H. Furushima et al., RELATION BETWEEN BRADYCARDIA DEPENDENT LONG QT SYNDROME AND QT PROLONGATION BY DISOPYRAMIDE IN HUMANS, HEART, 79(1), 1998, pp. 56-58
Background-Recent molecular biological investigations have identified
abnormal genes in familial forms of long QT syndrome, but in bradycard
ia dependent acquired long QT syndrome, no such genetic abnormality ha
s yet been identified. Objective-To investigate the relation between t
he responses of QT interval to pacing change and to disopyramide. Meth
ods-This study included 13 patients with bradyarrhythmia who had under
gone pacemaker implantation. The patients were divided into two groups
: group I (n = 8), patients with QT prolongation (QT interval greater
than or equal to 500 ms) during bradycardia; group II (n = 5), patient
s without QT prolongation (QT interval < 500 ms) during bradycardia. T
he responses of QT interval caused by the change of pacing rate were d
etermined and compared with the changes of the QT interval after disop
yramide administration. Results-The QT interval in group I was signifi
cantly 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 beat
s/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 di
sopyramide 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 pro
longation are also more markedly affected by disopyramide and that abn
ormal potassium channel may be the underlying mechanism.