Lown-Ganong-Levine syndrome: Difference between revisions

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{{Infobox_Disease |
  Name          = {{PAGENAME}} |
  Image          = |
  Caption        = |
  DiseasesDB    = 7599 |
  ICD10          = {{ICD10|I|45|6|i|30}}  |
  ICD9          = {{ICD9|426.81}} |
  ICDO          = |
  OMIM          = 108950 |
  MedlinePlus    = |
  eMedicineSubj  = |
  eMedicineTopic = |
  MeshID        = D008151 |
}}
{{SI}}
{{WikiDoc Cardiology Network Infobox}}
{{CMG}}
__NOTOC__
__NOTOC__
{{Lown-Ganong-Levine syndrome}}
                                                                 
{{CMG}} {{AE}} {{Usman Ali Akbar}}
{{SK}} Lown-Ganong-Levine [[Syndrome]], LGL syndrome, [[Pre-excitation syndrome|Pre-excitation syndromes]], [[Short PR interval|Short PR]] [[Normal]] [[QRS complex|QRS Complex]] [[Syndrome]], Clerc-Lévy-Cristesco syndrome, [[Coronary]] [[Node (physics)|nodal]] [[rhythm]] [[syndrome]], Short PQ [[Interval (mathematics)|interval]] [[syndrome]], Short [[P-R interval|P-R]] [[syndrome]].
==Overview==
==Overview==
'''Lown-Ganong-Levine syndrome''' ('''LGL''') is a syndrome of pre-excitation of the [[Ventricle (heart)|ventricles]] due to an accessory pathway providing an abnormal electrical communication from the [[atrium (anatomy)|atria]] to the ventricles. It is grouped with [[Wolff-Parkinson-White syndrome]] as an atrioventricular re-entry tachycardia (AVRT).
Lown-Ganong-Levine [[syndrome]] (LGL) is actually a [[pre-excitation syndrome|pre-excitation syndrome]] with [[EKG]] findings including short [[PR interval]], narrow or [[normal]] [[QRS complex]], and a [[normal]] [[P wave]]. It is [[Causes|caused]] by the [[Presenting symptom|presence]] of [[accessory]] [[Bundle branch|bundles]] of [[Fiber|fibers]] known as [[James fibers]] which lead to the [[development]] of [[abnormal]] [[Conduction System|conduction pathways]]. The LGL [[syndrome]] was named after Bernard Lown, William Francis Ganong, and Samual Levine who described it in 1952. [[Patients]] of LGL usually [[Presenting symptom|present]] with a [[History and Physical examination|history]] of [[Palpitation|palpitations]], [[lightheadedness]], [[shortness of breath]], and sometimes [[chest pain]]. There is an increased [[RiskMetrics|risk]] of [[tachyarrhythmias]] and [[syncope]]. [[EKG]] is the principal [[modality]] of [[Investigational product|investigation]] for establishing a [[diagnosis]]. Usually, [[antiarrhythmics]] are given to [[Prevention|prevent]] the [[Development (biology)|development]] of [[tachyarrhythmias]] but recently [[radiofrequency ablation]] of the [[accessory pathways]] has been the mainstay of [[treatment]] with a good [[prognosis]].
 
==Historical Perspective==
 
*Following is the timeline of LGL [[syndrome]] with its discovery and [[Development|developments]] of its [[Bypass tract|bypass tracts]]:<ref name="LOWN GANONG LEVINE 1952 pp. 693–706">{{cite journal | last=LOWN | first=BERNARD | last2=GANONG | first2=WILLIAM F. | last3=LEVINE | first3=SAMUEL A. | title=The Syndrome of Short P-R Interval Normal QRS Complex and Paroxysmal Rapid Heart Action | journal=Circulation | publisher=Ovid Technologies (Wolters Kluwer Health) | volume=5 | issue=5 | year=1952 | issn=0009-7322 | pmid=14926053 | doi=10.1161/01.cir.5.5.693 | pages=693–706}}</ref><ref name="Manning 1978 pp. 576–577">{{cite journal | last=Manning | first=G W | title=Lown-Ganong-Levine syndrome. | journal=Circulation | publisher=Ovid Technologies (Wolters Kluwer Health) | volume=58 | issue=3 | year=1978 | issn=0009-7322 | pmid=679452 | doi=10.1161/01.cir.58.3.576 | pages=576–577}}</ref><ref name="DOUGLAS 1972 pp. 1143–1144">{{cite journal | last=DOUGLAS | first=JOHN E. | title=Lown-Ganong-Levine Syndrome | journal=Circulation | publisher=Ovid Technologies (Wolters Kluwer Health) | volume=45 | issue=5 | year=1972 | issn=0009-7322 | pmid=5020803 | doi=10.1161/01.cir.45.5.1143 | pages=1143–1144}}</ref>
 
{| class="wikitable"
|+Historical timeline of LGL Syndrome
! style="background:#4479BA;width:200px; color: #FFFFFF;" + |Year
! style="background:#4479BA;width:200px; color: #FFFFFF;" + |Description
|-
| align="center" style="background:#DCDCDC;" + |'''1938'''
|
*Clerc, Levy, and Critesco in 1938 first [[Reporting results|reported]] [[Case Report Form|cases]] in which there was an occurrence of frequent [[Paroxysm|paroxysms]] of [[tachycardia]].
*The [[EKG]] of such [[patients]] consisted of a [[short PR interval]] and a [[normal]] [[QRS Interval|QRS interval]].
|-
| align="center" style="background:#DCDCDC;" + |'''1946'''
|
*Burch and Kimball hinted about the existence of the [[Atrio-Hisian fibers|Atrio-Hisian pathway.]]
|-
| align="center" style="background:#DCDCDC;" + |'''1952'''
|
*The Lown-Ganong-Levine (LGL) [[pattern]] was described in 1952 by Bernard Lown, William Francis Ganong, and Samual Levine.
|-
| align="center" style="background:#DCDCDC;" + |'''1961-1974'''
|
*In 1961 and subsequently, in 1974, an [[anatomic]] pathway was identified and reported by James and Brechemacher respectively.
|}
[[File:Timeline-LGL.jpg|600px|thumb|none|Historic Timeline of LGL Syndrome]]
 
==Classification==
 
*LGL [[syndrome]] can be [[Classification|classified]] based on the [[accessory pathways]] into the following categories:<ref name="LOWN GANONG LEVINE 1952 pp. 693–706">{{cite journal | last=LOWN | first=BERNARD | last2=GANONG | first2=WILLIAM F. | last3=LEVINE | first3=SAMUEL A. | title=The Syndrome of Short P-R Interval Normal QRS Complex and Paroxysmal Rapid Heart Action | journal=Circulation | publisher=Ovid Technologies (Wolters Kluwer Health) | volume=5 | issue=5 | year=1952 | issn=0009-7322 | pmid=14926053 | doi=10.1161/01.cir.5.5.693 | pages=693–706}}</ref><ref name="Manning 1978 pp. 576–577">{{cite journal | last=Manning | first=G W | title=Lown-Ganong-Levine syndrome. | journal=Circulation | publisher=Ovid Technologies (Wolters Kluwer Health) | volume=58 | issue=3 | year=1978 | issn=0009-7322 | pmid=679452 | doi=10.1161/01.cir.58.3.576 | pages=576–577}}</ref>
 
{| class="wikitable"
|+
! style="background:#4479BA;width:200px; color: #FFFFFF;" + |Accessory Pathway
! style="background:#4479BA;width:200px; color: #FFFFFF;" + |Description
|-
| align="center" style="background:#DCDCDC;" + |'''[[James fibers]]'''
|
*They can be [[Presenting symptoms|present]] as a [[normal]] part of the [[AV node]] but these [[Fiber|fibers]] have been established as an [[anatomic]] [[Reasoning|reason]] for LGL [[syndrome]].
|-
| align="center" style="background:#DCDCDC;" + |'''[[Brechenmacher fibers]]'''
|
*These [[Atrio-Hisian fibers|atrio-Hisian tracts]] have a [[frequency]] of 0.03% and contribute theoretically towards LGL [[syndrome]].
|-
| align="center" style="background:#DCDCDC;" + |'''Intra-[[Node (physics)|nodal]] [[Bypass tract|bypass tracts]]'''
|
*The intra-[[Node (physics)|nodal]] [[Bypass tract|bypass tracts]] allow the [[Conduction System|conduction]] of rapid [[action potential]] through [[Atrioventricular node|AV node]] [[Bypass|bypassing]] other pathways with [[slow]] [[Conduction System|conduction]].
|}


==Pathophysiology==
==Pathophysiology==


In normal individuals, electrical activity in the heart is initiated in the [[sinoatrial node|sinoatrial]] (SA) node (located in the [[right atrium]]), propagates to the [[atrioventricular node| atrioventricular]] (AV) node, and then through the [[bundle of His]] to the ventricles of the heart. (See [[electrical conduction system of the heart]]).
*The [[pathophysiology]] of LGL [[syndrome]] is not yet understood completely.
*Multiple [[Theory|theories]] have been proposed to [[Suggestion|suggest]] the [[Mechanism (biology)|mechanism]] of LGL.<ref name="LOWN GANONG LEVINE 1952 pp. 693–706">{{cite journal | last=LOWN | first=BERNARD | last2=GANONG | first2=WILLIAM F. | last3=LEVINE | first3=SAMUEL A. | title=The Syndrome of Short P-R Interval Normal QRS Complex and Paroxysmal Rapid Heart Action | journal=Circulation | publisher=Ovid Technologies (Wolters Kluwer Health) | volume=5 | issue=5 | year=1952 | issn=0009-7322 | pmid=14926053 | doi=10.1161/01.cir.5.5.693 | pages=693–706}}</ref>
*The [[current]] [[theory]] supporting the [[Mechanism (biology)|mechanism]] of LGL is that it may [[result]] from numerous underlying [[causes]] that involve [[junctional pathways]] which partially or wholly [[bypass]] the [[Atrioventricular node|AV node]] with subsequent [[normal]] [[Conduction System|conduction]] down the [[bundle of His]].<ref name="Benditt Pritchett Smith Wallace 1978 pp. 454–465">{{cite journal | last=Benditt | first=D G | last2=Pritchett | first2=L C | last3=Smith | first3=W M | last4=Wallace | first4=A G | last5=Gallagher | first5=J J | title=Characteristics of atrioventricular conduction and the spectrum of arrhythmias in lown-ganong-levine syndrome. | journal=Circulation | publisher=Ovid Technologies (Wolters Kluwer Health) | volume=57 | issue=3 | year=1978 | issn=0009-7322 | pmid=624155 | doi=10.1161/01.cir.57.3.454 | pages=454–465}}</ref>
*The three [[accessory pathways]] as discussed in the [[classification]] section have been [[Proposition|proposed]] to be the main [[Trigger|triggering]] factors for the [[development]] of LGL.<ref name="Denes Wu Rosen 1974 pp. 343–346">{{cite journal | last=Denes | first=Pablo | last2=Wu | first2=Delon | last3=Rosen | first3=Kenneth M. | title=Demonstration of Dual A-V Pathways in a Patient with Lown-Ganong-Levine Syndrome | journal=Chest | publisher=Elsevier BV | volume=65 | issue=3 | year=1974 | issn=0012-3692 | doi=10.1378/chest.65.3.343 | pages=343–346}}</ref>
*Lown-Ganong-Levine [[pattern]] may occur including the following [[Fiber|fibers]]:
**[[Brechenmacher fibers]] (account for 0.03% of the [[patients]] [[Presenting symptom|presenting]] with LGL)
**Intra-[[Node (physics)|nodal]] [[Bypass tract|bypass tracts]]
**[[James fibers]]
*The intra-[[Node (physics)|nodal]] [[Bypass tract|bypass tracts]] allow the rapid [[Conduction System|conduction]] of [[action potential]] through the [[AV node]] [[Bypass|bypassing]] the other [[slow]] pathways.
 
[[File:LGL-bypass.jpg|thumb|500px|none|LGL Syndrome associated bypass tracts ]]
 
==Causes==
 
*The exact [[causes]] of LGL [[syndrome]] have not been completely understood yet.
*However, the [[Presenting symptom|presence]] of following [[accessory pathways]] can predispose a [[patient]] to the [[development]] of LGL [[syndrome]]:<ref name="LOWN GANONG LEVINE 1952 pp. 693–706">{{cite journal | last=LOWN | first=BERNARD | last2=GANONG | first2=WILLIAM F. | last3=LEVINE | first3=SAMUEL A. | title=The Syndrome of Short P-R Interval Normal QRS Complex and Paroxysmal Rapid Heart Action | journal=Circulation | publisher=Ovid Technologies (Wolters Kluwer Health) | volume=5 | issue=5 | year=1952 | issn=0009-7322 | pmid=14926053 | doi=10.1161/01.cir.5.5.693 | pages=693–706}}</ref>
**[[James fibers]]
**[[Brechenmacher fibers]]
**Intra-[[Node (physics)|nodal]] [[Fiber|fibers]]
*Sometimes, [[patients]] with LGL [[syndrome]] have a [[History and Physical examination|history]] of [[congenital heart disease]].
 
==Differentiating Lown-Ganong-Levine Syndrome from other Diseases==
 
*The [[Differential Diagnosis Table|differential diagnosis]] for Lown-Ganong-Levine [[syndrome]] includes the following [[diseases]] as shown in the [[Differential Diagnosis Table|table]] below:
 
 
{| class="wikitable"
|+
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Arrhythmia
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Rhythm
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Rate
! align="center" style="background:#4479BA; color: #FFFFFF;" + |P wave
! align="center" style="background:#4479BA; color: #FFFFFF;" + |PR Interval
! align="center" style="background:#4479BA; color: #FFFFFF;" + |QRS Complex
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Response to Maneuvers
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Epidemiology
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Co-existing Conditions
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |'''LGL [[Syndrome]]'''
|
*[[Irregularly irregular pulse|Irregularly irregular]]
|
*On a 10-[[second]] [[12-lead ECG|12-lead EKG]] [[Stripping|strip]], multiply [[number]] of [[QRS complexes]] by 6
|
*Present
 
|
*[[Short PR interval]]
|
*[[Normal]]/Narrow [[QRS complex]], [[Consistency (statistics)|consistent]], and [[normal]] in [[Morphology (biology)|morphology]]
|
*Does break with [[adenosine]] or [[vagal maneuvers]]
|
*In a [[retrospective study]] conducted by Bernard Lown, William Francis Ganong, and Samual Levine, 200 [[electrocardiograms]] ([[EKG]]) of 13500 [[patients]] showed [[EKG]] findings with a [[prevalence]] of just over 1%.
*
|
*[[Congenital heart diseases]]
*[[Mitral valve disease]]
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |'''[[Atrial fibrillation|Atrial fibrillation (AFib)]]<ref name="pmid24837984">{{cite journal |vauthors=Lankveld TA, Zeemering S, Crijns HJ, Schotten U |title=The ECG as a tool to determine atrial fibrillation complexity |journal=Heart |volume=100 |issue=14 |pages=1077–84 |date=July 2014 |pmid=24837984 |doi=10.1136/heartjnl-2013-305149 |url=}}</ref><ref name="pmid22518390">{{cite journal |vauthors=Harris K, Edwards D, Mant J |title=How can we best detect atrial fibrillation? |journal=J R Coll Physicians Edinb |volume=42 Suppl 18 |issue= |pages=5–22 |date=2012 |pmid=22518390 |doi=10.4997/JRCPE.2012.S02 |url=}}</ref>'''
|
*[[Irregularly irregular pulse|Irregularly irregular]]
|
*On a 10-[[second]] [[12-lead ECG|12-lead EKG]] [[Stripping|strip]], multiply [[number]] of [[QRS complexes]] by 6
|
*Absent
*[[Fibrillation|Fibrillatory]] [[waves]]
|
*Absent
|
*Less than 0.12 [[Second|seconds]], [[Consistency (statistics)|consistent]], and [[normal]] in [[Morphology (biology)|morphology]] in the absence of aberrant [[Conduction System|conduction]]
|
*Does not break with [[adenosine]] or [[vagal maneuvers]]
|
*2.7–6.1 million [[People's Solidarity|people]] in the [[United States]] have [[Atrial fibrillation|AFib]]
*2% of [[People's Solidarity|people]] [[Young adult|younger]] than [[age]] 65 have [[Atrial fibrillation|AFib]], while about 9% of [[People's Solidarity|people]] [[Age|aged]] 65 [[Year|years]] or [[Old age|older]] have [[Atrial fibrillation|AFib]]
|
*[[Elderly]]
*Following [[Coronary artery bypass surgery|bypass surgery]]
*[[Mitral valve disease]]
*[[Hyperthyroidism]]
*[[Diabetes mellitus|Diabetes]]
*[[Heart failure]]
*[[Ischemic heart disease]]
*[[Chronic kidney disease]]
*Heavy [[Alcohol abuse|alcohol use]]
*Left chamber enlargement
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |'''[[Atrial Flutter|Atrial flutter]]'''<ref name="pmid28835836">{{cite journal |vauthors=Cosío FG |title=Atrial Flutter, Typical and Atypical: A Review |journal=Arrhythm Electrophysiol Rev |volume=6 |issue=2 |pages=55–62 |date=June 2017 |pmid=28835836 |pmc=5522718 |doi=10.15420/aer.2017.5.2 |url=}}</ref>
|
*Regular or [[Irregular heart rhythms|Irregular]]
|
*75 (4:1 [[Blocking (statistics)|block]]), 100 (3:1 [[Blocking (statistics)|block]]) and 150 (2:1 [[Blocking (statistics)|block]]) [[beats per minute]] ([[Beats per minute|bpm]]), but 150 is more common
|
*Sawtooth [[pattern]] of [[P waves]] at 250 to 350 [[Beats per minute|bpm]]
*[[Biphasic]] deflection in [[V1-morph|V1]]
|
*[[Variance|Varies]] [[Dependent variable|depending]] upon the [[Magnitude (mathematics)|magnitude]] of the [[Blocking (statistics)|block]], but is [[Shortening|short]]
|
*Less than 0.12 [[Second|seconds]], [[Consistency (statistics)|consistent]], and [[normal]] in [[Morphology (biology)|morphology]]
|
*[[Conduction System|Conduction]] may [[Variable|vary]] in [[Response variable|response]] to [[drugs]] and maneuvers [[Drop (liquid)|dropping]] the [[rate]] from 150 to 100 or to 75 [[Beats per minute|bpm]]
|
*[[Incidence]]: 88 per 100,000 [[Individual growth|individuals]]
|
*[[Elderly]]
*[[Alcohol]]
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |'''[[Atrioventricular nodal reentry tachycardia]] ([[AV nodal reentrant tachycardia|AVNRT]])<ref name="pmid27617092">{{cite journal |vauthors=Katritsis DG, Josephson ME |title=Classification, Electrophysiological Features and Therapy of Atrioventricular Nodal Reentrant Tachycardia |journal=Arrhythm Electrophysiol Rev |volume=5 |issue=2 |pages=130–5 |date=August 2016 |pmid=27617092 |pmc=5013176 |doi=10.15420/AER.2016.18.2 |url=}}</ref><ref name="pmid20458824">{{cite journal |vauthors=Letsas KP, Weber R, Siklody CH, Mihas CC, Stockinger J, Blum T, Kalusche D, Arentz T |title=Electrocardiographic differentiation of common type atrioventricular nodal reentrant tachycardia from atrioventricular reciprocating tachycardia via a concealed accessory pathway |journal=Acta Cardiol |volume=65 |issue=2 |pages=171–6 |date=April 2010 |pmid=20458824 |doi=10.2143/AC.65.2.2047050 |url=}}</ref>'''<ref name="urlAtrioventricular Nodal Reentry Tachycardia (AVNRT) - StatPearls - NCBI Bookshelf">{{cite web |url=https://www.ncbi.nlm.nih.gov/books/NBK499936/ |title=Atrioventricular Nodal Reentry Tachycardia (AVNRT) - StatPearls - NCBI Bookshelf |format= |work= |accessdate=}}</ref><ref name="pmid25196716">{{cite journal |vauthors=Schernthaner C, Danmayr F, Strohmer B |title=Coexistence of atrioventricular nodal reentrant tachycardia with other forms of arrhythmias |journal=Med Princ Pract |volume=23 |issue=6 |pages=543–50 |date=2014 |pmid=25196716 |pmc=5586929 |doi=10.1159/000365418 |url=}}</ref>
|
*Regular
|
*140-280 [[Beats per minute|bpm]]
|
*[[Slow]]-[[Fast and wide|Fast]] [[AVNRT]]:
**Pseudo-[[S wave]] in [[Lead|leads]] II, III, and AVF
**Pseudo-R' in [[lead]] [[V1-morph|V1]].
*[[Fast and wide|Fast]]-[[Slow]] [[AVNRT]]
**[[P waves]] between the [[QRS complex|QRS]] and [[T waves]] ([[QRS complex|QRS]]-[[P wave|P]]-[[T wave|T complexes]])
*[[Slow]]-[[Slow]] [[AVNRT]]
**Late [[P waves]] after a [[QRS complex|QRS]]
**Often [[Appearance|appears]] as [[atrial tachycardia]].
*[[Invert|Inverted]], [[Superimposition|superimposed]] on or buried within the [[QRS complex]] ([[Pseudo-Cushing syndrome|pseudo]] [[R wave|R]] [[Prime EKG|prime]] in [[V1-morph|V1]]/pseudo [[S wave]] in inferior [[Lead|leads]])
|
*Absent ([[P wave]] can [[Appearance|appear]] after the [[QRS complex]] and before the [[T wave]], and in [[Atypical AV nodal reentrant tachycardia|atypical AVNRT]], the [[P wave]] can [[Appearance|appear]] just before the [[QRS complex]])
|
*Less than 0.12 [[Second|seconds]], [[Consistency (statistics)|consistent]], and [[normal]] in [[Morphology (biology)|morphology]] in the absence of aberrant [[Conduction System|conduction]]
*[[QRS complex alternans|QRS alternans]] may be [[Presenting symptoms|present]]
|
*May break with [[adenosine]] or [[vagal maneuvers]]
|
*60%-70% of all [[supraventricular tachycardias]]
|
*[[Structural heart disease]]
*[[Atrial tachyarrhythmias]]
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |'''[[Multifocal atrial tachycardia (MAT)|Multifocal atrial tachycardia]]<ref name="pmid2570520">{{cite journal |vauthors=Scher DL, Arsura EL |title=Multifocal atrial tachycardia: mechanisms, clinical correlates, and treatment |journal=Am. Heart J. |volume=118 |issue=3 |pages=574–80 |date=September 1989 |pmid=2570520 |doi=10.1016/0002-8703(89)90275-5 |url=}}</ref><ref name="pmid11884328">{{cite journal |vauthors=Goodacre S, Irons R |title=ABC of clinical electrocardiography: Atrial arrhythmias |journal=BMJ |volume=324 |issue=7337 |pages=594–7 |date=March 2002 |pmid=11884328 |pmc=1122515 |doi=10.1136/bmj.324.7337.594 |url=}}</ref>'''
|
*[[Irregular heart rhythms|Irregular]]
|
*[[Atrial]] [[rate]] is > 100 [[beats per minute]]
|
*Varying [[morphology]] from at least three [[Differentiate|different]] [[Focusing|foci]]
*Absence of one [[dominant]] [[atrial]] [[pacemaker]], can be mistaken for [[atrial fibrillation]] if the [[P waves]] are of low [[amplitude]]
|
*[[Variable]] [[PR interval|PR intervals]], [[RR interval|RR intervals]], and [[PP interval|PP intervals]]
|
*Less than 0.12 [[Second|seconds]], [[Consistency (statistics)|consistent]], and [[normal]] in [[Morphology (biology)|morphology]]
|
*Does not [[Termination signal|terminate]] with [[adenosine]] or [[vagal maneuvers]]
|
*0.05% to 0.32% of [[electrocardiograms]] in [[Generalization|general]] [[hospital]] [[Admission note|admissions]]
|
*[[Elderly]]
*[[Chronic obstructive pulmonary disease]] ([[Chronic obstructive pulmonary disease|COPD]])
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |'''[[Paroxysmal supraventricular tachycardia]]'''
|
*Regular
|
*150 and 240 [[Beats per minute|bpm]]
|
*Absent
*Hidden in [[QRS complex|QRS]]
|
*Absent
|
*Narrow [[Complex (chemistry)|complexes]] (< 0.12 s)
|
*Breaks with [[vagal maneuvers]], [[adenosine]], [[diving reflex]], [[oculocardiac reflex]]
|
*[[Prevalence]]: 0.023 per 100,000
|
*[[Alcohol]]
*[[Caffeine]]
*[[Nicotine]]
*[[Psychological stress]]
*[[Wolff-Parkinson-White syndrome]]
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |'''[[Premature atrial contraction|Premature atrial contractrions]] ([[Premature atrial contraction|PAC]])'''<ref name="pmid26316525">{{cite journal |vauthors=Lin CY, Lin YJ, Chen YY, Chang SL, Lo LW, Chao TF, Chung FP, Hu YF, Chong E, Cheng HM, Tuan TC, Liao JN, Chiou CW, Huang JL, Chen SA |title=Prognostic Significance of Premature Atrial Complexes Burden in Prediction of Long-Term Outcome |journal=J Am Heart Assoc |volume=4 |issue=9 |pages=e002192 |date=August 2015 |pmid=26316525 |pmc=4599506 |doi=10.1161/JAHA.115.002192 |url=}}</ref><ref name="pmid18063110">{{cite journal |vauthors=Strasburger JF, Cheulkar B, Wichman HJ |title=Perinatal arrhythmias: diagnosis and management |journal=Clin Perinatol |volume=34 |issue=4 |pages=627–52, vii–viii |date=December 2007 |pmid=18063110 |pmc=3310372 |doi=10.1016/j.clp.2007.10.002 |url=}}</ref>
|
*Regular except when disturbed by [[premature]] [[Beats per minute|beat(s)]]
|
*80-120 [[Beats per minute|bpm]]
|
*Upright
|
*> 0.12 [[Second|seconds]]
*May be [[Shortening|shorter]] than that in [[normal sinus rhythm]] ([[Normal sinus rhythm|NSR]]) if the [[origin]] of [[PAC]] is [[Location parameter|located]] closer to the [[AV node]]
*[[Ashman phenomenon|Ashman’s Phenomenon]]:
**[[Premature atrial contraction|PAC]] displaying a [[right bundle branch block]] [[pattern]]
|
*Usually narrow (< 0.12 s)
|
*Breaks with [[vagal maneuvers]], [[adenosine]], [[diving reflex]], [[oculocardiac reflex]]
|_
|
*[[Infant|Infants]]
*[[Cardiomyopathy]]
*[[Myocarditis]]
*[[Elderly]]
*[[Coronary artery disease]]
*[[Stroke]]
*Increased [[atrial natriuretic peptide]] ([[Atrial natriuretic peptide|ANP]])
*[[Hypercholesterolemia]]
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |'''[[Wolff-Parkinson-White syndrome|Wolff-Parkinson-White Syndrome]]<ref name="pmid24982705">{{cite journal |vauthors=Rao AL, Salerno JC, Asif IM, Drezner JA |title=Evaluation and management of wolff-Parkinson-white in athletes |journal=Sports Health |volume=6 |issue=4 |pages=326–32 |date=July 2014 |pmid=24982705 |pmc=4065555 |doi=10.1177/1941738113509059 |url=}}</ref><ref name="pmid10597097">{{cite journal |vauthors=Rosner MH, Brady WJ, Kefer MP, Martin ML |title=Electrocardiography in the patient with the Wolff-Parkinson-White syndrome: diagnostic and initial therapeutic issues |journal=Am J Emerg Med |volume=17 |issue=7 |pages=705–14 |date=November 1999 |pmid=10597097 |doi=10.1016/s0735-6757(99)90167-5 |url=}}</ref>'''
|
*Regular
|
*[[Atrial]] rate is nearly 300 [[Beats per minute|bpm]] and [[ventricular]] rate is at 150 [[Beats per minute|bpm]]
|
*With [[orthodromic]] [[Conduction System|conduction]] due to a [[bypass tract]], the [[P wave]] [[Generalization|generally]] follows the [[QRS complex]], whereas in [[AVNRT]], the [[P wave]] is [[Generalization|generally]] buried in the [[QRS complex]].
|
*Less than 0.12 [[Second|seconds]]
|
*A [[delta wave]] and [[evidence]] of [[ventricular]] [[pre-excitation]] if there is [[Conduction System|conduction]] to the [[ventricle]] via ante-grade [[Conduction System|conduction]] down an [[accessory pathway]]
*A [[delta wave]] and [[pre-excitation]] may not be present because [[Bypass tract|bypass tracts]] do not [[conduct]] ante-grade.
|
*May break in [[Response variable|response]] to [[procainamide]], [[adenosine]], [[vagal maneuvers]]
|
*Worldwide [[prevalence]] of [[Wolff-Parkinson-White syndrome|WPW syndrome]] is 100 - 300 per 100,000
|
*[[Ebstein's anomaly]]
*[[Mitral valve prolapse]]: This [[cardiac]] [[Disorder (medicine)|disorder]], if [[Presenting symptom|present]], is [[Association (statistics)|associated]] with left-sided [[accessory pathways]].
*[[Hypertrophic cardiomyopathy]]: This [[Disorder (medicine)|disorder]] is [[Association (statistics)|associated]] with [[familial]]/[[inherited]] form of [[Wolff-Parkinson-White syndrome|WPW syndrome]].
*[[Hypokalemic periodic paralysis]]
*[[Pompe disease]]
*[[Tuberous sclerosis]]
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |'''[[Ventricular fibrillation|Ventricular fibrillation (VF)]]'''<ref name="pmid27899944">{{cite journal |vauthors=Glinge C, Sattler S, Jabbari R, Tfelt-Hansen J |title=Epidemiology and genetics of ventricular fibrillation during acute myocardial infarction |journal=J Geriatr Cardiol |volume=13 |issue=9 |pages=789–797 |date=September 2016 |pmid=27899944 |pmc=5122505 |doi=10.11909/j.issn.1671-5411.2016.09.006 |url=}}</ref><ref name="pmid11334828">{{cite journal |vauthors=Samie FH, Jalife J |title=Mechanisms underlying ventricular tachycardia and its transition to ventricular fibrillation in the structurally normal heart |journal=Cardiovasc. Res. |volume=50 |issue=2 |pages=242–50 |date=May 2001 |pmid=11334828 |doi=10.1016/s0008-6363(00)00289-3 |url=}}</ref><ref name="pmid20142817">{{cite journal |vauthors=Adabag AS, Luepker RV, Roger VL, Gersh BJ |title=Sudden cardiac death: epidemiology and risk factors |journal=Nat Rev Cardiol |volume=7 |issue=4 |pages=216–25 |date=April 2010 |pmid=20142817 |pmc=5014372 |doi=10.1038/nrcardio.2010.3 |url=}}</ref>
|
*[[Irregular heart rhythms|Irregular]]
|
*150 to 500 [[Beats per minute|bpm]]
|
*Absent
|
*Absent
|
*Absent ([[R wave|R]] on [[T wave|T]] [[Phenomenology|phenomenon]] in the [[Set|setting]] of [[ischemia]])
|
*Does not break in [[Response variable|response]] to [[procainamide]], [[adenosine]], [[vagal maneuvers]]
|
*3-12% [[Case-based reasoning|cases]] of [[acute myocardial infarction]] ([[Acute myocardial infarction|AMI]])
*Out of 356,500 out of [[hospital]] [[Cardiac arrest|cardiac arrests]], 23% have [[Ventricular fibrillation|VF]] as initial [[rhythm]]
|
*[[Myocardial ischemia]] / [[Myocardial infarction|infarction]]
*[[Cardiomyopathy]]
*[[Channelopathies]] e.g. [[Long QT]] ([[acquired]] / [[congenital]])
*[[Electrolyte abnormalities]] ([[hypokalemia]]/[[hyperkalemia]], [[hypomagnesemia]])
*[[Aortic stenosis]]
*[[Aortic dissection]]
*[[Myocarditis]]
*[[Cardiac tamponade]]
*[[Blunt trauma]] ([[Commotio cordis|Commotio Cordis]])
*[[Sepsis]]
*[[Hypothermia]]
*[[Pneumothorax]]
*[[Seizures]]
*[[Stroke]]
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |'''[[Ventricular tachycardia]]'''<ref name="pmid19252119">{{cite journal |vauthors=Koplan BA, Stevenson WG |title=Ventricular tachycardia and sudden cardiac death |journal=Mayo Clin. Proc. |volume=84 |issue=3 |pages=289–97 |date=March 2009 |pmid=19252119 |pmc=2664600 |doi=10.1016/S0025-6196(11)61149-X |url=}}</ref><ref name="pmid21505622">{{cite journal |vauthors=Levis JT |title=ECG Diagnosis: Monomorphic Ventricular Tachycardia |journal=Perm J |volume=15 |issue=1 |pages=65 |date=2011 |pmid=21505622 |pmc=3048638 |doi=10.7812/tpp/10-130 |url=}}</ref>
|
*Regular
|
*> 100 [[Beats per minute|bpm]] (150-200 [[Beats per minute|bpm]] common)
|
*Absent
|<br />
 
*Absent
*Initial [[R wave]] in [[V1-morph|V1]], initial [[R wave|r]] > 40 [[Millisecond|ms]] in V1/V2, [[Notch|notched]] [[S wave|S]] in [[V1-morph|V1]], initial [[R wave|R]] in [[aVR]], [[lead]] II [[R wave]] peak [[Time constant|time]] ≥50 [[Millisecond|ms]], no RS in [[V1-morph|V1]]-V6, and [[atrioventricular dissociation]]
|
*[[Wide complex tachycardia|Wide complex]], [[QRS complex|QRS]] duration > 120 [[Millisecond|milliseconds]]
|
*Does not break in [[Response variable|response]] to [[procainamide]], [[adenosine]], [[vagal maneuvers]]
|
*5-10% of [[patients]] [[Presenting symptom|presenting]] with [[Acute myocardial infarction|AMI]]
|
*[[Coronary artery disease]]
*[[Aortic stenosis]]
*[[Cardiomyopathy]]
*[[Electrolyte imbalance|Electrolyte imbalances]] (e.g., [[hypokalemia]], [[hypomagnesemia]])
*[[Inherited]] [[channelopathies]] (e.g., [[long-QT syndrome]])
*[[Catecholaminergic polymorphic ventricular tachycardia]]
*[[Arrhythmogenic right ventricular dysplasia]]
*[[Myocardial infarction]]
*[[Torsades de pointes]] is a form of [[polymorphic VT]] that is often [[Association (statistics)|associated]] with a [[Prolonged QT Interval|prolonged QT interval]]
|}
 
==Epidemiology and Demographics==
 
*In a [[Retrospective cohort study|retrospective study]] conducted by Bernard Lown, William Francis Ganong, and Samual Levine,  200 [[electrocardiograms]] ([[EKG|EKGs]]) of 13500 [[patients]] showed [[EKG]] findings with the [[prevalence]] of just over 1%.<ref name="LOWN GANONG LEVINE 1952 pp. 693–706">{{cite journal | last=LOWN | first=BERNARD | last2=GANONG | first2=WILLIAM F. | last3=LEVINE | first3=SAMUEL A. | title=The Syndrome of Short P-R Interval Normal QRS Complex and Paroxysmal Rapid Heart Action | journal=Circulation | publisher=Ovid Technologies (Wolters Kluwer Health) | volume=5 | issue=5 | year=1952 | issn=0009-7322 | pmid=14926053 | doi=10.1161/01.cir.5.5.693 | pages=693–706}}</ref>
===Age===
 
*There is currently insufficient data regarding [[age]] predilection of LGL [[syndrome]].
===Gender===
 
*There is currently insufficient data regarding gender predilection of LGL [[syndrome]] as the LGL [[pattern]] is not [[Association (statistics)|associated]] with an increased [[incidence]] in one particular [[Sex (activity)|sex]].
*However, Lown in 1952 reported 70.9% of the 34 cases in [[women]].<ref name="LOWN GANONG LEVINE 1952 pp. 693–706">{{cite journal | last=LOWN | first=BERNARD | last2=GANONG | first2=WILLIAM F. | last3=LEVINE | first3=SAMUEL A. | title=The Syndrome of Short P-R Interval Normal QRS Complex and Paroxysmal Rapid Heart Action | journal=Circulation | publisher=Ovid Technologies (Wolters Kluwer Health) | volume=5 | issue=5 | year=1952 | issn=0009-7322 | pmid=14926053 | doi=10.1161/01.cir.5.5.693 | pages=693–706}}</ref>
===Race===
 
*There is currently insufficient [[data]] regarding [[race]] predilection of LGL [[syndrome]] as the LGL [[pattern]] is not [[Association (statistics)|associated]] with an increased [[incidence]] in one particular [[Ethnic group|ethnic background]].
 
==Risk Factors==
 
*The [[data]] regarding the [[risk factors]] predisposing to LGL [[syndrome]] is insufficient. However, the following [[conditions]] or factors may lead to the various [[Pre-excitation syndrome|pre-excitation syndromes]]:<ref name="pmid14926053">{{cite journal| author=LOWN B, GANONG WF, LEVINE SA| title=The syndrome of short P-R interval, normal QRS complex and paroxysmal rapid heart action. | journal=Circulation | year= 1952 | volume= 5 | issue= 5 | pages= 693-706 | pmid=14926053 | doi=10.1161/01.cir.5.5.693 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14926053  }} </ref>
**Presence of [[Accessory pathway|accessory]] [[Bypass tract|bypass tracts]]
**The high-risk [[population]] for [[sudden cardiac death]] in [[patients]] with [[Pre-excitation syndrome|pre-excitation syndromes]] includes the following:
***Policemen
***[[Athletes]]
***Firemen
***Pilots
***Steelworkers
 
==Natural History, Complications and Prognosis==
===Natural History===
 
*LGL [[syndrome]] can be [[asymptomatic]] or can [[Presenting symptom|present]] with the following [[symptoms]]:
**[[Palpitation|Palpitations]]
**[[Lightheadedness]]
**[[Shortness of breath]]
**[[Syncope]]
*In the case of [[congenital heart disease]] or [[Genetic anomalies|genetic anomaly]], it can also [[Presenting symptom|present]] as [[Paroxysm|paroxysms]] of [[tachycardia]] or [[chest pain]].<ref name="LOWN GANONG LEVINE 1952 pp. 693–706">{{cite journal | last=LOWN | first=BERNARD | last2=GANONG | first2=WILLIAM F. | last3=LEVINE | first3=SAMUEL A. | title=The Syndrome of Short P-R Interval Normal QRS Complex and Paroxysmal Rapid Heart Action | journal=Circulation | publisher=Ovid Technologies (Wolters Kluwer Health) | volume=5 | issue=5 | year=1952 | issn=0009-7322 | pmid=14926053 | doi=10.1161/01.cir.5.5.693 | pages=693–706}}</ref>


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 [[electrocardiogram|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).
===Complications===


Individuals with LGL syndrome are thought to have an accessory pathway that connects the atria directly to the bundle of His. As in WPW syndrome, the accessory pathway does not share the rate-slowing properties of the AV node, and may 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 can fibrillate causing VF (ventricular fibrillation)- leading to sudden cardiac death (SCD).
*There is an increased risk of developing [[Tachyarrhythmias|tachyarrhythmias.]]
*Certain [[medications]] such as [[sympathomimetics]] should be used with caution in [[patients]] of LGL [[syndrome]].
*[[Digitalis]] does not produce any [[Effect size|effect]] on LGL [[syndrome]] but it can [[slow]] down the [[Conduction System|conduction]] in the [[AV node]] which [[Prevention (medical)|prevents]] [[AV reentrant tachycardia|AVRT]] in these [[patients]].
*Although [[beta-blockers]] do not directly [[affect]] the [[accessory pathway]], however, they can [[slow]] [[Conduction System|conduction]] through the [[AV node]] similar to [[Digoxin|digitalis]].


==Characteristic Findings==
===Prognosis===


* [[PR interval]] is shorter than normal, but no delta wave is present(in contrast to [[Wolff Parkinson White syndrome]] where there is a delta wave which is a slurring of the [[QRS]] upstroke)
*The overall [[prognosis]] of [[patients]] with LGL [[syndrome]] is good.
* LGL is due to intranodal bypass tracts (i.e. there is conduction down James fibers) 
*[[Patients]] are usually [[asymptomatic]] but some can [[Development|develop]] certain [[clinical]] [[Features (pattern recognition)|features]] such as:
* [[QRS duration]] is normal
**[[Palpitations]]
* [[PR interval]] is less than 0.12 seconds
**[[Shortness of breath]]
* [[P wave]] is normal
**Occasional episodes of:
***[[Atrial fibrillation]]
***[[Atrial flutter]]
***[[AV reentrant tachycardia|AVRT]]
***Other [[tachyarrhythmias]]
***They can also lead to the [[development]] of [[ventricular arrhythmias]] in [[rare]] cases.<ref name="LOWN GANONG LEVINE 1952 pp. 693–706">{{cite journal | last=LOWN | first=BERNARD | last2=GANONG | first2=WILLIAM F. | last3=LEVINE | first3=SAMUEL A. | title=The Syndrome of Short P-R Interval Normal QRS Complex and Paroxysmal Rapid Heart Action | journal=Circulation | publisher=Ovid Technologies (Wolters Kluwer Health) | volume=5 | issue=5 | year=1952 | issn=0009-7322 | pmid=14926053 | doi=10.1161/01.cir.5.5.693 | pages=693–706}}</ref><ref name="Benditt Pritchett Smith Wallace 1978 pp. 454–465">{{cite journal | last=Benditt | first=D G | last2=Pritchett | first2=L C | last3=Smith | first3=W M | last4=Wallace | first4=A G | last5=Gallagher | first5=J J | title=Characteristics of atrioventricular conduction and the spectrum of arrhythmias in lown-ganong-levine syndrome. | journal=Circulation | publisher=Ovid Technologies (Wolters Kluwer Health) | volume=57 | issue=3 | year=1978 | issn=0009-7322 | pmid=624155 | doi=10.1161/01.cir.57.3.454 | pages=454–465}}</ref>


==Diagnosis==
==Diagnosis==
LGL syndrome is commonly diagnosed on the basis of the surface [[electrocardiogram|EKG]] in an [[asymptomatic]] individual. In this case it is manifest as a PR interval less than or equal to 0.12 second (120 ms) with normal QRS complex duration.
===Diagnostic Criteria===
 
*Characteristic [[ECG]] findings of LGL [[syndrome]] are <ref name="LOWN GANONG LEVINE 1952 pp. 693–706">{{cite journal | last=LOWN | first=BERNARD | last2=GANONG | first2=WILLIAM F. | last3=LEVINE | first3=SAMUEL A. | title=The Syndrome of Short P-R Interval Normal QRS Complex and Paroxysmal Rapid Heart Action | journal=Circulation | publisher=Ovid Technologies (Wolters Kluwer Health) | volume=5 | issue=5 | year=1952 | issn=0009-7322 | pmid=14926053 | doi=10.1161/01.cir.5.5.693 | pages=693–706}}</ref>
**[[Short PR interval]] (<120ms)
**[[Normal]] [[P wave]] [[axis]]
**[[Normal]]/narrow [[QRS complex|QRS morphology]] in the presence of paroxysmal [[tachyarrhythmia]]
 
[[File:Lown-Ganong-Levine syndrome ECG.jpg|thumb|500px|none|Lown-Ganong-Levine syndrome ECG features. [https://upload.wikimedia.org/wikipedia/commons/b/bf/Lown-Ganong-Levine_syndrome_ECG.jpg]]]
 
===History and Symptoms===
 
*LGL [[syndrome]] is usually [[asymptomatic]].
*The [[symptoms]] of LGL [[syndrome]] usually overlap with those of [[pre-excitation syndrome]] and may include the following:<ref name="LOWN GANONG LEVINE 1952 pp. 693–706">{{cite journal | last=LOWN | first=BERNARD | last2=GANONG | first2=WILLIAM F. | last3=LEVINE | first3=SAMUEL A. | title=The Syndrome of Short P-R Interval Normal QRS Complex and Paroxysmal Rapid Heart Action | journal=Circulation | publisher=Ovid Technologies (Wolters Kluwer Health) | volume=5 | issue=5 | year=1952 | issn=0009-7322 | pmid=14926053 | doi=10.1161/01.cir.5.5.693 | pages=693–706}}</ref>
**[[Palpitations]]
**[[Dizziness]]
**[[Lightheadedness]]
**[[Shortness of breath]]
**[[Racing heart]]
**[[Syncope]]
**[[Chest pain]] or [[tachycardia]] (in case of an underlying [[cardiac]] [[Structural biology|structural]] [[defect]])
 
===Physical Examination===
 
*[[Patients]] with LGL [[syndrome]] usually [[Appearance|appear]] [[normal]].
*[[Physical examination]] findings are limited in LGL [[syndrome]].
*During [[cardiac]] [[auscultation]] or [[palpation]] of peripheral [[pulses]], there can be [[Irregular heart rhythms|irregular rhythm]].
 
===Imaging Findings===
 
====ECG====
 
*The [[diagnosis]] of LGL [[syndrome]] can be made by the use of resting [[The electrocardiogram|EKG]]. [[EKG]] findings usually show:
**[[Short PR interval]] (<120ms)
**[[Normal]] [[P wave]] [[axis]]
**[[Normal]]/narrow [[QRS complex|QRS]] [[morphology]] in the presence of paroxysmal [[tachyarrhythmia]]
 
[[File:Lown–Ganong–Levine-syndrome-LGL.jpg|thumb|500px|none|ECG showing LGL syndrome with short PR interval, narrow QRS complex, and normal P waves. [https://litfl.com/lown-ganong-levine-syndrome/ Source: LITFL]]]
 
===Other Diagnostic Studies===
 
*[[Holter monitors]] or [[Implant|implantable]] loop recorders may provide insight into the underlying [[Conduction disorders|conduction abnormalities]].
 
==Treatment==
===Medical Therapy===
 
*The mainstay of [[therapy]] for LGL [[syndrome]] is the use of [[Antiarrhythmic agents|antiarrhythmic]] [[medications]] to [[Prevention (medical)|prevent]] [[tachyarrhythmias]].
*[[Medications]] such as [[digitalis]], [[beta-blockers]], [[calcium channel blockers]] and [[Antiarrhythmic drugs|Class I and III antiarrhythmic drugs]] have been used to [[slow]] down [[Atrioventricular node|AV]] [[Conduction System|conduction]] and [[Prevention (medical)|prevent]] [[AV reentrant tachycardia|AVRT]] and other [[arrhythmias]].<ref name="Benditt Klein Kriett Dunnigan 1984 pp. 1088–1095">{{cite journal | last=Benditt | first=D G | last2=Klein | first2=G J | last3=Kriett | first3=J M | last4=Dunnigan | first4=A | last5=Benson | first5=D W | title=Enhanced atrioventricular nodal conduction in man: electrophysiologic effects of pharmacologic autonomic blockade. | journal=Circulation | publisher=Ovid Technologies (Wolters Kluwer Health) | volume=69 | issue=6 | year=1984 | issn=0009-7322 | pmid=6713613 | doi=10.1161/01.cir.69.6.1088 | pages=1088–1095}}</ref><ref name="Caracta Damato Gallagher Josephson 1973 pp. 245–253">{{cite journal | last=Caracta | first=Anthony R. | last2=Damato | first2=Anthony N. | last3=Gallagher | first3=John J. | last4=Josephson | first4=Mark E. | last5=Varghese | first5=P.Jacob | last6=Lau | first6=Sun H. | last7=Westura | first7=Edwin E. | title=Electrophysiologic studies in the syndrome of short P-R interval, normal QRS complex | journal=The American Journal of Cardiology | publisher=Elsevier BV | volume=31 | issue=2 | year=1973 | issn=0002-9149 | doi=10.1016/0002-9149(73)91037-0 | pages=245–253}}</ref>
*[[Drugs]] such as [[sotalol]] and [[amiodarone]] have promising [[Effect size|effects]] as a [[treatment]] option for LGL [[syndrome]] but are still under [[Investigational product|investigation]] and need further [[Study design|studies]].


It can be distinguished from WPW syndrome because:
===Surgery===
* The QRS complexes in LGL syndrome are normal because ventricular contraction is initiated in the normal manner. The broad complexes seen in the asymptomatic individual with WPW are not a feature of LGL.
* The delta waves seen in WPW syndrome are not seen in LGL syndrome as the accessory pathway does not connect to the ventricles and so ventricular contraction does not start early.


==Differential Diagnosis==
*[[Patients]] [[refractory]] to [[medical]] management can be [[Managed care|managed]] by the use of [[radiofrequency catheter ablation]] as it has become a primary treatment option in various [[Pre-excitation syndrome|pre-excitation syndromes]].
*[[Paroxysmal Atrial Tachycardia (PAT)]]
*This can be further implicated by the [[implantation]] of a [[permanent pacemaker]][[Artificial pacemaker|.]]
*[[Wolf-Parkinson-White syndrome|Wolf Parkinson White Syndrome]]
*[[Mahaim Type Preexcitation]]


==Related Chapters==
===Prevention===
* [[Wolff-Parkinson-White syndrome]]
* [[Cardiac electrophysiology]]
* [[Electrical conduction system of the heart]]
* [[Electrocardiogram]]
* [[Electrophysiologic study]]


{{Electrocardiography}}
*There are no [[Primary prevention|primary preventive]] measures available for LGL [[syndrome]].
{{Circulatory system pathology}}


[[Category:Electrophysiology]]
==References==
{{Reflist|2}}
[[Category:Cardiology]]
[[Category:Cardiology]]
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[[Category:Up-to-date]]
{{WikiDoc Sources}}

Latest revision as of 20:03, 28 April 2021

Lown-Ganong-Levine syndrome Microchapters

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Lown-Ganong-Levine Syndrome from other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

Treatment

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2] Associate Editor(s)-in-Chief: Usman Ali Akbar, M.B.B.S.[3]

Synonyms and keywords: Lown-Ganong-Levine Syndrome, LGL syndrome, Pre-excitation syndromes, Short PR Normal QRS Complex Syndrome, Clerc-Lévy-Cristesco syndrome, Coronary nodal rhythm syndrome, Short PQ interval syndrome, Short P-R syndrome.

Overview

Lown-Ganong-Levine syndrome (LGL) is actually a pre-excitation syndrome with EKG findings including short PR interval, narrow or normal QRS complex, and a normal P wave. It is caused by the presence of accessory bundles of fibers known as James fibers which lead to the development of abnormal conduction pathways. The LGL syndrome was named after Bernard Lown, William Francis Ganong, and Samual Levine who described it in 1952. Patients of LGL usually present with a history of palpitations, lightheadedness, shortness of breath, and sometimes chest pain. There is an increased risk of tachyarrhythmias and syncope. EKG is the principal modality of investigation for establishing a diagnosis. Usually, antiarrhythmics are given to prevent the development of tachyarrhythmias but recently radiofrequency ablation of the accessory pathways has been the mainstay of treatment with a good prognosis.

Historical Perspective

Historical timeline of LGL Syndrome
Year Description
1938
1946
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, an anatomic pathway was identified and reported by James and Brechemacher respectively.
Historic Timeline of LGL Syndrome

Classification

Accessory Pathway Description
James fibers
Brechenmacher fibers
Intra-nodal bypass tracts

Pathophysiology

LGL Syndrome associated bypass tracts

Causes

Differentiating Lown-Ganong-Levine Syndrome from other Diseases


Arrhythmia Rhythm Rate P wave PR Interval QRS Complex Response to Maneuvers Epidemiology Co-existing Conditions
LGL Syndrome
  • Present
Atrial fibrillation (AFib)[6][7]
  • Absent
Atrial flutter[8]
Atrioventricular nodal reentry tachycardia (AVNRT)[9][10][11][12]
  • Regular
Multifocal atrial tachycardia[13][14]
Paroxysmal supraventricular tachycardia
  • Regular
  • 150 and 240 bpm
  • Absent
  • Hidden in QRS
  • Absent
Premature atrial contractrions (PAC)[15][16]
  • Upright
  • Usually narrow (< 0.12 s)
_
Wolff-Parkinson-White Syndrome[17][18]
  • Regular
Ventricular fibrillation (VF)[19][20][21]
  • Absent
  • Absent
Ventricular tachycardia[22][23]
  • Regular
  • > 100 bpm (150-200 bpm common)
  • Absent

Epidemiology and Demographics

Age

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

Gender

  • There is currently insufficient data regarding gender predilection of LGL syndrome as the LGL pattern is not associated with an increased incidence in one particular sex.
  • However, Lown in 1952 reported 70.9% of the 34 cases in women.[1]

Race

Risk Factors

Natural History, Complications and Prognosis

Natural History

Complications

Prognosis

Diagnosis

Diagnostic Criteria

Lown-Ganong-Levine syndrome ECG features. [1]

History and Symptoms

Physical Examination

Imaging Findings

ECG

ECG showing LGL syndrome with short PR interval, narrow QRS complex, and normal P waves. Source: LITFL

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Prevention

References

  1. 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 1.9 LOWN, BERNARD; GANONG, WILLIAM F.; LEVINE, SAMUEL A. (1952). "The Syndrome of Short P-R Interval Normal QRS Complex and Paroxysmal Rapid Heart Action". Circulation. Ovid Technologies (Wolters Kluwer Health). 5 (5): 693–706. doi:10.1161/01.cir.5.5.693. ISSN 0009-7322. PMID 14926053.
  2. 2.0 2.1 Manning, G W (1978). "Lown-Ganong-Levine syndrome". Circulation. Ovid Technologies (Wolters Kluwer Health). 58 (3): 576–577. doi:10.1161/01.cir.58.3.576. ISSN 0009-7322. PMID 679452.
  3. DOUGLAS, JOHN E. (1972). "Lown-Ganong-Levine Syndrome". Circulation. Ovid Technologies (Wolters Kluwer Health). 45 (5): 1143–1144. doi:10.1161/01.cir.45.5.1143. ISSN 0009-7322. PMID 5020803.
  4. 4.0 4.1 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.
  5. Denes, Pablo; Wu, Delon; Rosen, Kenneth M. (1974). "Demonstration of Dual A-V Pathways in a Patient with Lown-Ganong-Levine Syndrome". Chest. Elsevier BV. 65 (3): 343–346. doi:10.1378/chest.65.3.343. ISSN 0012-3692.
  6. Lankveld TA, Zeemering S, Crijns HJ, Schotten U (July 2014). "The ECG as a tool to determine atrial fibrillation complexity". Heart. 100 (14): 1077–84. doi:10.1136/heartjnl-2013-305149. PMID 24837984.
  7. Harris K, Edwards D, Mant J (2012). "How can we best detect atrial fibrillation?". J R Coll Physicians Edinb. 42 Suppl 18: 5–22. doi:10.4997/JRCPE.2012.S02. PMID 22518390.
  8. Cosío FG (June 2017). "Atrial Flutter, Typical and Atypical: A Review". Arrhythm Electrophysiol Rev. 6 (2): 55–62. doi:10.15420/aer.2017.5.2. PMC 5522718. PMID 28835836.
  9. Katritsis DG, Josephson ME (August 2016). "Classification, Electrophysiological Features and Therapy of Atrioventricular Nodal Reentrant Tachycardia". Arrhythm Electrophysiol Rev. 5 (2): 130–5. doi:10.15420/AER.2016.18.2. PMC 5013176. PMID 27617092.
  10. Letsas KP, Weber R, Siklody CH, Mihas CC, Stockinger J, Blum T, Kalusche D, Arentz T (April 2010). "Electrocardiographic differentiation of common type atrioventricular nodal reentrant tachycardia from atrioventricular reciprocating tachycardia via a concealed accessory pathway". Acta Cardiol. 65 (2): 171–6. doi:10.2143/AC.65.2.2047050. PMID 20458824.
  11. "Atrioventricular Nodal Reentry Tachycardia (AVNRT) - StatPearls - NCBI Bookshelf".
  12. Schernthaner C, Danmayr F, Strohmer B (2014). "Coexistence of atrioventricular nodal reentrant tachycardia with other forms of arrhythmias". Med Princ Pract. 23 (6): 543–50. doi:10.1159/000365418. PMC 5586929. PMID 25196716.
  13. Scher DL, Arsura EL (September 1989). "Multifocal atrial tachycardia: mechanisms, clinical correlates, and treatment". Am. Heart J. 118 (3): 574–80. doi:10.1016/0002-8703(89)90275-5. PMID 2570520.
  14. Goodacre S, Irons R (March 2002). "ABC of clinical electrocardiography: Atrial arrhythmias". BMJ. 324 (7337): 594–7. doi:10.1136/bmj.324.7337.594. PMC 1122515. PMID 11884328.
  15. Lin CY, Lin YJ, Chen YY, Chang SL, Lo LW, Chao TF, Chung FP, Hu YF, Chong E, Cheng HM, Tuan TC, Liao JN, Chiou CW, Huang JL, Chen SA (August 2015). "Prognostic Significance of Premature Atrial Complexes Burden in Prediction of Long-Term Outcome". J Am Heart Assoc. 4 (9): e002192. doi:10.1161/JAHA.115.002192. PMC 4599506. PMID 26316525.
  16. Strasburger JF, Cheulkar B, Wichman HJ (December 2007). "Perinatal arrhythmias: diagnosis and management". Clin Perinatol. 34 (4): 627–52, vii–viii. doi:10.1016/j.clp.2007.10.002. PMC 3310372. PMID 18063110.
  17. Rao AL, Salerno JC, Asif IM, Drezner JA (July 2014). "Evaluation and management of wolff-Parkinson-white in athletes". Sports Health. 6 (4): 326–32. doi:10.1177/1941738113509059. PMC 4065555. PMID 24982705.
  18. Rosner MH, Brady WJ, Kefer MP, Martin ML (November 1999). "Electrocardiography in the patient with the Wolff-Parkinson-White syndrome: diagnostic and initial therapeutic issues". Am J Emerg Med. 17 (7): 705–14. doi:10.1016/s0735-6757(99)90167-5. PMID 10597097.
  19. Glinge C, Sattler S, Jabbari R, Tfelt-Hansen J (September 2016). "Epidemiology and genetics of ventricular fibrillation during acute myocardial infarction". J Geriatr Cardiol. 13 (9): 789–797. doi:10.11909/j.issn.1671-5411.2016.09.006. PMC 5122505. PMID 27899944.
  20. Samie FH, Jalife J (May 2001). "Mechanisms underlying ventricular tachycardia and its transition to ventricular fibrillation in the structurally normal heart". Cardiovasc. Res. 50 (2): 242–50. doi:10.1016/s0008-6363(00)00289-3. PMID 11334828.
  21. Adabag AS, Luepker RV, Roger VL, Gersh BJ (April 2010). "Sudden cardiac death: epidemiology and risk factors". Nat Rev Cardiol. 7 (4): 216–25. doi:10.1038/nrcardio.2010.3. PMC 5014372. PMID 20142817.
  22. Koplan BA, Stevenson WG (March 2009). "Ventricular tachycardia and sudden cardiac death". Mayo Clin. Proc. 84 (3): 289–97. doi:10.1016/S0025-6196(11)61149-X. PMC 2664600. PMID 19252119.
  23. Levis JT (2011). "ECG Diagnosis: Monomorphic Ventricular Tachycardia". Perm J. 15 (1): 65. doi:10.7812/tpp/10-130. PMC 3048638. PMID 21505622.
  24. LOWN B, GANONG WF, LEVINE SA (1952). "The syndrome of short P-R interval, normal QRS complex and paroxysmal rapid heart action". Circulation. 5 (5): 693–706. doi:10.1161/01.cir.5.5.693. PMID 14926053.
  25. Benditt, D G; Klein, G J; Kriett, J M; Dunnigan, A; Benson, D W (1984). "Enhanced atrioventricular nodal conduction in man: electrophysiologic effects of pharmacologic autonomic blockade". Circulation. Ovid Technologies (Wolters Kluwer Health). 69 (6): 1088–1095. doi:10.1161/01.cir.69.6.1088. ISSN 0009-7322. PMID 6713613.
  26. Caracta, Anthony R.; Damato, Anthony N.; Gallagher, John J.; Josephson, Mark E.; Varghese, P.Jacob; Lau, Sun H.; Westura, Edwin E. (1973). "Electrophysiologic studies in the syndrome of short P-R interval, normal QRS complex". The American Journal of Cardiology. Elsevier BV. 31 (2): 245–253. doi:10.1016/0002-9149(73)91037-0. ISSN 0002-9149.