Lown-Ganong-Levine syndrome: Difference between revisions

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=== Laboratory Findings ===
=== Laboratory Findings ===
*There are no specific laboratory findings associated with [disease name].
*There are no specific laboratory findings associated with LGL syndrome.


*A  [positive/negative] [test name] is diagnostic of [disease name].
*An [elevated/reduced] concentration of [serum/blood/urinary/CSF/other] [lab test] is diagnostic of [disease name].
*Other laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].
===Imaging Findings===
===Imaging Findings===
*There are no [imaging study] findings associated with [disease name].
*There are no [imaging study] findings associated with [disease name].

Revision as of 07:21, 20 August 2020

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Usman Ali Akbar, M.B.B.S.[2]

Overview

Historical Perspective

Historical timeline of LGL Syndrome
Year Description
1938 Clerc, Levy and Critesco in 1938 first reported cases in which there was occurence of frequent paroxysms of tachycardia. The EKG of such patients consist of a short PR interval and normal QRS interval
1946 Burch and Kimball hinted on existence of the atrio-Hisian pathway
1952 The Lown-Ganong-Levine (LGL) pattern was described in 1952 by Bernard Lown, William Francis Ganong and Samual Levine.
1961,1974 In 1961 and subsequently in 1974 anatomic pathway was identified and reported by James and Brechemacher respectively.

Classification

  • LGL syndrome can be classified based on the accessory pathways into following categories
Accessory Pathway Description
James Fibers They can be present as normal part of AV node but these fibers have been established as anatomic reason for LGL syndrome
Brechmacher fibers These atrio-Hisian tracts are reported to have a frequency of 0.03 % and can be theoratically a cause of LGL syndrome
Intra-nodal bypass tracts Intra-nodal bypass tracts would allow the conduction of rapid action potential through AV node bypassing the other slow pathways.

Pathophysiology

  • The pathophysiology of LGL syndrome has not yet been completely understood.
  • Multiple theories have been proposed to suggest the mechanism of LGL.
  • The current theory supporting the mechanism of LGL is that it may result from numerous underlying causes that involve junctional pathways that partially or wholly bypass the AV node with subsequent normal conduction down the bundle of His.
  • The three accessory pathways as discussed in classification has been proposed to be the main triggering factors for the development of LGL.
  • Lown-Ganong-Levine pattern may occur include Brechenmacher fibers or intranodal bypass tracts and James Fibers. Brenchmacher fibers account for 0.03% of the patients presenting with LGL.
  • The intra-nodal bypass tracts allow the conduction of rapid action potential through AV-node bypassing the other slow pathways.

Clinical Features

The clinical features of LGL overlap with other pre-excitation syndromes. Patient can present with following features.

  • Palpitations
  • Lightheadedness
  • Shortness of breath.
  • Syncope
  • In case of an underlying cardiac structural defect, it can also present with chest pain or episodes of tachycardia.

Differentiating [disease name] from other Diseases

The differential diagnosis for Lown-Ganong-Levine includes

  • Supraventricular tachycardia
  • Atrial fibrillation or flutter with a rapid ventricular response
  • AV nodal reentry tachycardia
  • Wolf-Parkinson-White Syndrome

Epidemiology and Demographics

  • The Lown-Ganong-Levine pattern does not show an increased incidence in one particular sex or ethnic background.
  • In a retrospective study conducted by Bernard Lown, William Francis Ganong and Samual Levine 200 electrocardiograms (EKG) of 13500 patients showed EKG findings with prevalence of just over 1%

Age

  • There is currently insufficient data regarding age predilection of LGL syndrome.

Gender

  • There is currently insufficient data regarding gender predilection of LGL syndrome.However, Lown in 1952 reported 70.9% of the 34 cases in women.

Race

  • There is currently insufficient data regarding race predilection of LGL syndrome.].

Risk Factors

The data regarding the risk factors predisposing to LGL syndrome is insufficient. However following conditions or factor may lead to various pre-excitation syndromes.

  • Presence of accessory bypass tracts
  • High risk population for sudden cardiac death in Pre-excitation syndromes include
    • Policemen
    • Athletes
    • Firemen
    • Pilots
    • Steelworkers

Natural History, Complications and Prognosis

Natural History

  • LGL syndrome can be asymptomatic or can present with palpitations, lightheadedness, shortness of breath, and syncope. In the case of congenital heart disease or genetic anomaly, it can also present as paroxysms of tachycardia or chest pain.

Complications

  • There is an increased risk of developing tachyarrythmias.
  • Certain medications such as sympathomimetics should be used with caution in the patients of LGL syndrome. Digitalis does not have any effect in LGL syndrome but it can slow conduction via the AV-node. This can prevent AVRT in these patients.
  • Beta-blockers do not affect the accessory pathway directly but can slow conduction through AV node similar to digitalis.

Prognosis=

There is an overall good prognosis in patients with LGL syndrome. Patients are usually asymptomatic but some can develop certain clinical features such as palpitations, shortness of breath, and occasional episodes of atrial fibrillation, atrial flutter, AVRT, and other tachyarrhythmias. They can also lead to the development of ventricular arrhythmias in rare cases.[1]

Diagnosis

Diagnostic Criteria

Characteristic ECG findings of LGL syndrome are

  • Short PR interval (<120ms)
  • Normal P wave axis
  • Normal/narrow QRS morphology in the presence of paroxysmal tachyarrhythmia.

Symptoms

  • LGL syndrome is usually asymptomatic.
  • Symptoms of LGL syndrome may include the following:
  • palpitations
  • chest pain
  • dizziness
  • lightheadedness
  • shortness of breath
  • Racing heart

Physical Examination

  • Patients with LGL syndrome usually appear normal.
  • Physical examination findings are limited in LGL syndrome.
  • During cardiac auscultation or palpation of peripheral pulses, there can be irregular rhythm.

Laboratory Findings

  • There are no specific laboratory findings associated with LGL syndrome.

Imaging Findings

  • There are no [imaging study] findings associated with [disease name].
  • [Imaging study 1] is the imaging modality of choice for [disease name].
  • On [imaging study 1], [disease name] is characterized by [finding 1], [finding 2], and [finding 3].
  • [Imaging study 2] may demonstrate [finding 1], [finding 2], and [finding 3].

Other Diagnostic Studies

  • [Disease name] may also be diagnosed using [diagnostic study name].
  • Findings on [diagnostic study name] include [finding 1], [finding 2], and [finding 3].

Treatment

Medical Therapy

  • There is no treatment for [disease name]; the mainstay of therapy is supportive care.
  • The mainstay of therapy for [disease name] is [medical therapy 1] and [medical therapy 2].
  • [Medical therapy 1] acts by [mechanism of action 1].
  • Response to [medical therapy 1] can be monitored with [test/physical finding/imaging] every [frequency/duration].

Surgery

  • Surgery is the mainstay of therapy for [disease name].
  • [Surgical procedure] in conjunction with [chemotherapy/radiation] is the most common approach to the treatment of [disease name].
  • [Surgical procedure] can only be performed for patients with [disease stage] [disease name].

Prevention

  • There are no primary preventive measures available for [disease name].
  • Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].
  • Once diagnosed and successfully treated, patients with [disease name] are followed-up every [duration]. Follow-up testing includes [test 1], [test 2], and [test 3].

References

  1. Benditt, D G; Pritchett, L C; Smith, W M; Wallace, A G; Gallagher, J J (1978). "Characteristics of atrioventricular conduction and the spectrum of arrhythmias in lown-ganong-levine syndrome". Circulation. Ovid Technologies (Wolters Kluwer Health). 57 (3): 454–465. doi:10.1161/01.cir.57.3.454. ISSN 0009-7322. PMID 624155.

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