eMedicine Specialties > Cardiology > Arrhythmias

Lown-Ganong-Levine Syndrome

Daniel M Beyerbach, MD, PhD,, Consulting Staff, Florida Electrophysiology Associates; Affiliate Clinical Assistant Professor of Biomedical Science, Florida Atlantic University, Regional Campus of University of Miami Miller School of Medicine
Christopher Cadman, MD, Director of Arrhythmia Service, Assistant Professor, Department of Internal Medicine, Division of Cardiology, University of New Mexico

Updated: Sep 4, 2009

Introduction

Background

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. LGL is usually categorized in a class of preexcitation syndromes that includes the Wolff-Parkinson-White syndrome (WPW), LGL, and Mahaim-type preexcitation. 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.

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.¹ This syndrome was again described in 1952 by Lown, Ganong, and Levine, whose names form the eponym now used to describe it.² 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.³ In 1961, James described fibers that originate in the low atrium and terminate low in the AV node.⁴ Brechenmacher et al reported anatomic findings of an AH bundle in 1974.⁵ 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.⁶

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.^2,7,8

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 atrioventricular nodal conduction.

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.⁹

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.

Pathophysiology

The syndrome described by Lown, Ganong, and Levine in 1952 associated the occurrence of tachycardia with presence of a short PR interval and normal QRS. Subsequent investigations have failed to identify a unifying anatomic basis that accounts for both occurrence of tachycardia and presence of a short PR interval. Rather, several mechanisms have been proposed for the coexistence of a short PR interval and normal QRS^10,11,12 , while the occurrence of tachycardias has separately been found to be largely based on previously identified conditions, such as AV nodal reentry tachycardia, atrial fibrillation, and ventricular tachycardia.^13,14

No single structural anomaly has been implicated directly as the cause of the short PR interval and normal QRS in LGL. Indeed, most authors believe that LGL does not exist as a phenomenon separate from other known conditions. Several structural anomalies have been proposed as the possible basis for LGL,^15,16 including the presence of James fibers,¹⁷ Mahaim fibers,¹⁸ Brechenmacher-type fibers,⁵ and an anatomically underdeveloped (hypoplastic)¹⁹ or small AV node.^20,13

James fibers run from the upper portion of the AV node and insert into the lower portion of the AV node, or into the bundle of His.⁴ Thus, conduction over James fibers bypasses some of the intrinsic AV nodal delay, which shortens the PR interval; the QRS configuration remains normal, as ventricular activation occurs normally via His-Purkinje system. 

Mahaim fibers are muscular bridges, almost exclusively right-sided in occurrence, that may originate in the lower portion of the AV node, the upper portion of the bundle of His, or the bundle branches. Mahaim fibers terminate in the interventricular septum or in a bundle branch. 

Brechenmacher described fibers that run from the atrium to the His bundle, bypassing the AV node altogether. 

Each of these fibers has been identified histologically. However, none of these anomalous communications has been uniquely linked to the presence of LGL. Moreover, the histologic presence of fibers does not speak to whether these fibers are functional, with conductive properties.

EAVNC has been investigated as a possible functional basis for LGL.²¹ The criteria for EAVNC were established arbitrarily on the basis of observations of some patients with what seemed to be abnormally rapid AV nodal conduction times. However, in 1980, Bauernfeind and colleagues described a unimodal distribution of PR intervals in a series of 65 patients with AV nodal reentrant tachycardia.²²  

Further, in 1983 Jackman et al provided convincing evidence that EAVNC does not exist as a phenomenon separate from normal AV nodal physiology, but that AV nodal conduction physiology comprises a spectrum of AH intervals.⁹ In their series of 160 consecutive patients, they failed to identify a distinct group of patients with abnormally rapid AV nodal conduction. Rather, they found a broad spectrum of AH intervals in a unimodal, continuous distribution. Importantly, among patients with dual pathways, patients with shorter AH intervals do have a greater likelihood of developing AV nodal reentrant tachycardia.²³

The modern view of LGL is that no convincing evidence suggests that this is a syndrome separate from other known phenomena. LGL was identified as a clinical syndrome prior to the advent of catheter-based electrophysiologic (EP) studies. EP studies and histopathologic studies have identified several underlying mechanisms that can account for the presence of a short PR interval and normal QRS. These mechanisms include enhanced AV nodal conduction, several types of fibers that bypass all or part of the AV node, and an anatomically small AV node. Studies incorporating electrophysiologic data have separately identified several types tachycardias that occur in patients with LGL. The most common tachycardias include AV nodal reentry, accessory pathway mediated tachycardia, atrial fibrillation, atrial flutter, and ventricular tachycardia.^24,21  

To date, the underlying mechanisms that generate a short PR interval in LGL have not been found to be necessary for the development of the tachycardias identified in patients with LGL. In the case of enhanced AV nodal conduction, the short PR interval reflects anterograde conduction over the fast AV nodal pathway; however, during the most common form of AV nodal reentry, which is the most common tachycardia in patients with LGL, conduction occurs anterograde over the AV nodal slow pathway and retrograge up the AV nodal fast pathway. 

Enhanced conduction over the fast pathway is not necessary for existence of the tachycardia (normal fast pathway conduction would suffice). Even the rate of the tachycardia is largely determined by slow pathway conduction, which is independent of the short PR interval mechanism.²²  Similarly, the presence of fibers that bypass all or part of the AV node is not necessary for the occurrence of atrial fibrillation or atrial flutter; functionally, these fibers may facilitate more rapid conduction of atrial arrhythmias to the ventricles. 

In summary, LGL is a clinical diagnosis born of the era before EP study. Many mechanisms have been identified to describe the coexistence of a short PR interval and normal QRS and many tachycardias have been identified in patients with LGL. However, none of the identified short PR interval mechanisms is necessary for the generation of LGL tachycardias.

Frequency

United States

Lown and associates described tachyarrhythmias in 17% of patients with a short PR interval.² Some 2-4% of the adult population has a PR interval less than or equal to 0.12 second.²¹ Taken together, these data provide an estimate of the frequency of LGL as 0.5% of the adult population.

International

Frequency mirrors that in the United States.

Mortality/Morbidity

Paroxysms of tachycardia represent the primary morbidity of LGL. Few data are available regarding the frequency of these paroxysms. Data regarding mortality from LGL are scant. In their original report, Lown, Ganong, and Levine reported 6 patients with paroxysmal atrial fibrillation, 2 of whom suffered sudden cardiac death.²  Numbers in published studies are too small to estimate mortality rate with significant accuracy or confidence. In the absence of significant structural heart disease, the mortality rate appears to be very low.

Sex

In their 1952 manuscript, Lown, Ganong, and Levine reported 70.9% of their 34 cases to have occurred in women.²

Age

The average age of onset of tachycardia in LGL is 33.5 years.²

Clinical

History

Symptoms of paroxysmal tachycardia must be elicited. Manifestations of such paroxysms include palpitations, lightheadedness, and shortness of breath. In cases of underlying structural heart disease or coronary artery disease, episodes of tachycardia may induce cardiac stress and produce symptoms of chest pain or possibly of hypotension or other hemodynamic instability. At higher ventricular rates, syncope may occur, particularly if ventricular tachycardia or ventricular fibrillation are initiated.

Physical

An accentuated first heart sound of mitral valve closure may be present in 87% of cases.²  During paroxysms of tachycardia, cardiovascular examination may reveal a rapid heart rate. Absence of a rapid heart rate does not exclude LGL as a possible diagnosis, as the tachycardia of LGL is paroxysmal.

Causes

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.

Differential Diagnoses

Other Problems to Be Considered

Sinoatrial reentrant tachycardia
Mahaim-type preexcitation
Sinus tachycardia
Atypical AV nodal reentrant tachycardia
Persistent form of juvenile reentrant tachycardia

Workup

Laboratory Studies

• Workup is directed at determining the cause of tachycardia. LGL is an outdated diagnosis, and as such no workup is directed at making this diagnosis. However, identification of a short PR interval during sinus rhythm in a patient with paroxysmal supraventricular tachycardia (PSVT) should raise suspicion of a possible underlying bypass tract (ie, WPW). In the case of isolated short PR interval with no history of tachycardia or symptoms suggestive of paroxysms of tachycardia, no further workup is indicated.
• Patients may present in an acute episode of tachycardia or with a history of symptoms suggestive of paroxysms of tachycardia.
  • In the acute setting, institute a standard workup for tachycardia, including an ECG to document the rhythm, serum electrolytes, calcium, magnesium levels, and serum thyroid-stimulating hormone (TSH) levels.
  • For a history suggestive of recurrent paroxysms of tachycardia, a Holter monitor or event recorder may prove useful for documenting the rhythm during acute symptomatic episodes. Less commonly, particularly when paroxysms of tachycardia are more rare, an implantable loop recorder may prove helpful.

Imaging Studies

• In the case of shortness of breath, posteroanterior and lateral chest films are indicated.

Other Tests

• To meet criteria for LGL, the 12-lead ECG taken during a period of normal sinus rhythm must demonstrate a PR interval less than or equal to 0.12 second and a normal QRS upstroke and duration (see Media file 1).
  
  

  

  ECG demonstrating a short PR interval of approximately 100 ms and normal QRS.

  
  
• One of the most useful diagnostic tools is a 12-lead ECG recorded during a paroxysm of tachycardia. Such documentation satisfies the LGL criterion of tachycardia.
• A delta wave on the QRS complex precludes the diagnosis of LGL, because one of the criteria for LGL is a normal QRS complex. A delta wave suggests the presence of an accessory pathway; occurrence of supraventricular tachycardia in the presence of an accessory pathway suggests WPW, another preexcitation syndrome (see Media file 2).
  
  

  

  ECG demonstrating ventricular preexcitation. A delta wave, which corresponds to initial myocardial depolarization via a bypass tract, appears at the beginning of each QRS complex.

  
  

Procedures

• If tachycardia is present, diagnostic workup to determine the cause may include Valsalva maneuvers.
• If blood pressure is stable, the patient has no angina, is not presyncopal, and no carotid bruits are present, carotid massage may provide diagnostic information. Ideally, carotid massage should be performed during continuous 12-lead rhythm strip monitoring. The result of carotid massage may be termination of the tachycardia, or transient AV block that may provide a ventricular pause long enough to reveal an underlying atrial arrhythmia.
• If these maneuvers fail to terminate the tachycardia, a trial of intravenous adenosine administration, again with simultaneous rhythm strip recording, may reveal the rhythm.  Adenosine should not be administered if there is any indication of pre-excitation on the surface ECG.
• In cases of recurrent tachycardia, an invasive electrophysiology study is warranted.  This is particularly true when symptoms become intolerable, medical therapy is failing to prevent episodes of tachycardia, or when a ventricular arrhythmia is suspected.

Treatment

Medical Care

In the outpatient setting, empiric therapies for recurrent PSVT may be instituted. These therapies may include beta-blockers, calcium channel blockers, and digoxin. A full discussion of these therapies lies outside the scope of this article (see Paroxysmal Supraventricular Tachycardia).

Surgical Care

Rare patients for whom the criteria of LGL are met may have no inducibility of tachyarrhythmias by EP study. Rarely, medical therapy fails in these patients, who continue to have recurrent, intolerable symptoms. In such extreme cases, pacemaker implantation, followed by
radiofrequency (RF) ablation of the AV node or bundle of His may be considered.

Consultations

• Conditions appropriate for consideration of RF catheter ablation and referral to an electrophysiologist include the following:
  • Failure of pharmacologic therapy to control symptoms
  • Recurrence of any signs of hemodynamic instability or of intolerable symptoms under medical management
  • Patient's desire to avoid daily medication
  • Intolerable adverse effects of medication

Diet

No dietary restrictions are required.

Activity

Patients who have experienced an episode of syncope should be counseled to not drive or operate vehicles of public transport for 6 months from the time of the most recent episode of syncope, or until the cause of syncope has been identified and adequately treated.

Medication

No medication therapy is specific to LGL. The goals of therapy are to identify the cause of tachycardia and to treat this cause appropriately.

Beta-blockers

Inhibit chronotropic, inotropic, and vasodilatory responses to beta-adrenergic stimulation and slow AV nodal conduction.

Metoprolol (Lopressor, Toprol XL)

Selective beta1-adrenergic receptor blocker that decreases automaticity of contractions. During IV administration, carefully monitor BP, heart rate, and ECG.

Dosing

Adult

50 mg/d PO qd or divided bid/tid initially and increase at 1-wk intervals prn to total of 200 mg/d if necessary

Pediatric

1-5 mg/kg/24h PO divided bid

Interactions

Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels of metoprolol, possibly resulting in decreased pharmacologic effects
Sparfloxacin, phenothiazines, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives may increase toxicity
May increase toxicity of digoxin, flecainide, clonidine, epinephrine, nifedipine, prazosin, verapamil, and lidocaine

Contraindications

Documented hypersensitivity; uncompensated CHF; bradycardia; asthma; cardiogenic shock; AV conduction abnormalities

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Beta-adrenergic blockade may reduce signs and symptoms of acute hypoglycemia and may decrease clinical signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; monitor patient closely and withdraw the drug slowly; during IV administration, carefully monitor blood pressure, heart rate, and ECG

Atenolol (Tenormin)

Selectively blocks beta1-receptors with little or no effect on beta2 types.

Dosing

Adult

50 mg PO qd; increase to 100 mg/d if necessary

Pediatric

1-2 mg/kg/dose PO qd

Interactions

Aluminum salts, barbiturates, calcium salts, cholestyramine, NSAIDs, penicillins, and rifampin may decrease effects; haloperidol, hydralazine, loop diuretics, and MAOIs may increase toxicity

Contraindications

Documented hypersensitivity; CHF; pulmonary edema; cardiogenic shock; AV conduction abnormalities; heart block (without pacemaker)

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Beta-adrenergic blockade may reduce symptoms of acute hypoglycemia and mask signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism and cause thyroid storm; monitor patients closely and withdraw drug slowly; during IV, carefully monitor BP, heart rate, and ECG

Calcium channel blockers (nondihydropyridine)

In specialized conducting and automatic cells in the heart, calcium is involved in the generation of the action potential. Calcium channel blockers inhibit movement of calcium ions across the cell membrane, depressing both impulse formation (automaticity) and conduction velocity.

Verapamil (Calan, Covera, Isoptin)

Can diminish PVCs associated with perfusion therapy and decrease risk of ventricular fibrillation and ventricular tachycardia. By interrupting reentry at AV node, can restore normal sinus rhythm in patients with PSVT.

Dosing

Adult

80-120 mg PO tid or 120-360 mg SR formulation; alternatively, 5-10 mg IV followed by second dose 15-30 min later if PSVT does not respond satisfactorily to initial dose

Pediatric

Not established

Interactions

May increase carbamazepine, digoxin, and cyclosporine levels; amiodarone can cause bradycardia and decrease in cardiac output; beta-blockers may increase cardiac depression; cimetidine may increase levels; may increase theophylline levels

Contraindications

Documented hypersensitivity; severe CHF; sick sinus syndrome; second- or third-degree AV block; hypotension (<90 mm Hg systolic)

Precautions

Pregnancy

B - Usually safe but benefits must outweigh the risks.

Precautions

Hepatocellular injury may occur; transient elevations of transaminases with and without concomitant elevations in alkaline phosphatase and bilirubin have occurred (elevations have been transient and may disappear with continued treatment); monitor liver functions periodically

Diltiazem (Cardizem)

During depolarization, inhibits calcium ions from entering slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium.

Dosing

Adult

30-90 mg PO tid, or 120-300 mg PO qd of CD formulation

Pediatric

Not established

Interactions

May increase carbamazepine, digoxin, cyclosporine, and theophylline levels; amiodarone may cause bradycardia and decrease in cardiac output; beta-blockers may increase cardiac depression; cimetidine may increase levels

Contraindications

Documented hypersensitivity; severe CHF; sick sinus syndrome; second- or third-degree AV block; hypotension (<90 mm Hg systolic)

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Caution in impaired renal or hepatic function; may increase LFT levels, and hepatic injury may occur

Cardiac glycosides

Decrease AV nodal conduction, primarily by increasing vagal tone.

Digoxin (Lanoxin)

Cardiac glycoside with direct inotropic effects in addition to indirect effects on cardiovascular system. Acts directly on cardiac muscle, increasing myocardial systolic contractions. Indirect actions result in increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increase in mean arterial pressure.

Dosing

Adult

0.125-0.375 mg PO qd

Pediatric

<5 years: Not established
5-10 years: 20-35 mcg/kg loading dose PO
>10 years: 10-15 mcg/kg loading dose PO
Maintenance dose: 25-35% of PO loading dose administered qd

Interactions

Alprazolam, benzodiazepines, bepridil, captopril, cyclosporine, propafenone, propantheline, quinidine, diltiazem, aminoglycosides, oral amiodarone, anticholinergics, diphenoxylate, erythromycin, felodipine, flecainide, hydroxychloroquine, itraconazole, nifedipine, omeprazole, quinine, ibuprofen, indomethacin, esmolol, tetracycline, tolbutamide, and verapamil may increase levels
Aminoglutethimide, antihistamines, cholestyramine, neomycin, penicillamine, aminoglycosides, oral colestipol, hydantoins, hypoglycemic agents, antineoplastic treatment combinations (including carmustine, bleomycin, methotrexate, cytarabine, doxorubicin, cyclophosphamide, vincristine, procarbazine), aluminum or magnesium antacids, rifampin, sucralfate, sulfasalazine, barbiturates, kaolin/pectin, and aminosalicylic acid may decrease levels

Contraindications

Documented hypersensitivity; beriberi heart disease; idiopathic hypertrophic subaortic stenosis; constrictive pericarditis; carotid sinus syndrome

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Hypokalemia may reduce positive inotropic effect; IV calcium may produce arrhythmias in digitalized patients; hypercalcemia predisposes patient to digitalis toxicity, and hypocalcemia can make digoxin ineffective until serum calcium levels are normal; magnesium replacement therapy must be instituted in patients with hypomagnesemia to prevent digitalis toxicity; patients with incomplete AV block may progress to complete block when treated with digoxin; use caution in hypothyroidism, hypoxia, and acute myocarditis

Follow-up

Further Inpatient Care

• Admit patients in unstable condition to telemetry.
• Institute pharmacologic therapy as dictated by symptoms and documented tachycardia.
• Order consultations as discussed in Treatment.
• Consider exercise treadmill testing if tachycardia is induced by exercise.

Further Outpatient Care

• If no arrhythmia is documented on ECG or telemetry, and symptoms occur on a daily basis, consider Holter monitor with diary to document cardiac rhythm during symptomatic episodes.
• If no arrhythmia is documented on ECG or telemetry, and symptoms occur less frequently than daily, consider an event recorder to document cardiac rhythm during symptomatic episodes.
• If patient is in stable condition and does not require hospitalization, and if no tachyarrhythmia has been documented but symptoms are induced by exercise, consider outpatient exercise treadmill testing.
• If symptoms persist, but no tachyarrhythmia can be documented by any of these methods, consider referral to an electrophysiologist for an outpatient EP study.

Inpatient & Outpatient Medications

• Refer to section on Medical Care.

Complications

• Complications vary by the underlying condition.

Prognosis

• No studies have shown an increased risk of sudden death or decreased survival for patients meeting criteria for diagnosis of LGL.

Patient Education

• LGL is an outdated clinical diagnosis with no known unique underlying anatomic correlate. No specific risks are conferred with the diagnosis.
• For excellent patient education resources, visit eMedicine's Heart Center. Also, see eMedicine's patient education article Supraventricular Tachycardia.

Miscellaneous

Medicolegal Pitfalls

• Advise patients who have experienced syncope to not drive or operate vehicles of public transport for 6 months after the occurrence of the most recent episode of syncope, or until the cause of syncope has been identified and adequately treated. Within the United States, laws regarding restrictions on driving and operating vehicles of public transport after an episode of syncope vary by state.

Multimedia

Media file 1: ECG demonstrating a short PR interval of approximately 100 ms and normal QRS.

Media file 2: ECG demonstrating ventricular preexcitation. A delta wave, which corresponds to initial myocardial depolarization via a bypass tract, appears at the beginning of each QRS complex.

References

1. Clerc A, Levy R, Critesco C. A propos du raccourcissement permanent de l'espace P-R de l'electrocardiogramme sans deformation du complex ventriculaire. Arch Mal Coeur. 1938;31:569.

2. LOWN B, GANONG WF, LEVINE SA. The syndrome of short P-R interval, normal QRS complex and paroxysmal rapid heart action. Circulation. May 1952;5(5):693-706. [Medline].

3. Burch GE, Kimball JL. Notes on the similarity of QRS complex configuration in Wolff-Parkinson-White syndrome. Am Heart J. 1946;32:560.

4. James TN. Morphology of the human atrioventricular node, with remarks pertinent to its electrophysiology. Am Heart J. 1961;62:756-71.

5. 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. [Medline].

6. Josephson ME, Kastor JA. Supraventricular tachycardia in Lown-Ganong-Levine syndrome: atrionodal versus intranodal reentry. Am J Cardiol. Oct 1977;40(4):521-7. [Medline].

7. Chou TC. Wolff-Parkinson-White syndrome and its variants. In: Electrocardiography in Clinical Practice, Adult and Pediatric. 4th ed. Philadelphia:. WB Saunders Co;1996.

8. Moller P. Letter: Criteria for the LGL syndrome. Am Heart J. Apr 1976;91(4):539-41. [Medline].

9. Jackman WM, Prystowsky EN, Naccarelli GV, et al. Reevaluation of enhanced atrioventricular nodal conduction: evidence to suggest a continuum of normal atrioventricular nodal physiology. Circulation. Feb 1983;67(2):441-8. [Medline].

10. Ward DE, Camm AJ, Spurrell RA. Re-entrant tachycardia using two bypass tracts and excluding AV node in short PR interval, normal QRS syndrome. Br Heart J. Oct 1978;40(10):1127-33. [Medline].

11. Zipes DP, DeJoseph RL, Rothbaum DA. Unusual properties of accessory pathways. Circulation. Jun 1974;49(6):1200-11. [Medline].

12. Ward DE, Camm AJ, Spurrell RAJ. Dual AH pathways in patients with and without the Lown-Ganong-Levine syndrome. Br Heart J. 1981;45:356.

13. 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. [Medline].

14. Denes P, Wu D, Dhingra RC, et al. Demonstration of dual A-V nodal pathways in patients with paroxysmal supraventricular tachycardia. Circulation. Sep 1973;48(3):549-55. [Medline].

15. Mandel WJ, Danzig R, Hayakawa H. Lown-Ganong-Levine syndrome. A study using His bundle electrograms. Circulation. Oct 1971;44(4):696-708. [Medline].

16. Douglas JE, Mandel WJ, Danzig R, Hayakawa H. Lown-Ganong-Levine syndrome. Circulation. May 1972;45(5):1143-4. [Medline].

17. Durrer D, Schuilenburg RM, Wellens HJ. Pre-excitation revisited. Am J Cardiol. Jun 1970;25(6):690-7. [Medline].

18. 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.

19. 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. [Medline].

20. Caracta AR, Damato AN, Gallagher JJ, et al. Electrophysiologic studies in the syndrome of short P-R interval, normal QRS complex. Am J Cardiol. Feb 1973;31(2):245-53. [Medline].

21. Wiener I. Syndromes of Lown-Ganong-Levine and enhanced atrioventricular nodal conduction. Am J Cardiol. Sep 1 1983;52(5):637-9. [Medline].

22. Bauernfeind RA, Ayres BF, Wyndham CC, et al. Cycle length in atrioventricular nodal reentrant paroxysmal tachycardia with observations on the Lown-Ganong-Levine syndrome. Am J Cardiol. Jun 1980;45(6):1148-53. [Medline].

23. Bauernfeind RA, Swiryn S, Strasberg B, et al. Analysis of anterograde and retrograde fast pathway properties in patients with dual atrioventricular nodal pathways: observations regarding the pathophysiology of the Lown-Ganong-Levine syndrome. Am J Cardiol. Feb 1 1982;49(2):283-90. [Medline].

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Keywords

Lown-Gangong-Levine syndrome, LGL syndrome, Clerc-Levy-Critesco syndrome, enhanced atrioventricular nodal conduction, accelerated atrioventricular nodal conduction, short PR/normal QRS syndrome, short PR/narrow QRS syndrome, accessory pathway, WPW syndrome, Wolff-Parkinson-White syndrome

Contributor Information and Disclosures

Author

Daniel M Beyerbach, MD, PhD,, Consulting Staff, Florida Electrophysiology Associates; Affiliate Clinical Assistant Professor of Biomedical Science, Florida Atlantic University, Regional Campus of University of Miami Miller School of Medicine
Daniel M Beyerbach, MD, PhD, is a member of the following medical societies: American College of Cardiology
Disclosure: Nothing to disclose.

Coauthor(s)

Christopher Cadman, MD, Director of Arrhythmia Service, Assistant Professor, Department of Internal Medicine, Division of Cardiology, University of New Mexico
Christopher Cadman, MD is a member of the following medical societies: American College of Cardiology and Phi Beta Kappa
Disclosure: Nothing to disclose.

Medical Editor

Justin D Pearlman, MD, PhD, ME, MA, Director of Advanced Cardiovascular Imaging, Professor of Medicine, Professor of Radiology, Adjunct Professor, Thayer Bioengineering and Computer Science, Dartmouth-Hitchcock Medical Center
Justin D Pearlman, MD, PhD, ME, MA is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Federation for Medical Research, International Society for Magnetic Resonance in Medicine, and Radiological Society of North America
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Frank M Sheridan, MD, Cardiology, Providence Everett Medical Center
Frank M Sheridan, MD is a member of the following medical societies: American College of Cardiology, American Heart Association, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

Michael E Zevitz, MD, Assistant Professor of Medicine, Finch University of the Health Sciences, The Chicago Medical School; Consulting Staff, Private Practice
Michael E Zevitz, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Medical Association, and Michigan State Medical Society
Disclosure: Nothing to disclose.

Christopher Cadman, MD, contributed to the original version of this article.

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