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1/4. Enhanced A-V nodal conduction (lown-ganong-levine syndrome) by congenitally hypoplastic A-V node.

    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-delaying function, and thus allowed rapid, unfiltered atrial impulses to reach the lower A-V junction and ventricles. ( info)

2/4. lown-ganong-levine syndrome in pregnancy.

    BACKGROUND: lown-ganong-levine syndrome is characterized by paroxysmal supraventricular tachycardia, a short PR interval, and normal QRS. CASE: A gravida 3, para 2 was diagnosed with lown-ganong-levine syndrome at 16 weeks' gestation after an episode of chest pain and shortness of breath. She was hospitalized and treated with digoxin, and her symptoms subsided. The remainder of her pregnancy was uneventful. CONCLUSION: lown-ganong-levine syndrome is a rare complication most commonly seen in young to middle-aged women. This syndrome can be treated and controlled medically with a good outcome. ( info)

3/4. Pulmonary developmental anomaly associated with klippel-feil syndrome and anomalous atrioventricular conduction.

    We report the findings in a patient with klippel-feil syndrome and associated agenesis of right upper and middle lobes, hypoplasia of the right lower lobe of the lung, and lown-ganong-levine syndrome. To our knowledge, such an association has not been previously described. ( info)

4/4. Supraventricular tachycardia in a patient with lown-ganong-levine syndrome associated with apical hypertrophic cardiomyopathy.

    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. ( info)

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