Lown–Ganong–Levine syndrome

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Lown–Ganong–Levine syndrome
Classification and external resources
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ICD-10 I45.6
ICD-9-CM 426.81
OMIM 108950
DiseasesDB 7599
eMedicine med/2954
Patient UK Lown–Ganong–Levine syndrome
MeSH D008151
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Lown–Ganong–Levine syndrome (LGL) is a syndrome of pre-excitation of the ventricles due to an accessory pathway providing an abnormal electrical communication from the atria to the ventricles. It is grouped with Wolff–Parkinson–White syndrome as an atrioventricular re-entrant tachycardia (AVRT). The syndrome is named after Bernard Lown, William Francis Ganong, Jr., and Samuel A. Levine.[1][2]

A short PR is seen.[3]


In normal individuals, electrical activity in the heart is initiated in the sinoatrial (SA) node (located in the right atrium), propagates to the atrioventricular (AV) node, and then through the bundle of His to the ventricles of the heart. (See electrical conduction system of the heart).

The AV node acts as a gatekeeper, limiting the electrical activity that reaches the ventricles of the heart. This is an important function of the AV node, because if the signals generated in the atria of the heart were to increase in rate (such as during atrial fibrillation or atrial flutter), the AV node will limit the electrical activity that conducts to the ventricles. For instance, if the atria are electrically activated at 300 beats per minute, half those electrical impulses are blocked by the AV node, so that the ventricles are activated at 150 beats per minute (giving a pulse of 150 beats per minute). Another important property of the AV node is that it slows down individual electrical impulses. This is manifest on the EKG as the PR interval, the time from activation of the atria (manifest as the P wave) and activation of the ventricles (manifest as the QRS complex).

Individuals with LGL syndrome were once thought to have an accessory pathway that connects the atria directly to the bundle of His. As in WPW syndrome, the concern was that the accessory pathway would not share the rate-slowing properties of the AV node, and could potentially conduct electrical activity at a significantly higher rate than the AV node. For instance, in the example above, if an individual had an atrial rate of 300 beats per minute, the accessory bundle may conduct all the electrical impulses from the atria to the ventricles, causing the ventricles to activate at 300 beats per minute. Because the ventricles are the main pumping chambers of the heart, the body depends on the proper filling and emptying (contraction) of them. When conducted too rapidly (i.e. 300 beats per minute), the body would become hemodynamically unstable. If not corrected quickly, the ventricles could then fibrillate causing VF (ventricular fibrillation) – leading to sudden cardiac death (SCD).

Fortunately this proved not to be the case. Following the advent of His-bundle recordings further studies demonstrated that these patients simply have more rapid AV nodal conduction but that decremental AV nodal conduction is still present. These patients do not carry an increased sudden death risk. Their risk of SVT is no different from the general population. Since this is now known to be an EKG variant without adverse prognosis, the diagnosis of LGL Syndrome has been abandoned in electrophysiology.


LGL syndrome was diagnosed on the basis of the surface EKG in an asymptomatic individual with a PR interval less than or equal to 0.12 second (120 ms) with normal QRS complex duration. It can be distinguished from WPW syndrome because the delta waves seen in WPW syndrome are not seen in LGL syndrome as there is normal ventricular activation.

See also


  1. Rull G (2009). "Lown–Ganong–Levine Syndrome". Patient UK. EMIS. Retrieved 2011-05-29.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
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