Key Points
- To determine whether a presentation of Lown-Ganong-Levine syndrome was caused by an accessory pathway of James fibers or enhanced atrioventricular nodal conduction.
- Evaluated a 17-year-old male with recurrent narrow-complex and wide-complex tachycardia using surface electrocardiography.
- Conducted an invasive electrophysiologic study and pharmacological adenosine challenge to assess atrioventricular conduction dynamics.
- Performed catheter ablation targeting the atrioventricular nodal region.
- Electrophysiologic testing demonstrated an abnormally short atrial-to-His conduction interval, two coexisting conduction pathways at identical pacing cycle lengths, and resistance to adenosine challenge.
- Following the emergence of intermittent conduction, an adenosine challenge triggered conduction over the short atrial-to-His interval without producing atrioventricular block.
- Catheter ablation in the atrioventricular nodal area normalized the atrial-to-His interval, restored decremental conduction properties, and reestablished sensitivity to adenosine.
Structured PICO
PPopulation17-year-old man with a history of recurrent narrow-complex and wide-complex tachycardia on ECG (Lown-Ganong-Levine syndrome)
IInterventionElectrophysiologic study and catheter ablation of the AV nodal region
OOutcomeElectrophysiologic characteristics and response to ablationsurrogate
Electrophysiologic studies and successful ablation in a case of Lown-Ganong-Levine syndrome supported the pathophysiological role of James fibers.