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• Re: Flecainide induced ventricular fibrillation in a neonate
  Shubhayan Sanatani
  Published on: 2 February 2004
• Lights and shadows of Flecainide use in the pediatric patient
  Alessandro Giardini
  Published on: 21 November 2003

• Published on: 2 February 2004

  Re: Flecainide induced ventricular fibrillation in a neonate

  • Shubhayan Sanatani, Physician

  Dear Editor

  I was disappointed to read the case report describing a catastrophic outcome in a neonate with an arrhythmia. While I agreed with each statement in the Discussion, the title suggested a direct causal relationship between the flecainide and ventricular fibrillation. In my opinion, this relationship was not proven, nor could it be.

  There are several important data not available in this case....

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  Dear Editor

  I was disappointed to read the case report describing a catastrophic outcome in a neonate with an arrhythmia. While I agreed with each statement in the Discussion, the title suggested a direct causal relationship between the flecainide and ventricular fibrillation. In my opinion, this relationship was not proven, nor could it be.

  There are several important data not available in this case. It is not clear what the original arrhythmia diagnosis in this patient was, the duration of the episode, nor the degree of cardiac dysfunction present at birth. The lack of response to vagal maneuvers (ice) and adenosine are not specific but do raise the possibility that an automatic focus was involved as opposed to a nodal dependent tachycardia. The working diagnosis was excluded by the authors when facing a broad complex tachycardia at 170 bpm. Following the resuscitation, the “ECG showed broad complex tachycardiac arrests and re-entrant supraventricular tachycardia…”. While I am not familiar with the first term, I find it difficult to conceive how the diagnosis of re-entrant SVT was made, particularly in the absence of a response to adenosine. Perhaps an illustrative tracing would be helpful.

  I share the authors’ view that neonates with arrhythmias are a clinical challenge, and that the medications we use have potentially life- threatening adverse effects. However, this case has not demonstrated unequivocally that flecainide caused VF in this neonate when there are so many issues not addressed in this report. More importance is sometimes placed on case reports in pediatric cardiology since there are relatively fewer cases than in the adult cardiology sphere, and caution must be used when “sounding the alarm”.

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  Conflict of Interest:
  None declared.

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• Published on: 21 November 2003

  Lights and shadows of Flecainide use in the pediatric patient

  • Alessandro Giardini
  • Other Contributors:
    • Gabriele Bronzetti, Fernando M. Picchio

  Dear Editor

  Like all medals, also flecainide has two faces. One is that of a fast and efficient antiarrhythmic drug, the other one being that of a drug with a very bad reputation.[1]

  In the October issue of Heart, Ackland et al. [2] briefly reported their experience concerning the occurrence of ventricular fibrillation in a neonate suffering from supraventricular tachycardia (SVT), likely due to the pro...

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  Dear Editor

  Like all medals, also flecainide has two faces. One is that of a fast and efficient antiarrhythmic drug, the other one being that of a drug with a very bad reputation.[1]

  In the October issue of Heart, Ackland et al. [2] briefly reported their experience concerning the occurrence of ventricular fibrillation in a neonate suffering from supraventricular tachycardia (SVT), likely due to the proarrhytmic effect of flecainide. However, in their presentation several issues might be misleading or neglected.

  First of all, it is unclear what kind of rhythm disturbance the neonate suffered from and if a specific pharmacological therapy had been used during pregnancy, since an urgent caesarean section was necessary for child delivery. Then, if the arrhythmia was not tolerated, it is unclear why they chased an oral administration protocol of flecainide over an intravenous one or why external electric cardioversion was not preferred over drug therapy. The authors describe that after flecainide administration, heart rate decreased from 240 beats/min to 170 beats/min and then QRS complex duration increased. This behaviour is rather typical of flecainide effect, relying on its own pharmacodynamics. Flecainide acts blocking Na+ channels in myocardial cells membrane, thus prolonging the duration of the action potential, possibly prolonging QRS duration. Thus, the broad complex tachycardia seen after flecainide may well be the same SVT with an aberrant conduction. Indeed, heart rate was the same for both arrhythmias (170 beats/min). Flecainide administration in children has been reported to be associated to a significant risk for arrhythmias and fatal events,[3] as amiodarone.[4] Potential advantages of flecainide over amiodarone are a faster effect, due to its high early uptake from the heart, a shortest elimination (half-life of about 6 hours), and as reported by Dr Ackland,[2] the plasmatic dosability, which may help to avoid toxicity.

  In a recently published paper [5] we reported our very good results with the use of intravenous flecainide for the treatment of postoperative junctional ectopic tachycardia in neonates, which is often a lifethreatening arrhythmia. About 35 children followed-up at our centre (with an age range at administration from 2 days to 13 years) currently receive daily flecainide for their arrhythmias and only one adverse event occurred in a 5-years-old girl who presented with a sinus rhythm at 65 beats/min and a QRS duration of about 200 milliseconds. Parent’s interview revealed an over-administration of the drug. Blood sample revealed a plasmatic drug concentration of 720 mcg/l at about 12 hours after the last administration. Owing a flecainide elimination half life of 6 hours, we presumed peak plasmatic values exceeding 1000 mcg/l (which is the upper limit to avoid toxicity). Further caution should be taken with flecainide administration in critically ill infants, since drug metabolism may be impaired, thus accumulating in the blood. Therefore, in the setting of resistant SVT, we endorse the use of intravenous flecainide at the loading dose of 0.5-2 mg/kg with continuous infusion of 0.4 mg/Kg/h when the arrhythmia is tolerated, using a smaller bolus (0.5-1 mg/kg) when the clinical condition suggests an impaired metabolism, like in low cardiac output patients. Immediate external electric cardioversion represents the treatment of choice when collapse is pending. In conclusion, we do not think that the case report by Ackland [2] should discourage the use of flecainide in neonates with SVT, but it rather draws the attention to the fact that all care providers should be aware of drug toxicity and of possible proarrhythmic effects related to the administration of this powerful drug.

  References

  (1) The Cardiac Arrhythmia Suppression Trial (CAST) Investigators: Preliminary report: effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction. N Engl J Med 1989;321:406-412.

  (2) Ackland F, Singh R, Thayyil S. Flecainide induced ventricular fibrillation in a neonate.Heart 2003;89:1261

  (3) Fish FA, Gillette PC, Benson DW Jr. Proarrhythmia, cardiac arrest and death in young patients receiving encainide and flecainide. The Pediatric Electrophysiology Group. J Am Coll Cardiol 1991;18:356-365.

  (4) Figa FH, Gow RM, Hamilton RM, Freedom RM. Clinical efficacy and safety of intravenous Amiodarone in infants and children. Am J Cardiol 1994;74:573-577.

  (5) Bronzetti G, Formigari R, Giardini A, et al. Intravenous Flecainide for the Treatment of Junctional Ectopic Tachycardia after Surgery for Congenital Heart Disease. Ann Thorac Surg 2003:76:148-151.

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  Conflict of Interest:
  None declared.

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