Lown-Ganong-Levine syndrome: Difference between revisions

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In [[cardiology]], '''Lown-Ganong-Levine syndrome''' is "a form of [[Pre-excitation syndrome|ventricular pre-excitation]] characterized by a short PR interval and a normal QRS complex. In this syndrome, the atrial impulse conducts via [a nonstandard pathway] which connect the atrium to bundle of [[bundle of His]] bypassing the upper [[atrioventricular node]]. [[Heart ventricles]] are depolarized normally through the His-Purkinje system."<ref>{{MeSH}}</ref>  It may not be diagnosed until well into adulthood, but it can produce bursts of dizziness or fainting through paroxysmal tachycardia.  A broader term for conditions including the syndrome is enhanced atrioventricular nodal conduction, (EAVNC)<ref></ref>, which defines a continuum containing "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."<ref>{{citation
In [[cardiology]], '''Lown-Ganong-Levine syndrome''' is "a form of [[Pre-excitation syndrome|ventricular pre-excitation]] characterized by a short PR interval and a normal QRS complex. In this syndrome, the atrial impulse conducts via [a nonstandard pathway] which connect the atrium to bundle of [[bundle of His]] bypassing the upper [[atrioventricular node]]. [[Heart ventricles]] are depolarized normally through the His-Purkinje system."<ref>{{MeSH}}</ref>  It may not be diagnosed until well into adulthood, but it can produce bursts of dizziness or fainting through paroxysmal tachycardia.  A broader term for conditions including the syndrome is enhanced atrioventricular nodal conduction, (EAVNC), which defines a continuum containing "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."<ref>{{citation
  | url = http://circ.ahajournals.org/cgi/reprint/67/2/441
  | url = http://circ.ahajournals.org/cgi/reprint/67/2/441
  | title = Reevaluation of enhanced atrioventricular nodal conduction: evidence to suggest a continuum of normal atrioventricular nodal physiology.
  | title = Reevaluation of enhanced atrioventricular nodal conduction: evidence to suggest a continuum of normal atrioventricular nodal physiology.
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  | author = Durrer D, Schuilenburg RM, Wellens HJ}}</ref> Mahaim fibers,<ref>Mahaim I. Kent fibers and the A-V paraspecific conduction through the upper connections of the bundle of His-Tawara. Am Heart J. 1947;33:651.</ref> Brechenmacher-type fibers,<ref>Brechenmacher C, Laham J, Iris L, et al. [Histological study of abnormal conduction pathways in the Wolff-Parkinson-White syndrome and Lown-Ganong-Levine syndrome]. Arch Mal Coeur Vaiss. May 1974;67(5):507-19.</ref> and an anatomically underdeveloped (hypoplastic)<ref>Ometto R, Thiene G, Corrado D, et al. Enhanced A-V nodal conduction (Lown-Ganong-Levine syndrome) by congenitally hypoplastic A-V node. Eur Heart J. Nov 1992;13(11):1579-84.</ref> or small AV node.<ref>Benditt DG, Pritchett LC, Smith WM, et al. Characteristics of atrioventricular conduction and the spectrum of arrhythmias in Lown-Ganong-Levine syndrome. Circulation. Mar 1978;57(3):454-65. </ref>
  | author = Durrer D, Schuilenburg RM, Wellens HJ}}</ref> Mahaim fibers,<ref>Mahaim I. Kent fibers and the A-V paraspecific conduction through the upper connections of the bundle of His-Tawara. Am Heart J. 1947;33:651.</ref> Brechenmacher-type fibers,<ref>Brechenmacher C, Laham J, Iris L, et al. [Histological study of abnormal conduction pathways in the Wolff-Parkinson-White syndrome and Lown-Ganong-Levine syndrome]. Arch Mal Coeur Vaiss. May 1974;67(5):507-19.</ref> and an anatomically underdeveloped (hypoplastic)<ref>Ometto R, Thiene G, Corrado D, et al. Enhanced A-V nodal conduction (Lown-Ganong-Levine syndrome) by congenitally hypoplastic A-V node. Eur Heart J. Nov 1992;13(11):1579-84.</ref> or small AV node.<ref>Benditt DG, Pritchett LC, Smith WM, et al. Characteristics of atrioventricular conduction and the spectrum of arrhythmias in Lown-Ganong-Levine syndrome. Circulation. Mar 1978;57(3):454-65. </ref>


Current thinking is that treatment is only relevant in the context of symptomatic tachycardia and syncope. <ref>{{citation
| title = Lown-Ganong-Levine Syndrome: Treatment & Medication
| author = Daniel M Beyerbach,  Christopher Cadman
| date = 4 September 2009
| url =http://emedicine.medscape.com/article/160097-treatment
| journal = eMedicine}}</ref>
==References==
==References==
{{reflist|2}}
{{reflist|2}}

Latest revision as of 13:48, 23 June 2010

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In cardiology, Lown-Ganong-Levine syndrome is "a form of ventricular pre-excitation characterized by a short PR interval and a normal QRS complex. In this syndrome, the atrial impulse conducts via [a nonstandard pathway] which connect the atrium to bundle of bundle of His bypassing the upper atrioventricular node. Heart ventricles are depolarized normally through the His-Purkinje system."[1] It may not be diagnosed until well into adulthood, but it can produce bursts of dizziness or fainting through paroxysmal tachycardia. A broader term for conditions including the syndrome is enhanced atrioventricular nodal conduction, (EAVNC), which defines a continuum containing "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."[2]

A variety of supraventricular tachycardias can come from pathology where there is an abnormal conduction path, a normal one only, or both; the diagnosis may require invasive electrophysiological studies of the heart.[3] This has been reported in Wolff-Parkinson-White syndrome as well as Lown-Ganong-Levine. [4]

The pathological pathway may involve James fibers[5] Mahaim fibers,[6] Brechenmacher-type fibers,[7] and an anatomically underdeveloped (hypoplastic)[8] or small AV node.[9]

Current thinking is that treatment is only relevant in the context of symptomatic tachycardia and syncope. [10]

References

  1. Anonymous (2024), Lown-Ganong-Levine syndrome (English). Medical Subject Headings. U.S. National Library of Medicine.
  2. Jackman WM; Prystowsky EN; Naccarelli GV; Fineberg NS; Rahilly GT; Heger JJ; Zipes DP (1983), "Reevaluation of enhanced atrioventricular nodal conduction: evidence to suggest a continuum of normal atrioventricular nodal physiology.", Circulation 67 (2): 441-8
  3. Benditt DG et al. (August 1, 1979), "Ventriculoatrial Intervals: Diagnostic Use in Paroxysmal Supraventricular Tachycardia", Ann Internal Medicine 91 (2): 161-166
  4. D E Ward, A J Camm, and R A Spurrell (1978 October), "Re-entrant tachycardia using two bypass tracts and excluding AV node in short PR interval, normal QRS syndrome.", Br Heart J. 40 (10): 1127–1133
  5. Durrer D, Schuilenburg RM, Wellens HJ (1970 Jun), "Pre-excitation revisited", Am J Cardiol 25 (6): 690-7.
  6. Mahaim I. Kent fibers and the A-V paraspecific conduction through the upper connections of the bundle of His-Tawara. Am Heart J. 1947;33:651.
  7. Brechenmacher C, Laham J, Iris L, et al. [Histological study of abnormal conduction pathways in the Wolff-Parkinson-White syndrome and Lown-Ganong-Levine syndrome]. Arch Mal Coeur Vaiss. May 1974;67(5):507-19.
  8. Ometto R, Thiene G, Corrado D, et al. Enhanced A-V nodal conduction (Lown-Ganong-Levine syndrome) by congenitally hypoplastic A-V node. Eur Heart J. Nov 1992;13(11):1579-84.
  9. Benditt DG, Pritchett LC, Smith WM, et al. Characteristics of atrioventricular conduction and the spectrum of arrhythmias in Lown-Ganong-Levine syndrome. Circulation. Mar 1978;57(3):454-65.
  10. Daniel M Beyerbach, Christopher Cadman (4 September 2009), "Lown-Ganong-Levine Syndrome: Treatment & Medication", eMedicine