Infants presenting with paroxysmal supraventricular tachycardia may have an inapparent bypass tract and WPW syndrome, which may only become apparent on ECG after long-term follow-up.
May support adding propranolol or verapamil for digoxin-refractory infant PSVT; leaves open bypass tract prevalence and long-term ECG monitoring needs.
We report 3 infants with Wolff-Parkinson-White (WPW) syndrome who presented with life-threatening paroxysmal reciprocating atrioventricular tachycardia in their first month of life. The diagnosis was confirmed by electrophysiological studies at ages 2--4 years, but the characteristic ECG of pre-excitation has not been shown in one patient and was first recorded at 2 and 3 years in the other two. In 2 patients the tachycardia proved refractory to treatment with digoxin alone but responded to the addition of propranalol or verapamil. One of these infants was converted to sinus rhythm by DC countershock, giving time to reconsider his treatment with drugs. Digoxin is a well-tried treatment acting by slowing AV conduction and interrupting the re-entry circuit. However, it may act more slowly than other agents that act on the AV node--such as intravenous verapamil. Our patients illustrate the value of long follow-up as the diagnosis of WPW syndrome could not be made in infancy. Many infants who present with paroxysmal supraventricular tachycardia in infancy may have an inapparent bypass and be examples of the WPW syndrome.
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Hallidie-Smith et al. (1978) studied this question.
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