Sa. Zamora et al., Effects of cisapride on ventricular depolarization-repolarization and arrhythmia markers in infants, BIOL NEONAT, 80(1), 2001, pp. 30-34
To study prospectively the effects of cisapride on ventricular repolarizati
on, depolarization, and arrhythmia markers in neonates, we determined befor
e and three days after starting cisapride (1 mg/kg/day): corrected QT inter
val (QTc) and QT dispersion (QTd) on standard ECGs, and duration of filtere
d QRS (fQRS) and of low amplitude (< 40 muV) terminal signals (LAS40, ms) a
nd root mean square of the last 40 ms (RMS40, muV) using high-gain signal-a
veraged ECG (SAECG). Twenty-four term and 11 preterm infants (gestational a
ge 23-35 weeks) were studied at a median chronological age of 32 days. QTc
and QTd were not different between term and preterm infants. Cisapride leng
thened QTc (mean +/- SD; ms: 396.6 +/- 24.8 before vs. 417.0 +/- 35.2 after
, p < 0.001). Three term and two preterm infants (5/35 = 14%; 95% Cl: 5-30%
) had a QTc > 450 ms after cisapride. QTd after cisapride increased signifi
cantly in all infants with prolonged QTc. Filtered QRS, LAS40, and RMS40 be
fore and after cisapride were within our normal values. We conclude that ci
sapride prolongs ventricular repolarization in neonates and infants without
altering depolarization. Although no clinical arrhythmias were observed th
e dose of 0.8 mg/kg/day should not be exceeded. Copyright (C) 2001 S. Karge
r AG, Basel.