Literature DB >> 3964800

Wolff-Parkinson-White syndrome and supraventricular tachycardia during infancy: management and follow-up.

B J Deal, J F Keane, P C Gillette, A Garson.   

Abstract

The records of 90 patients with Wolff-Parkinson-White syndrome who presented with supraventricular tachycardia in the first 4 months of life were reviewed. Among these, 63% were male. Structural heart disease was present in 20%, most commonly Ebstein's anomaly. All patients presented with a regular narrow QRS tachycardia, and pre-excitation became evident only when normal sinus rhythm was established. Only one infant had atrial flutter and none had atrial fibrillation. Type A Wolff-Parkinson-White syndrome was most common (49%), with heart disease occurring in only 5% of these patients. In contrast, heart disease was identified in 45% of those with type B syndrome. Initially, normal sinus rhythm was achieved in 88% of the 66 infants treated with digoxin with no deaths. Normal sinus rhythm resumed after electrical countershock in 87% of the 15 infants so treated. Maintenance digoxin therapy was used in 85 patients. The Wolff-Parkinson-White pattern disappeared in 36% of the patients. Four infants died of cardiac causes during the mean follow-up period of 6.5 years. Two of these four infants had congenital heart disease; the third, with a normal heart initially, developed ventricular fibrillation and died from a cardiomyopathy considered related to resuscitation. The remaining infant, with a normal heart, died suddenly at 1 month of age. All were receiving digoxin. A wide QRS tachycardia later appeared in three patients, all with heart disease, one of whom died.(ABSTRACT TRUNCATED AT 250 WORDS)

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Year:  1985        PMID: 3964800     DOI: 10.1016/s0735-1097(85)80095-4

Source DB:  PubMed          Journal:  J Am Coll Cardiol        ISSN: 0735-1097            Impact factor:   24.094


  52 in total

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7.  Acceleration of the ventricular response to atrial flutter by amiodarone in an infant with Wolff-Parkinson-White syndrome.

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9.  20p12.3 microdeletion predisposes to Wolff-Parkinson-White syndrome with variable neurocognitive deficits.

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