What is Lown-Ganong-Levine syndrome (LGL)?

Updated: Dec 09, 2020
  • Author: Daniel M Beyerbach, MD, PhD; Chief Editor: Jose M Dizon, MD  more...
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The Lown-Ganong-Levine syndrome (LGL) is a clinical syndrome consisting of paroxysms of tachycardia and electrocardiogram (ECG) findings of a short PR interval and normal QRS duration. The accessory pathway partly or completely bypasses the atrioventricular node, leading to the direct activation of the His bundle by the sinoatrial node. [1]

LGL is usually categorized in a class of preexcitation syndromes that includes the Wolff-Parkinson-White syndrome (WPW), LGL, and Mahaim-type preexcitation. [2] Investigations into WPW have revealed that an accessory pathway for conduction, called a bundle of Kent, from the atria to the ventricles underlies the preexcitation observed in patients with WPW. Less is known regarding the structural anomalies underlying LGL. Theories proposed to explain LGL have centered around the possible existence of intranodal or paranodal fibers that bypass all or part of the atrioventricular (AV) node.

Historically, some authors have referred to patients with a short PR interval and normal QRS duration as having LGL. However, this practice has been largely abandoned as more evidence has accumulated demonstrating that such patients without a history of tachycardia likely fall into a class of normal variants. Patients with an isolated finding of short PR interval may be characterized as having accelerated AV nodal conduction.

In 1938, Clerc, Levy, and Critesco first described the occurrence of frequent paroxysms of tachycardia in patients with a short PR interval and normal QRS duration. [3] This syndrome was again described in 1952 by Lown, Ganong, and Levine, whose names form the eponym now used to describe it. [4] In 1946, Burch and Kimball proposed that an atrio-Hisian (AH) pathway might explain the findings of the syndrome, although no such pathway had yet been identified anatomically. [5] In 1961, James described fibers that originate in the low atrium and terminate low in the AV node. [6] Brechenmacher et al reported anatomic findings of an AH bundle in 1974. [7] Subsequent investigations into the origin of LGL have largely involved invasive electrophysiologic studies that have sought to identify structural and functional anomalies that might explain the findings of LGL. [8, 9]

Criteria for LGL include a PR interval less than or equal to 0.12 second (120 ms), normal QRS complex duration of less than 120 ms, and occurrence of a clinical tachycardia. [4, 10, 11]

The term enhanced atrioventricular nodal conduction (EAVNC) refers to a set of functional criteria that includes an AH interval less than or equal to 60 ms, 1-to-1 AV nodal conduction at rates as high as 200 beats per minute, and an abnormally small increase in AH interval as atrial pacing rate is increased. [12]

EAVNC represents a functional characterization of the AV node, whereas LGL refers to a syndrome of supraventricular tachycardia in association with a short PR interval. The short PR interval in LGL may be related to the presence of EAVNC. LGL and EAVNC may coexist, or either may exist alone in a given patient.

No environmental factors that contribute to occurrence of LGL have been identified. Some evidence suggests that both WPW and LGL may be hereditary in certain families.

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