This report describes the first known case of Lown-Ganong-Levine syndrome associated with apical hypertrophic cardiomyopathy, demonstrating that the short P-R interval and tachycardia were due to intranodal reentry through dual A-V nodal pathways.
Extends LGL syndrome to apical HCM; leaves open mechanistic link and clinical relevance pending larger studies.
Electrophysiologic study of a 55-year-old patient with Lown-Ganong-Levine syndrome associated with apical hypertrophic cardiomyopathy is reported. The patient had a history of recurrent attacks of tachyarrhythmia and his electrocardiogram showed a short P-R interval (0.10 sec) with narrow QRS complex and left ventricular hypertrophy with giant negative T waves. His cineangiogram showed severe apical hypertrophy. An electrophysiologic study was performed. The results of programmed atrial pacing show the existence of the dual A-V nodal pathways. The A-H interval at rapid atrial pacing increased maximally by 103 msec. Atrial stimulation could depolarize parts of the atrium without altering the supraventricular tachycardia. These findings suggested that preferential rapidly conducting A-V nodal and intranodal reentry are the responsible mechanisms in this reciprocating tachycardia. We conclude that the short P-R interval was due to intranodal reentry through the dual A-V nodal pathways. To our knowledge, a case of Lown-Ganong-Levine syndrome with apical hypertrophic cardiomyopathy has not been previously described in the literature.
No takes yet. Share an insight, caveat, or question.
Hayano et al. (1988) studied this question.
Synapse has enriched 2 closely related papers on similar clinical questions. Consider them for comparative context: