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European Heart Journal 1992 13(11):1579-1584;
Copyright © 1992 by the European Society of Cardiology.
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© 1992 The European Society of Cardiology

Enhanced A-V nodal conduction (Lown-Ganong-Levine syndrome) by congenitally hypoplastic A-V node

R. OMETTO, G. THIENE*,, D. CORRADO*, M. VINCENZI and L. ROSSI*

Department of Cardiology, City Hospital Vicenza
*Department of Pathology, University of Padua Italy

Received 5 September 1991; revised 22 January 1990; .

Correspondence Gaetano Thiene, MD, Istituto di Anatomia Palologica, Via A. Gabelli, 61, 35121 Padova, Italy

Abstract

The basic anatomical substrate of enhanced A-V nodal conduction, manifesting or not as Lown-Ganong-Levine syndrome, is still a controversial issue. We describe the case of a 34-year-old man who presented episodes of ventricular fibrillation. Electrophysiological studies showed that the AH interval was 55 ms, and increased by only 20 ms at paced cycle lengths of 300 ms; atrial pacing induced atrial fibrillation, with a shortest RR interval of 240 ms. Despite verapamil therapy, this patient died suddenly at home. Histological study disclosed a severe A-V node hypoplasia that was evidently congenital in nature; the rest of the conduction system was normal, and no accessory A-V pathways were present. We suggest that enhanced A-V nodal conduction in this patient was due to the developmental defect in the A-V node; this abnormality caused a loss of specific impulse-delay ing function, and thus allowed rapid, unfiltered atrial impulses to reach the lower A-V junction and ventricles.

Key Words: Conduction system • congenital heart disease • enhanced A-V nodal conduction • Lown-Ganong-Levine syndrome


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