The Lown-Ganong-Levine (LGL) syndrome occurs when an accessory pathway is congenitally present that directly connects the atria to the ventricles, bypassing the AV node similar to the Wolff-Parkinson-White (WPW) syndrome. Thus, when the sinus node fires, the electrical activation does not need to travel through the AV node like in a normal person (which usually delays the impulse from getting to the ventricles). Instead, the action potential can travel down the accessory pathway and activate the ventricles rapidly. This short duration between the sinus node firing and the ventricles being depolarized results in a short PR interval on the ECG.
The main distinguishing feature between LGL and WPW syndromes is that the accessory pathway in LGL syndrome connects distally to the normal conduction pathway (bundle of His), and in WPW the accessory pathway connects to the ventricular myocardium. Thus, both disease states can have a short PR interval, however LGL syndrome will not have a delta wave or widened QRS complex as seen in WPW syndrome. This is because ventricular activation occurs normally in LGL syndrome instead of occurring from myocyte to myocyte as seen in WPW.
Similar arrhythmias occur with LGL syndrome and WPW syndrome, including atrioventricular reentrant tachycardia (AVRT) and rapidly conducting atrial fibrillation. Treatment is similar to WPW and procainamide is frequently utilized. Ablation of the accessory pathway is more difficult in LGL syndrome compared to WPW syndrome since it is located very close to the AV node and there is risk of causing complete heart block necessitating permanent pacemaker implantation.
- Surawicz B, et al. Circulation. 2009;119:e235-240.
- Chou's Electrocardiography in Clinical Practice: Adult and Pediatric, Sixth Edition, Saunders, Philadelphia, 2008.