Amiodarone treatment of junctional ectopic tachycardia in a neonate receiving extracorporeal membrane oxygenation.

OBJECTIVE: To describe the administration of amiodarone and the resulting serum concentrations in a neonate receiving extracorporeal membrane oxygenation (ECMO). CASE SUMMARY: A 3463 g, 38 week gestational age male diagnosed with tetralogy of Fallot developed junctional ectopic tachycardia (JET) and required ECMO support following cardiac surgery. The patient continued to show JET despite cooling, pacing, and intravenous amiodarone infusion, with the dose initiated at 10 microg/kg/min. Sinus rhythm was achieved following 5 days of treatment, additional amiodarone boluses, and an increase in the infusion rate to 20 microg/kg/min. Two serum concentrations of amiodarone were obtained during therapy. On day 4, the concentration was 0.9 mg/L at the 20 microg/kg/min infusion rate; a bolus dose of 5 mg/kg was administered 1 hour later. The serum concentration the following day, with the infusion rate unchanged, was 2 mg/L. DISCUSSION: ECMO is used increasingly postoperatively in patients with congenital cardiac abnormalities. The incidence of JET following repair of tetralogy of Fallot is 22%. Despite the minimal information on the pharmacokinetics of amiodarone in neonates, it has been used in doses up to 20 microg/kg/min for the treatment of postoperative JET. As of August 25, 2006, we found no reports describing its dosage and use in patients undergoing ECMO. CONCLUSIONS: The delivery of amiodarone to a patient receiving ECMO may be complicated by the administration of large blood volumes, circuit changes, and binding to the circuit. Neonates receiving ECMO may require larger amiodarone doses to achieve a therapeutic effect. Further investigation is required to define the pharmacokinetics and pharmacodynamics of amiodarone in neonates receiving ECMO.

[A new cause of increased troponin levels: junctional tachycardia]. / Une nouvelle cause d'élévation de la troponine: la tachycardie jonctionnelle.

The authors report 4 cases of acute coronary syndromes with increased troponine levels during junctional tachycardia in patients with angiographically normal coronary arteries. ST segment changes during junctional tachycardia have no predictive value for the detection of coronary artery disease. Increased troponine, a marker of myocardial cellular necrosis, is not a sign of coronary lesions. A disequilibrium between the increased metabolic and energetic requirements of the myocardium and decreased perfusion due to the tachycardia could explain this observation. The recommended management of these patients is not to perform coronary angiography initially in the absence of cerebrovascular risk factors, but rather to document myocardial ischaemia by a non-invasive method such as echocardiography or scintigraphy.

Magnesium supplementation in the prevention of arrhythmias in pediatric patients undergoing surgery for congenital heart defects.

BACKGROUND: The efficacy of magnesium in the prevention of arrhythmias in pediatric patients after heart surgery remains unknown. Therefore we prospectively examined the effect of magnesium treatment on the incidence of postoperative arrhythmias in pediatric patients undergoing surgical repair of congenital heart defects. METHODS AND RESULTS: Twenty-eight pediatric patients undergoing heart surgery with cardiopulmonary bypass were prospectively, randomly assigned in a double-blind fashion to receive intravenous magnesium (magnesium group, n = 13; 30 mg/kg) or saline (placebo group, n = 15) immediately after cessation of cardiopulmonary bypass. Magnesium, potassium, and calcium levels were measured at defined intervals during surgery and 24 hours after surgery. Continuous electrocardiographic documentation by Holter monitor was performed for 24 hours after surgery. Magnesium levels were significantly decreased below the normal reference range for patients in the placebo group compared with the magnesium group on arrival in the intensive care unit and for 20 hours after surgery. Magnesium levels remained in the normal range for patients in the magnesium group after magnesium supplementation. In 4 patients in the placebo group (27%), junctional ectopic tachycardia developed within the initial 20 hours in the intensive care unit. No junctional ectopic tachycardia was observed in the magnesium group (P =.026). CONCLUSIONS: Although this study was originally targeted to include 100 patients, the protocol was terminated because of the unacceptable incidence of hemodynamically significant junctional ectopic tachycardia that was present in the placebo group. Thus low magnesium levels in pediatric patients undergoing heart surgery are associated with an increased incidence of junctional ectopic tachycardia in the immediate postoperative period.

Pharmacokinetics of moricizine in young patients.

Moricizine is a novel phenothiazine antiarrhythmic agent that depresses the activity of ectopic foci, has a low incidence of adverse effects relative to other agents, and is useful in treating pediatric atrial ectopic tachycardia. A study was conducted to determine the pharmacokinetics of moricizine in children after oral administration. Moricizine was isolated from frozen serum obtained from four male patients (ages 7, 8, 9, and 18 years) receiving the drug for supraventricular tachycardia and analyzed by high-performance liquid chromatography with ultraviolet detection according to an established protocol. Peak serum levels were between 400 and 2000 ng/mL. Elimination of moricizine did not follow simple single-compartment pharmacokinetics. In three patients we observed an increase or slower decline in blood level occurring after 4 hours. Because of the paroxysmal nature of the tachycardias, decreases in patient heart rate could not be correlated with moricizine blood level. These results suggest that the pediatric pharmacokinetics of moricizine excretion are complex and may differ from those seen in adults.

Clinical experience with propafenone for cardiac arrhythmias in the young.

Seventy-two children were treated with propafenone between 1980 and 1990. The mean age was 34 months (range 0-192). Arrhythmias included atrioventricular re-entry tachycardia in 32 patients (44%), atrial flutter in 16 (22%), atrial or junctional ectopic tachycardia in 10 (14%), atrial re-entry tachycardias in three (4%) and ventricular arrhythmias in 11 patients (16%). The efficacy of oral treatment was good in patients with atrio-ventricular re-entry tachycardia (80%), atrial flutter (71%) and atrial ectopic tachycardia (83%); it was poor in ventricular arrhythmias (40%). The mean oral dose was 13.5 mg.kg-1. day-1. Dosage and serum levels of propafenone did not differ whether the patients were treated successfully or not. No correlation between dosage and serum level was observed. Intravenous propafenone administration was only partially successful in suppressing supraventricular tachycardias (6 of 11 patients). The presence of a congenital heart defect and the time of onset of the arrhythmias had a significant influence on the efficacy of propafenone. Better results were observed in patients with normal hearts and in whom onset of arrhythmia was pre-natal (success 80%) as well as in patients with arrhythmias seen early after surgery for congenital heart defects (success 87%). Success (65%) was also observed in patients without congenital heart defects and postnatal onset of supraventricular arrhythmias. Patients with ventricular or supraventricular arrhythmias late after corrective surgery showed the poorest response (31%).