the pacing rate was
decreased from 110 to 50 beats/min: mean (SD) 451 (16) v
416 (17) ms at 90 beats/min (p = 0.0033), and 490 (19)
v 432 (18) ms at 70 beats/min (p = 0.0002), respectively. The QT interval was prolonged significantly by
disopyramide in both groups, but the change was more pronounced in
group I than in group II: 78 (33) v 35 (10) ms
(p < 0.05).
Conclusions
This study suggests that the patients
showing bradycardia dependent QT prolongation are also more markedly
affected by disopyramide and that abnormal potassium channel may be the
underlying mechanism.
© 1998 by Heart
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