The T wave as a marker of dispersion of ventricular repolarization in premature infants before and while on treatment with the I(Kr) channel blocker cisapride.
OBJECTIVE
Measurement of electrocardiographic intervals to assess dispersion in ventricular repolarization may be helpful in the assessment of the risk of ventricular arrhythmia. We measured QTc, QT dispersion, and T wave intervals in premature infants before and while on treatment with the I(Kr) blocker cisapride as markers for dispersion in ventricular repolarization.


RESULTS
We enrolled 15 non-ventilated premature infants with a mean gestational age of 30.5 weeks, ranging from 26.5 to 33.5 weeks, and mean postnatal age of 24 days, with a range from 5 to 51 days. A digital 12 lead electrocardiogram was recorded prior to and 3 days after administering cisapride at a dose of 0.8 mg/kg/day. Serum electrolytes were simultaneously measured. Electrocardiographic measurements before and after included: QT, QTc Bazett, QT dispersion, R-R, T wave interval peak to end, T wave interval peak to end/onset Q to T wave peak, T wave axis, T wave maximum voltage and QRS-T angle. A paired t test and analysis of variance was used to compare the variables before and during treatment. The QTc, T wave interval peak to end and the ratio T wave interval peak to end/onset Q to T peak increased significantly following treatment with cisapride. Results expressed as before and during treatment were for QTc: 429 (65) ms versus 454 (29) ms p < 0.02; for T wave interval peak to end: 65 (11) ms versus 103 (24) p <0.01, for the ratio T wave interval peak to end/onset Q to T peak: 0.32 (0.06) versus 0.55 (0.16) p < 0.001. Treatment with the I(Kr) blocker did not significantly alter the QT dispersion, T wave voltage, angle or QRS-T angle.


CONCLUSIONS
The interval from the peak to the end of the T wave and the ratio of this value to the onset Q to T peak interval, represents regional dispersion of repolarization across the ventricular wall. This is a potentially useful clinical index in the assessment of arrhythmic risk in premature infants being treated by blockade of the I(Kr) channels.
Benatar
Avram
A
Department of Pediatric Cardiology, Academic Hospital, Free University of Brussels, Belgium. Abraham.Benatar@az.vub.ac.be
Cools
Filip
F
Decraene
Tine
T
Bougatef
Adel
A
Vandenplas
Yvan
Y
D001530:Belgium; D027682:Cation Transport Proteins; D020117:Cisapride / Q000008:administration & dosage / Q000037:antagonists & inhibitors*; D004268:DNA-Binding Proteins; D000072237:ERG1 Potassium Channel; D004562:Electrocardiography; D051638:Ether-A-Go-Go Potassium Channels; D006801:Humans; D007223:Infant; D007229:Infant Welfare; D007231:Infant, Newborn; D007234:Infant, Premature; D008133:Long QT Syndrome / Q000150:complications / Q000188:drug therapy / Q000453:epidemiology; D026902:Potassium Channel Blockers; D015221:Potassium Channels / Q000008:administration & dosage; D024642:Potassium Channels, Voltage-Gated; D012307:Risk Factors; D015534:Trans-Activators; D000071230:Transcriptional Regulator ERG; D018879:Ventricular Premature Complexes / Q000453:epidemiology / Q000209:etiology
D027682:Cation Transport Proteins; D004268:DNA-Binding Proteins; C072312:ERG protein, human; D000072237:ERG1 Potassium Channel; D051638:Ether-A-Go-Go Potassium Channels; C092509:KCNH6 protein, human; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D024642:Potassium Channels, Voltage-Gated; D015534:Trans-Activators; D000071230:Transcriptional Regulator ERG; D020117:Cisapride