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__NOTOC__
__NOTOC__
{{Pre-excitation syndrome}}
{{Pre-excitation syndrome}}
{{CMG}} {{AE}} {{Shivam Singla}}


{{CMG}}, '''Associate Editor-In-Chief:''' {{Shivam Singla}}
{{SK}} Pre Excitation [[Syndromes]]; [[Lown-Ganong-Levine syndrome|Lown-Ganong-Levine Syndrome]]; Pre-Excitation, [[Mahaim type preexcitation|Mahaim-Type Pre-excitation]]; [[Wolff-Parkinson-White syndrome|Wolff-Parkinson-White Syndrome]]


==Overview==
==Overview==
'''Pre-excitation syndrome''' is a condition where [[ventricles]] of the [[heart]] depolarize earlier than the normal leading to [[premature contraction]]. Normally the [[atria]] and the [[ventricles]] are isolated [[electrically]] and only electrical passage existing in between [[atria]] and [[ventricles]] is at [[Atrioventricular Node]]. In all [[pre-excitation syndromes]], there is also present an additional conducting pathway beside the [[AV junction]]. So the [[electrical impulses]] pass to the [[ventricles]] even before the normal wave of [[depolarization]] that is about to conduct through the [[AV node]]. This mechanism of [[depolarization]] of [[ventricles]] through an additional [[bypass]] pathway ( [[Bundle of Kent]]) much earlier than the usual [[depolarization]] pathway (through [[AV node]]) is referred to as "[[Pre- Excitation]]". The secondary [[conduction pathways]] are generally named as [[Bundle of His]].
'''Pre-excitation syndrome''' is a [[condition]] in which the [[ventricles]] of [[heart]] [[depolarize]] earlier than expected via some [[accessory pathway]] [[conduction]], leading to a [[premature contraction]]. Normally, [[atria]] and [[ventricles]] are interconnected with each other via the [[AV node]] ([[atrioventricular node]]). However, in all the [[pre-excitation]] [[syndromes]], an [[accessory]] [[pathway]] is present that [[conducts]] [[impulses]] to [[ventricles]] besides the [[AV node]]. The [[accessory pathway]] passes the [[electrical]] [[impulses]] to the [[ventricles]] before the normal [[impulse]] of [[depolarization]] passes through the [[AV node]]. The phenomenon of [[depolarizing]] [[ventricles]] through the [[accessory pathway]] [[earlier]] than the usual [[depolarization]] is supposed to happen through the [[AV node]] is referred to as [["Pre- Excitation"]]. [[WPW syndrome]] was described in 1930 and named after [[John Parkinson]], [[Paul Dudley White]], and [[Louis Wolff]]. The [[accessory pathways]] are named depending upon the regions of [[atria]] and [[ventricles]] they are connecting such as [[Bundle of His]], [[Mahaim fibers]], and [[James fibers]]. The typical [[ECG]] findings associated with [[WPW syndrome]] are shortened [[PR interval]], [[widened QRS]] complex and [[Delta wave]] which is a slurring in the [[upstroke]] of [[QRS]] complex due to [[preexcitation]] of [[ventricles]] via the [[accessory pathway]]. [[ECG]] findings along with [[symptomatic]] [[tachyarrhythmias]] are referred to as '''[[Wolff-Parkinson-White syndrome]]'''. Although it is more common in [[Adult|adults]], [[males]] have an [[incidence rate]] of 0.1-0.3 %, [[WPW]] can be considered as a [[congenital anomaly]] in some cases where it is usually present since the [[birth]] and in others, it is considered as a [[developmental]] [[anomaly]]. Studies have proven its [[lower]] [[prevalence]] in [[children]] [[aged]] between 6-13 than those in the [[age]] group of 14-15 years of [[age]]. [[Hemodynamically]] [[unstable]] [[patients]] should be managed with a [[direct cardioversion]]. For the stable [[patients]], [[medical]] [[management]] should be used first before using acceptable options of [[catheter ablation]] or [[surgical]] [[intervention]]. Although [[catheter ablation]] has widely replaced the [[surgical]] option, as it is a less [[invasive]] technique with better [[Outcome|outcomes]], in cases where [[catheter]] [[ablation]] cannot be done or doesn't prove to be effective, the [[surgical]] option is worth considering with a [[Cure|curative]] [[rate]] of nearly 100%.
 
The typical [[ECG]] findings are shortened [[PR interval]] and [[widened QRS interval]] with a slight slurring in the [[upstroke]] region. The [[clinical syndrome]] of the above clinical finding of [[ECG]] and history of [[SVT]] is referred to as '''[[Wolff-Parkinson-White syndrome]]'''. [[pre-excitation syndromes]] are getting more common in the [[pediatric population]] as well. The main component is the presence of an additional [[accessory]] bypass [[pathway]] in the [[heart]] through which the impulse conducts faster than than the [[physiological conduction]] through [[AV node]], resulting in quick [[depolarization]] of[[ventricles]] and leads to [[dangerous]] [[arrhythmias]]. The most common subtype is [[Wolf-Parkinson -White syndrome]]. The severe consequences range from [[arrhythmias]], [[SVT]], and [[sudden cardiac death]]. The main therapeutic measures for managing the patients are [[pharmacotherapy]] and [[ablation therapy]].


==Historical Perspective==
==Historical Perspective==


*WPW syndrome was described in 1930 and named for the John Parkinson, [[Paul Dudley White]], and Louis Wolff.
*In 1915, [[Frank Norman Wilson]] became the first to describe the [[condition]] which was later referred to as [[Wolff–Parkinson–White syndrome]].
*They successfully interpreted a series of 11 healthy young patients who had repeated attacks of tachycardia's in the presence os short PR interval and bundle branch block pattern on the ECG findings.
*In 1930, [[WPW syndrome]] was first described and named after [[John Parkinson]], [[Paul Dudley White]], and [[Louis Wolff]]. They successfully interpreted a series of 11 [[healthy]] young [[patients]] who had repeated [[Attack rate|attacks]] of [[tachycardia]] in the presence of [[short PR interval]] and [[bundle branch block]] [[pattern]] on the [[ECG]] findings. They also found the [[Association (statistics)|association]] of [[WPW]] with increasing the [[risk]] of [[sudden cardiac death]].<ref>https://doi.org/10.1016/j.eupc.2004.09.005</ref>
*British physiologist "Albert Frank Stanley Kent" (1863 - 1958), first described the lateral branches of [[AV grove]] of the [[monkey]] [[heart]], which were later named as the [[accessory]] [[bundle of Kent]].


*British physiologist "Albert Frank Stanley Kent" (1863 - 1958), first described the lateral branches of AV grove of the monkey heart, which was later named accessory [[bundle of Kent]].
[[File:Wolf-parkinson-white.jpg|thumb|300px|none|WPW Syndrome was given its name in 1930 by Wolf, Parkinson, and White. [https://en.ecgpedia.org/index.php?title=File:Wolffparkinsonwhite.jpg Source: Ecgpedia.org]]]
 
*In 1915, Frank Norman Wilson became the first to describe the condition which would later be referred to as Wolff–Parkinson–White syndrome.
 
*In 1930, it was first described by Louis Wolff, John Parkinson, and Paul Dudley White.
*They also found the association of WPW with increasing the risk of [[sudden cardiac death]].


==Classification==
==Classification==


*Pre-excitation syndrome may be classified into sub-types
*Based on the [[Conduction System|conduction]] pathway or [[fiber]] subtype, pre-excitation syndrome may be [[Classification|classified]] into the following sub-types:<ref name="pmid1111564">{{cite journal |vauthors=Lowe KG, Emslie-Smith D, Ward C, Watson H |title=Classification of ventricular pre-excitation. Vectorcardiographic study |journal=Br Heart J |volume=37 |issue=1 |pages=9–19 |date=January 1975 |pmid=1111564 |pmc=484149 |doi=10.1136/hrt.37.1.9 |url=}}</ref><ref name="pmid14563598">{{cite journal| author=Blomström-Lundqvist C, Scheinman MM, Aliot EM, Alpert JS, Calkins H, Camm AJ et al.| title=ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias--executive summary. a report of the American college of cardiology/American heart association task force on practice guidelines and the European society of cardiology committee for practice guidelines (writing committee to develop guidelines for the management of patients with supraventricular arrhythmias) developed in collaboration with NASPE-Heart Rhythm Society. | journal=J Am Coll Cardiol | year= 2003 | volume= 42 | issue= 8 | pages= 1493-531 | pmid=14563598 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14563598  }} </ref>


{| class="wikitable"
{| class="wikitable"
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|Wide/long
|Wide/long
|Usually short
|Usually short
|yes
|Yes
|-
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |[[Lown-Ganong-Levine syndrome]]
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |[[Lown-Ganong-Levine syndrome]]
|"James bundle" (atria to bundle of His)
|"[[James fibers|James bundle]]" ([[atria]] to [[bundle of His]])
|Normal/Unaffected
|Normal/Unaffected
|Short
|Short
|no
|No
|-
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |Mahaim-type
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |[[Mahaim type preexcitation|Mahaim-type Pre-excitation]]
|[[Mahaim fibers]]
|[[Mahaim fibers]]
|long
|Long
|normal
|Normal
|
|No
|}<br />
|}


*
*Based on their [[conduction]] properties, following three types of [[accessory pathways]] are there:<ref name="pmid4561817">{{cite journal |vauthors=Kuramoto K, Matsushita S |title=[Classification and interpretation of WPW syndrome] |language=Japanese |journal=Nippon Rinsho |volume=30 |issue=8 |pages=1770–8 |date=August 1972 |pmid=4561817 |doi= |url=}}</ref>
**'''[[Accessory pathway|Manifest Accessory Pathways]]:'''
***[[Conduct|Conducts]] more rapidly as compared to [[AV nodal conduction]].
***[[Delta waves]] are commonly seen in [[ECG]].
**'''[[Concealed accessory pathway|Concealed Accessory Pathways]]:'''
***[[Conduct]] in the [[retrograde direction]].
***As the name represents, the changes in [[ECG]] are [[concealed]] and no [[delta waves]] are seen.
**'''Latent [[Accessory]] Pathways:'''
***These are located in the [[lateral]] part of the [[heart]] as compared to [[AV node]].
***Hence, the [[impulses]] are delayed in traveling to the [[ventricles]] through the [[AV node]] which is at a much shorter [[distance]] as compared to the [[latent fibers]] located at the farther end.


==Pathophysiology==
==Pathophysiology==
===Normal electrical conduction pathway of heart===


[[File:Basics of pre ex.jpg|thumb|Basics of Pre excitation sydrome|alt=|320x320px]]Basic concept of Pathophysiology in pre excitation syndrome lies with the concept of by passing the AV node conduction and letting the impulse conduct faster from the atria to ventricles via these channels or accessory pathways.
*Normally, the [[electrical]] activity of the [[heart]] starts from [[SA node]].
[[File:WPW- ECG findings.png|thumb|408x408px|'''WPW- ECG findings''']]
*The [[impulse]] [[generation]] usually happens in the right [[atrium]] near the [[entrance]] of [[superior vena cava]] and it travels from [[SA node]] to the [[AV node]].
These pathways usually conducts impulses in forward( not common), backward ( around 15-20%) and both directions ( Most common) as well. The accessory pathways also mediates the formation of tachyarrhythmia's by forming a re-entry circuit which is known as AVRT. The direct conduction of impulses from atria to ventricles can also result in development of tachyarrhythmia's under the condition of A. Fib with RVR
*The [[AV node ]] modulates the rate and number of impulses to be conducted to the [[ventricles]]. It also modulates the [[speed]] of [[transmission]] from [[atria]] to [[ventricles]] which represents the [[PR interval]] on ECG.
*From the [[AV node]], an [[electrical]] [[impulse]] is transmitted to the [[bundle of His]], to left and right branches extending to the [[ventricular]] [[myocardium]].


===WPW Syndrome===
===Pre-excitation pathway===
 
*WPW syndrome is a combination of WPW pattern on ECG + Paroxysmal arrhythmias. The accessory pathways are usually named as Bundle of Kent or AV bypass tracts.
 
*ECG features of WPW syndrome are
**Short PR interval <120 ms ( < .12 seconds) with Normal P wave morphology.
**Widened QRS complex ( >.12 seconds)
**Delta wave- slurring upstroke of the initial QRS complex, most important criteria for the diagnosis of WPW syndrome.
**Deflection of T waves opposite to the direction of QRS complexes / Secondary changes in ST segment and T wave.
**Mainly categorized into 2 subtypes
***Type A - Positive delta wave
***Type B - Negative delta wave
 
<br />
 
===Lown-Ganong-Levine(LGL) Syndrome===
 
*The accessory pathways here are named as James fibers, also known as atrionodal fibers connecting the atrium to the distal AV node. These usually conduct the impulses from atria to the initial portion of the AV node.
 
*ECG features:
**PR interval is less than 120ms or .12 seconds with usual normal P wave morphology
**Normal QRS complex
**Absence of delta waves
**Episodic paroxysmal SVT
 
<br />
 
*
 
===Mahaim-Type Pre-excitation===
 
*The accessory pathways named as mahaim fibers connect the Atrium, AV node, or bundle of His to the Purkinje fibers or ventricular myocardium.
 
*ECG findings are usually normal


*[[WPW]] is another word for [[pre-excitation]] of the [[ventricle]] through the [[accessory]] [[pathway]] instead of going through the usual pathway of [[AV node]] which usually slows down the [[speed]] of [[conduction]] of [[impulses]] transmitted to the [[ventricles]].
*The [[accessory]] pathway creates a channel directly to [[conduct]] the [[impulses]] to [[ventricles]] resulting in a [[premature]] [[excitation]].
*In "Type A [[Pre-excitation]]", the [[accessory]] pathway lies between [[left atria]] and [[ventricles]] whereas in Type B [[Pre-excitation]], [[Fiber|fibers]] carry impulses between [[right atria]] and [[ventricles]].
*Basic [[concept]] of [[pathophysiology]] in pre-excitation syndrome lies in the [[concept]] of [[Bypass|bypassing]] the [[AV node]] [[conduction]] and letting the [[impulse conduct]] faster through [[atria]] to [[ventricles]] via [[accessory pathways]].
*These [[accessory pathways]] usually known as [[Bundle of Kent]] in [[WPW syndrome]], [[James fiber]] in [[LGL syndrome]], and [[Mahaim fibers]] in [[Mahaim type preexcitation|Mahaim type pre-excitation syndrome]].
*These [[conduct]] [[impulses]] in forward (not common), backward (around 15-20%), and in both directions (most common type) as well.
*The [[accessory pathways]] mediate the occurrence of [[tachyarrhythmia]] by forming a [[re-entry]] circuit and commonly known as [[AVRT]].<ref name="pmid28328711">{{cite journal |vauthors=Moskowitz A, Chen KP, Cooper AZ, Chahin A, Ghassemi MM, Celi LA |title=Management of Atrial Fibrillation with Rapid Ventricular Response in the Intensive Care Unit: A Secondary Analysis of Electronic Health Record Data |journal=Shock |volume=48 |issue=4 |pages=436–440 |date=October 2017 |pmid=28328711 |pmc=5603354 |doi=10.1097/SHK.0000000000000869 |url=}}</ref>
*The direct [[conduction]] of [[impulses]] from [[atria]] to [[ventricles]] can also [[result]] in the [[development]] of [[tachyarrhythmias]] when there is a [[development]] of [[atrial fibrillation]] with [[RVR]].
*[[WPW syndrome]] is a combination of [[WPW]] [[pattern]] on [[ECG]] plus [[paroxysmal arrhythmias]].
*The [[accessory pathways]] are usually named as [[Bundle of Kent]] or [[AV node|AV]] [[Bypass tract|bypass tracts]].
*[[Accessory pathways|The accessory pathways]] here are named as [[James fibers]], also known as [[atrionodal fibers]] connecting the [[atrium (heart)|atrium]] to the distal [[Atrioventricular node|AV node]].
*These usually [[conduct]] the [[impulses]] from [[atria]] to the initial portion of the [[AV node]].
*[[Accessory pathways|The accessory pathways]] named as [[Mahaim fibers]] connect the [[atrium (heart)|Atrium]], [[AV node]], or [[bundle of His]] to the [[Purkinje fibers]] or [[ventricular myocardium]].


==Differentiating Pre-excitation Syndrome from other Diseases==
==Differentiating Pre-excitation Syndrome from other Diseases==
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! style="background: #4479BA; width: 200px;" |{{fontcolor|#FFF|Co-existing Conditions}}
! style="background: #4479BA; width: 200px;" |{{fontcolor|#FFF|Co-existing Conditions}}
|-
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |[[Atrial fibrillation|Atrial Fibrillation]] (AFib)
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |[[Atrial fibrillation|Atrial Fibrillation]] ([[Atrial fibrillation|AFib]])<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><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>
|
|
*Irregularly irregular
*[[Irregularly irregular pulse|Irregularly irregular]]
|
|
*On a 10-second 12-lead [[The electrocardiogram|EKG]] strip, multiply number of [[QRS complexes]] by 6
*On a 10-[[second]] 12-[[lead]] [[The electrocardiogram|EKG]] strip, multiply the number of [[QRS complexes]] by 6
|
|
*Absent
*Absent
*Fibrillatory waves
*[[Fibrillation|Fibrillatory waves]]
|
|
*Absent
*Absent
|
|
*Less than 0.12 seconds, consistent, and normal in morphology in the absence of aberrant conduction
*Less than 0.12 [[Second|seconds]], consistent, and [[normal]] in [[morphology]] in the absence of [[aberrant]] [[conduction]]
|
|
*Does not break with [[adenosine]] or [[vagal maneuvers]]
*Does not break with [[adenosine]] or [[vagal maneuvers]]
|
|
*2.7–6.1 million people in the United States have AFib
*2.7–6.1 million people in the [[United States]] have [[Atrial fibrillation|AFib]]
*2% of people younger than age 65 have AFib, while about 9% of people aged 65 years or older have AFib
*2% of people younger than [[age]] 65 have [[Atrial fibrillation|AFib]], while about 9% of people [[Age|aged]] 65 years or older have [[Atrial fibrillation|AFib]]
|
|
*Elderly
*[[Elderly]]
*Following [[Coronary artery bypass surgery|bypass surgery]]
*Following [[Coronary artery bypass surgery|bypass surgery]]
*[[Mitral valve disease]]
*[[Mitral valve disease]]
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*Left chamber enlargement
*Left chamber enlargement
|-
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |'''[[Atrial Flutter]]'''
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |'''[[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
*Regular or [[Irregular heart rhythms|Irregular]]
|
|
*75 (4:1 block), 100 (3:1 block) and 150 (2:1 block) beats per minute (bpm), but 150 is more common
*75 (4:1 block), 100 (3:1 block) and 150 (2:1 block) [[Beats per minute|beats per minute (bpm)]], but 150 is more common
|
|
*Sawtooth pattern of P waves at 250 to 350 bpm
*Sawtooth [[pattern]] of [[P waves]] at 250 to 350 [[Beats per minute|bpm]]
*Biphasic deflection in V1
*[[Biphasic]] deflection in V1
|
|
*Varies depending upon the magnitude of the block, but is short
*Varies depending upon the [[Magnitude (mathematics)|magnitude]] of the block, but is short
|
|
*Less than 0.12 seconds, consistent, and normal in morphology
*Less than 0.12 [[Second|seconds]], [[consistent|consistent,]] and [[normal]] in [[morphology]]
|
|
*Conduction may vary in response to drugs and maneuvers dropping the rate from 150 to 100 or to 75 bpm
*[[Conduction]] may vary in response to [[drugs]] and maneuvers dropping the [[rate]] from 150 to 100 or to 75 [[Beats per minute|bpm]]
|
|
*[[Incidence]]: 88 per 100,000 individuals
*[[Incidence]]: 88 per 100,000 individuals
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*[[Alcohol]]
*[[Alcohol]]
|-
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |'''[[Atrioventricular nodal reentry tachycardia]] ([[AV nodal reentrant tachycardia|AVNRT]])<nowiki>''''</nowiki>'''
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |'''[[Atrioventricular nodal reentry tachycardia]] ([[AV nodal reentrant tachycardia|AVNRT]])'''<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="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="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
*Regular
|
|
*140-280 bpm
*140-280 [[Beats per minute|bpm]]
|
|
*slow-fast AVNRT:
*[[Slow]]-fast [[AVNRT]]:
**Pseudo-S wave in leads II, III, and AVF
**Pseudo-[[S wave]] in [[Lead|leads]] II, III, and AVF
**Pseudo-R' in lead V1.
**Pseudo-R' in [[lead]] V1
*Fast-Slow AVNRT
*Fast-[[Slow]] [[AVNRT]]
**[[P waves]] between the [[QRS complex|QRS]] and [[T waves]] (QRS-P-T complexes)
**[[P waves]] between the [[QRS complex|QRS]] and [[T waves]] ([[QRS complex|QRS]]-[[P wave|P]]-[[T wave|T]] complexes)
*Slow-Slow AVNRT
*[[Slow]]-[[Slow]] [[AVNRT]]
**Late [[P waves]] after a [[QRS complex|QRS]]
**Late [[P waves]] after a [[QRS complex|QRS]]
**Often appears as [[atrial tachycardia]].
**Often appears as [[atrial tachycardia]].
*Inverted, superimposed on or buried within the [[QRS complex]] (pseudo R prime in V1/pseudo S wave in inferior leads)
*[[Invert|Inverted]], superimposed on or buried within the [[QRS complex]] (pseudo [[R wave|R]] prime in V1/pseudo [[S wave]] in inferior [[Lead|leads]])
|
|
*Absent ([[P wave]] can appear after the QRS complex and before the T wave, and in atypical AVNRT, the [[P wave]] can appear just before the [[QRS complex]])
*Absent ([[P wave]] can appear after the [[QRS complex]] and before the [[T wave]], and in atypical [[AVNRT]], the [[P wave]] can appear just before the [[QRS complex]])
|
|
*Less than 0.12 seconds, consistent, and normal in morphology in the absence of aberrant conduction
*Less than 0.12 [[Second|seconds]], consistent, and [[normal]] in [[morphology]] in the absence of [[aberrant]] [[conduction]]
*[[QRS complex alternans|QRS alternans]] may be present
*[[QRS complex alternans|QRS alternans]] may be present
|
|
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*[[Atrial tachyarrhythmias]]
*[[Atrial tachyarrhythmias]]
|-
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |[[Multifocal atrial tachycardia|Multifocal Atrial Tachycardia]]
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |[[Multifocal atrial tachycardia|Multifocal Atrial Tachycardia]]<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><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>
|
|
*Irregular
*[[Irregular Heart Rhythms|Irregular]]
|
|
*[[Atrial]] rate is > 100 beats per minute
*[[Atrial]] [[rate]] is > 100 [[beats per minute]]
|
|
*Varying morphology from at least three different foci
*Varying [[morphology]] from at least three different foci
*Absence of one dominant atrial pacemaker, can be mistaken for [[atrial fibrillation]] if the [[P waves]] are of low amplitude
*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 intervals, and PP intervals
*Variable [[PR interval|PR intervals]], [[RR intervals]], and [[PP interval|PP intervals]]
|
|
*Less than 0.12 seconds, consistent, and normal in morphology
*Less than 0.12 [[Second|seconds]], consistent, and [[normal]] in [[morphology]]
|
|
*Does not terminate with [[adenosine]] or [[vagal maneuvers]]
*Does not terminate with [[adenosine]] or [[vagal maneuvers]]
|
|
*0.05% to 0.32% of [[electrocardiograms]] in general hospital admissions
*0.05% to 0.32% of [[electrocardiograms]] in general [[hospital]] [[Admission note|admissions]]
|
|
*[[Elderly]]
*[[Elderly]]
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*Regular
*Regular
|
|
*150 and 240 bpm
*150 and 240 [[Beats per minute|bpm]]
|
|
*Absent
*Absent
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*Absent
*Absent
|
|
*Narrow complexes (< 0.12 s)
*Narrow [[QRS complexes|complexes]] (< 0.12 [[Second|s]])
|
|
*Breaks with [[vagal maneuvers]], [[adenosine]], [[diving reflex]], [[oculocardiac reflex]]
*Breaks with [[vagal maneuvers]], [[adenosine]], [[diving reflex]], [[oculocardiac reflex]]
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*[[Wolff-Parkinson-White syndrome]]
*[[Wolff-Parkinson-White syndrome]]
|-
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |'''[[Premature atrial contraction|Premature Atrial Contractrions]] ([[Premature atrial contraction|PAC]])'''
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |'''[[Premature atrial contraction|Premature Atrial Contractrions]] ([[Premature atrial contraction|PAC]])'''<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><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>
|
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*Regular except when disturbed by premature beat(s)
*Regular except when disturbed by [[premature beat(s)]]
|
|
*80-120 bpm
*80-120 [[Beats per minute|bpm]]
|
|
*Upright
*Upright
|
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*> 0.12 second
*> 0.12 [[second]]
*Maybe shorter than that in normal sinus rhythm (NSR) if the origin of PAC is located closer to the AV node
*Maybe shorter than that in [[Normal sinus rhythm|normal sinus rhythm (NSR)]] if the [[origin]] of [[PAC]] is located closer to the [[AV node]]
*Ashman’s Phenomenon:
*[[Ashman phenomenon|Ashman’s Phenomenon]]:
**[[Premature atrial contraction|PAC]] displaying a [[right bundle branch block]] pattern
**[[Premature atrial contraction|PAC]] displaying a [[right bundle branch block]] [[pattern]]
|
|
*Usually narrow (< 0.12 s)
*Usually narrow (< 0.12 [[Second|s]])
|
|
*Breaks with [[vagal maneuvers]], [[adenosine]], [[diving reflex]], [[oculocardiac reflex]]
*Breaks with [[vagal maneuvers]], [[adenosine]], [[diving reflex]], [[oculocardiac reflex]]
Line 256: Line 242:
*[[Hypercholesterolemia]]
*[[Hypercholesterolemia]]
|-
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |[[Wolff-Parkinson-White syndrome|Wolff-Parkinson-White Syndrome]]
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |[[Wolff-Parkinson-White syndrome|Wolff-Parkinson-White Syndrome]]<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><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>
|
|
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*Regular
*Regular
|
|
*Atrial rate is nearly 300 bpm and the ventricular rate is at 150 bpm
*[[Atrial]] [[rate]] is nearly 300 [[Beats per minute|bpm]] and the [[ventricular]] [[rate]] is at 150 [[Beats per minute|bpm]]
|
|
*With [[orthodromic]] conduction due to a bypass tract, the [[P wave]] generally follows the [[QRS complex]], whereas in [[AVNRT]], the [[P wave]] is generally buried in the [[QRS complex]].
*With [[orthodromic]] [[Conduction System|conduction]] due to a [[bypass tract]], the [[P wave]] generally follows the [[QRS complex]], whereas in [[AVNRT]], the [[P wave]] is generally buried in the [[QRS complex]].
|
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*Less than 0.12 seconds
*Less than 0.12 [[Second|seconds]]
|
|
*A [[delta wave]] and evidence of [[ventricular]] pre-excitation if there is conduction to the ventricle via ante-grade conduction down an accessory pathway
*A [[delta wave]] and [[evidence]] of [[ventricular]] [[Pre-excitation of the ventricles|pre-excitation]] if there is [[Conduction System|conduction]] to the [[ventricle]] via ante-grade [[conduction]] down an [[accessory pathway]]
*A [[delta wave]] and pre-excitation may not be present because bypass tracts do not conduct ante-grade.
*A [[delta wave]] and [[Pre-excitation of the ventricles|pre-excitation]] may not be present because [[Bypass tract|bypass tracts]] do not [[conduct]] ante-grade.
|
|
*May break in response to [[procainamide]], [[adenosine]], [[vagal maneuvers]]
*May break in response to [[procainamide]], [[adenosine]], [[vagal maneuvers]]
Line 275: Line 260:
|
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*[[Ebstein's anomaly]]
*[[Ebstein's anomaly]]
*[[Mitral valve prolapse]]: This cardiac disorder, if present, is associated with left-sided accessory pathways.
*[[Mitral valve prolapse]]: This [[cardiac]] [[disorder]], if present, is associated with left-sided [[accessory pathways]].
*[[Hypertrophic cardiomyopathy]]: This disorder is associated with familial/inherited form of [[Wolff-Parkinson-White syndrome|WPW syndrome]].
*[[Hypertrophic cardiomyopathy]]: This [[disorder]] is associated with [[familial]]/[[inherited]] form of [[Wolff-Parkinson-White syndrome|WPW syndrome]].
*[[Hypokalemic periodic paralysis]]
*[[Hypokalemic periodic paralysis]]
*[[Pompe disease]]
*[[Pompe disease]]
*[[Tuberous sclerosis]]
*[[Tuberous sclerosis]]
|-
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |'''[[Ventricular fibrillation|Ventricular Fibrillation]] (VF)'''
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |'''[[Ventricular fibrillation|Ventricular Fibrillation]] ([[Ventricular fibrillation|VF]])'''<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><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>
|
|
*Irregular
*[[Irregular heart rhythms|Irregular]]
|
|
*150 to 500 bpm
*150 to 500 [[Beats per minute|bpm]]
|
|
*Absent
*Absent
Line 291: Line 276:
*Absent
*Absent
|
|
*Absent (R on T phenomenon in the setting of ischemia)
*Absent (R on T phenomenon in the setting of [[ischemia]])
|
|
*Does not break in response to [[procainamide]], [[adenosine]], [[vagal maneuvers]]
*Does not break in response to [[procainamide]], [[adenosine]], [[vagal maneuvers]]
|
|
*3-12% cases of [[acute myocardial infarction]] (AMI)
*3-12% cases of [[acute myocardial infarction]] (AMI)
*Out of 356,500 out of hospital cardiac arrests, 23% have VF as initial rhythm
*Out of 356,500 out of [[hospital]] [[Cardiac arrest|cardiac arrests]], 23% have [[Ventricular fibrillation|VF]] as initial [[rhythm]]
|
|
*[[Myocardial ischemia]] / [[Myocardial infarction|infarction]]
*[[Myocardial ischemia]] / [[Myocardial infarction|infarction]]
*[[Cardiomyopathy]]
*[[Cardiomyopathy]]
*Channelopathies e.g. Long QT (acquired / congenital)
*[[Channelopathies]] e.g. [[Long QT Syndrome|Long QT]] ([[acquired]]/ [[congenital]])
*Electrolyte abnormalities ([[hypokalemia]]/[[hyperkalemia]], [[hypomagnesemia]])
*[[Electrolyte abnormalities]] ([[hypokalemia]]/[[hyperkalemia]], [[hypomagnesemia]])
*[[Aortic stenosis]]
*[[Aortic stenosis]]
*[[Aortic dissection]]
*[[Aortic dissection]]
*[[Myocarditis]]
*[[Myocarditis]]
*[[Cardiac tamponade]]
*[[Cardiac tamponade]]
*Blunt trauma (Commotio Cordis)
*[[Blunt trauma]] (Commotio Cordis)
*[[Sepsis]]
*[[Sepsis]]
*[[Hypothermia]]
*[[Hypothermia]]
Line 313: Line 298:
*[[Stroke]]
*[[Stroke]]
|-
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |'''[[Ventricular tachycardia|Ventricular Tachycardia]]'''
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" |'''[[Ventricular tachycardia|Ventricular Tachycardia]]'''<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><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>


|
|
*Regular
*Regular
|
|
*> 100 bpm (150-200 bpm common)
*> 100 [[Beats per minute|bpm]] (150-200 [[Beats per minute|bpm]] common)
|
|
*Absent
*Absent
|
|
*Absent
*Absent
*Initial [[R wave]] in V1, initial r > 40 ms in V1/V2, notched S in V1, initial R in aVR, lead II R wave peak time ≥50 ms, no RS in V1-V6, and atrioventricular dissociation
*Initial [[R wave]] in [[V1-morph|V1]], initial r > 40 [[Millisecond|ms]] in [[V1-morph|V1]]/V2, notched [[S wave|S]] in [[V1-morph|V1]], initial [[R wave|R]] in aVR, [[lead]] II [[R wave]] peak time ≥50 [[Millisecond|ms]], no RS in [[V1-morph|V1]]-V6, and [[atrioventricular dissociation]]
|
|
*Wide complex, [[QRS complex|QRS]] duration > 120 milliseconds
*Wide complex, [[QRS complex|QRS]] duration > 120 [[Millisecond|milliseconds]]
|
|
*Does not break in response to [[procainamide]], [[adenosine]], [[vagal maneuvers]]
*Does not break in response to [[procainamide]], [[adenosine]], [[vagal maneuvers]]
|
|
*5-10% of patients presenting with AMI
*5-10% of [[patients]] presenting with AMI
|
|
*[[Coronary artery disease]]
*[[Coronary artery disease]]
Line 335: Line 320:
*[[Cardiomyopathy]]
*[[Cardiomyopathy]]
*[[Electrolyte imbalance|Electrolyte imbalances]] (e.g., [[hypokalemia]], [[hypomagnesemia]])
*[[Electrolyte imbalance|Electrolyte imbalances]] (e.g., [[hypokalemia]], [[hypomagnesemia]])
*Inherited [[channelopathies]] (e.g., [[long-QT syndrome]])
*[[Inherited]] [[channelopathies]] (e.g., [[long-QT syndrome]])
*[[Catecholaminergic polymorphic ventricular tachycardia]]
*[[Catecholaminergic polymorphic ventricular tachycardia]]
*[[Arrhythmogenic right ventricular dysplasia]]
*[[Arrhythmogenic right ventricular dysplasia]]
*[[Myocardial infarction]]
*[[Myocardial infarction]]
*[[Torsades de pointes]] is a form of polymorphic VT that is often associated with a prolonged [[QT interval]]
*[[Torsades de pointes]] is a form of [[polymorphic VT]] that is often associated with a prolonged [[QT interval]]
|}
|}


==Epidemiology and Demographics==
==Epidemiology and Demographics==


*Incidence 0.1 – 3.0 per 1000
*[[WPW]] is commonly found with an [[incidence]] of around 0.1-3.0 per thousand [[population]].<ref name="pmid22579340">{{cite journal |vauthors=Cohen MI, Triedman JK, Cannon BC, Davis AM, Drago F, Janousek J, Klein GJ, Law IH, Morady FJ, Paul T, Perry JC, Sanatani S, Tanel RE |title=PACES/HRS expert consensus statement on the management of the asymptomatic young patient with a Wolff-Parkinson-White (WPW, ventricular preexcitation) electrocardiographic pattern: developed in partnership between the Pediatric and Congenital Electrophysiology Society (PACES) and the Heart Rhythm Society (HRS). Endorsed by the governing bodies of PACES, HRS, the American College of Cardiology Foundation (ACCF), the American Heart Association (AHA), the American Academy of Pediatrics (AAP), and the Canadian Heart Rhythm Society (CHRS) |journal=Heart Rhythm |volume=9 |issue=6 |pages=1006–24 |date=June 2012 |pmid=22579340 |doi=10.1016/j.hrthm.2012.03.050 |url=}}</ref>
*[[Lown-Ganong-Levine syndrome|LGL syndrome]] is a rare Man > woman.
*More common in the [[male]] [[population]] as compared to [[females]].
*prognosis is good with [[SCD]] is noted in only 0.1% (rare)<br />
*[[Familial studies]] have found that it is 0.55% more commonly found amoung [[first degree]] relatives.
*More common in [[young]] and [[healthy]] [[individuals|individuals,]] and as the [[age]] advances, the [[prevalence]] of [[disease]] [[decreases]] because of loss of [[pre-excitation]].
*[[WPW]] can be considered as a [[congenital]] [[anomaly]] in some cases where it is usually present since [[birth]] whereas in others, it is regarded as a [[developmental]] [[anomaly]]. Studies have shown a [[lower]] [[prevalence]] in [[children]] [[aged]] between 6-13 than those in the [[age]] group of 14-15 [[Year|years]] of [[age]].


==Risk Factors==
==Risk Factors==
High risk population for [[sudden cardiac death]] in [[Wolff-Parkinson-White syndrome]] include:


*Policemen
*High-risk [[population]] for [[development]] of [[atrial fibrillation]] or [[sudden cardiac death]] include:<ref name="pmid22532593">{{cite journal |vauthors=Obeyesekere MN, Leong-Sit P, Massel D, Manlucu J, Modi S, Krahn AD, Skanes AC, Yee R, Gula LJ, Klein GJ |title=Risk of arrhythmia and sudden death in patients with asymptomatic preexcitation: a meta-analysis |journal=Circulation |volume=125 |issue=19 |pages=2308–15 |date=May 2012 |pmid=22532593 |doi=10.1161/CIRCULATIONAHA.111.055350 |url=}}</ref>
*Athletes
**[[Pilots]]
*Firemen
**[[Male]] [[gender]]
*Pilots
**[[Athletes]]
*Steelworkers
**[[Policemen]]
**[[Steelworkers]]
**[[Firemen]]
**Past history of [[syncope]]
**[[Age]] (peak [[Age|ages]] for the [[development]] of [[atrial fibrillation]] include 30 [[Year|years]] and 50 [[Year|years]])


Risk factors for the development of [[atrial fibrillation]] in WPW syndrome include:
==Natural History, Complications, and Prognosis==
===Natural History===


*Male gender
*Numerous [[studies]] have been published to [[describe]] the [[natural history]] or [[disease]] course of pre-excitation syndrome. [[Data]] from a recent study- "[[Long term]] [[natural]] [[history]] of [[patients]] with [[WPW]] treated with or without [[catheter ablation]]" showed promising [[results]] in explaining the reduced [[long-term]] [[mortality]] rates in [[WPW]] [[patients]] who are matched for [[age]] and [[gender]]. It also explained that there is a lower [[mortality]] rate among [[catheter]] ablated [[patients]] as compared to the non-ablated ones. Although the [[patients]] can die with [[sudden cardiac death]], death is uncommon.<ref name="pmid22532593">{{cite journal |vauthors=Obeyesekere MN, Leong-Sit P, Massel D, Manlucu J, Modi S, Krahn AD, Skanes AC, Yee R, Gula LJ, Klein GJ |title=Risk of arrhythmia and sudden death in patients with asymptomatic preexcitation: a meta-analysis |journal=Circulation |volume=125 |issue=19 |pages=2308–15 |date=May 2012 |pmid=22532593 |doi=10.1161/CIRCULATIONAHA.111.055350 |url=}}</ref>
*Age (peak ages for the development of atrial fibrillation include 30 years and 50 years)
*Past history of [[syncope]]


<br />
===Complications===
==Natural History, Complications and Prognosis==


*The majority of patients with [disease name] remain asymptomatic for [duration/years].
*Most common [[complications]] studied in [[patients]] having [[accessory pathway]] [[Conduction basics|conduction]] are [[arrhythmias]] and [[sudden cardiac death]].
*Early clinical features include [manifestation 1], [manifestation 2], and [manifestation 3].
**'''[[Tachyarrhythmias]]:'''
*If left untreated, [#%] of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].
***If there is a [[development]] of [[atrial fibrillation]] or [[flutter]], then there is [[fast conduction]] across the [[tracts]] which leads to an increased risk of dangerous [[ventricular arrhythmias]].
*Common complications of [disease name] include [complication 1], [complication 2], and [complication 3].
***[[AV nodal blocks|AV nodal blocking agents]] may also be the factor responsible for the [[increased]] [[Conduction System|conduction]] through [[accessory pathways]] causing life-threatening [[ventricular arrhythmias]] or [[hemodynamic]] instability resulting in a worse [[prognosis]].
*Prognosis is generally [excellent/good/poor], and the [1/5/10­year mortality/survival rate] of patients with [disease name] is approximately [#%].
**'''[[Sudden cardiac death]]:'''
***[[Sudden cardiac death]] is a more common [[complication]] in [[patients]] with the following characteristics:
****A young [[male]] with [[age]] less than 35
****Past history of [[arrhythmias]]
****[[Anatomical|Anatomical location]] of [[accessory pathway]]- that is the [[septal]] [[Location parameter|location]] of the [[accessory pathway]]
****Having multiple [[accessory pathways]]
***The studies proved the risk of [[sudden cardiac death]] related to the pre-excitation syndrome is around 1.5% in [[childhood]] with the highest [[risk]] in the first two decades of [[life]].


<br />
===Prognosis===
 
*[[Prognosis]] is usually very good if the [[patient]] is being [[Managed care|managed]] and [[Treatment|treated]] appropriately.
*[[Catheter ablation]] showed promising [[Result|results]] in the [[curative]] [[treatment]] of [[patients]] suffering from this [[disorder]].
*[[Sudden cardiac death]] is rarely seen in [[patients]] with this [[syndrome]] but when it happens, it is most commonly related to [[arrhythmias]].
*The most common [[misconception]] about the [[prognosis]] of [[WPW syndrome]] is related to the severity of [[symptoms]] in a [[patient]] but the most important determinant of [[prognosis]] is dependent on the [[electrophysiologic]] properties of the [[accessory pathways]].
*The [[conduction]] through [[accessory pathways]] usually decreases with [[age]]. This is due to [[fibrotic changes]] that happen with time.<br />


==Diagnosis==
==Diagnosis==
===WPW Syndrome===


====<u>[[Atrioventricular (AV) reentrant tachycardia|Atrioventricular Reentry Tachycardia's (AVRT)]]</u>====
*[[WPW syndrome]] is a combination of [[WPW]] [[pattern]] on [[ECG]] and paroxysmal [[arrhythmias]]. The [[accessory pathways]] are usually named as [[Bundle of Kent]] or [[AV]] [[bypass tracts]].
[[File:Orth.gif|thumb|AVRT ( Orthodromic and Antidromic)]]AVRT is a form of PSVT. Reentry circuit results from the combination of signal transduction from normal conduction system and [[accessory pathway]].( See: Diagram)
*[[ECG]] [[Features (pattern recognition)|features]] of [[WPW]] syndrome are:
**[[Short PR interval]] <120 ms (<0.12 [[Second|seconds]]) with [[normal]] [[P wave]] [[morphology]]
**[[Wide QRS complexes|Widened QRS complex]] (>0.12 [[Second|seconds]])
**[[Delta wave]] - slurring upstroke of the initial [[QRS complex]] due to the early and [[rapid depolarization]] of [[ventricles]] (the most important [[criteria]] for the [[diagnosis]] of [[WPW syndrome]]).
**Deflection of [[T waves]] [[opposite]] to the [[direction]] of [[QRS complexes]]/[[secondary]] changes in [[ST-segment]] and [[T wave]]
**Types of [[AVRT]] varies depending on the [[direction]] of the [[impulse conduction]] in the [[re-entry circuit]] ([[orthodromic]] or [[antidromic]]):
***[[Orthodromic AVRT|'''Orthodromic AVRT''']] means the [[antegrade conduction]] is through the [[AV node]] and [[retrograde]] through the [[accessory pathway]]. It presents with [[narrow QRS]] complexes on [[ECG]].
***[[Antidromic AVRT|'''Antidromic AVRT''']] means the [[antegrade]] [[conduction]] is through the AP and [[retrograde]] conduction through [[AV node]]. It presents with [[Wide QRS complex tachycardias|wide QRS complexes]] on [[ECG]].
**So in short, the [[Orthodromic AVRT]] [[preexcitation]] [[syndrome]] presents with [[narrow complex tachycardia]] and [[Antodromic AVRT|Antidromic AVRT]] [[pre-excitation]] [[syndrome]] presents with [[wide complex]] [[Tachycardias|tachycardia]].
**[[AF]] with [[RVR]] can be [[diagnosed]] in [[patients]] with [[WPW]] by comparing it with the baseline [[ECG]]. Look for comparison between [[pre-excited]] [[QRS]] complexes on the baseline [[ECG]] vs those seen during [[irregular tachycardia]].
**Mainly categorized into 2 subtypes
***Type A - Positive [[delta wave]]
***Type B - Negative [[delta wave]]


*During tachyarrythmias, the [[accessory pathway]] forms part of the reentry circuit that results in the disappearance of features of tachyarrhythmias.
[[File:WPW Syndrome - ECG changes with delta wave.png|thumb|300px|none|WPW ECG changes with significant 1) Delta wave 2) PR interval shortening 3) Wide QRS complexes. [https://openi.nlm.nih.gov/detailedresult?img=PMC4944806_wjem-17-469-g002&query=WPW%20syndrome&it=xg&req=4&npos=35]]]
*[[AV reentrant tachycardia|AVRT]] are further divided into
**Orthodromic or Antidromic conduction based on ECG morphology and direction of formation of re-entry circuit.


===History and Symptoms===
===Lown-Ganong-Levine (LGL) Syndrome===
People with Pre- Excitation syndromes may be asymptomatic, however, the individual may experience following symptoms


*'''[[Palpitation|Palpitations]]'''
*The [[accessory pathways]] [[LGL syndrome]] are named as [[James fibers]], also known as [[atrionodal fibers]] connecting the [[Atrium (heart)|atrium]] to the distal [[Atrioventricular node|AV node]]. These usually [[conduct]] the [[impulses]] from [[atria]] to the initial portion of the [[AV node]].
*'''[[Dizziness]]''' or lightheadedness.
*[[ECG]] features:
*[[Dyspnea|'''Shortness of breath'''.]]
**[[PR interval]] is less than 120 ms or 0.12 [[Second|seconds]] with [[normal]] [[P wave]] [[morphology]]
*[[Chest pain]]
**[[Normal]] [[QRS complex]]
*Fatigue.
**Absence of [[Delta wave|delta waves]]
*[[Anxiety]].
**Episodic [[Paroxysmal supraventricular tachycardia|paroxysmal SVT]]
*Fainting
*Difficulty breathing


======1) AVRT with Orthodromic Conduction======
===Mahaim-Type Pre-excitation===
In this, the anterograde conduction occurs via the [[AV node]] and retrograde conduction occurs via an accessory pathway. 


ECG features of [[AV reentrant tachycardia|AVRT]] with orthodromic conduction
*The [[accessory pathways]] named as [[Mahaim fibers]] connect the [[atrium (heart)|atrium]], [[AV node]], or [[bundle of His]] to the [[Purkinje fibers]] or [[ventricular myocardium]].<ref name="pmid15489095">{{cite journal |vauthors=Sternick EB, Timmermans C, Sosa E, Cruz FE, Rodriguez LM, Fagundes MA, Gerken LM, Wellens HJ |title=The electrocardiogram during sinus rhythm and tachycardia in patients with Mahaim fibers: the importance of an "rS" pattern in lead III |journal=J. Am. Coll. Cardiol. |volume=44 |issue=8 |pages=1626–35 |date=October 2004 |pmid=15489095 |doi=10.1016/j.jacc.2004.07.035 |url=}}</ref>
*[[ECG]] findings are usually [[normal]].


*Rate usually 200 – 300 bpm
===History and Symptoms===


*P waves may be buried in QRS complex or retrograde
*[[Patients]] with pre-excitation syndromes maybe [[Asymptomatic|asymptomatic,]] however, they can commonly experience the following [[symptoms]]:
*QRS Complex usually <120 ms unless pre-existing bundle branch block, or rate-related aberrant conduction
**[[Palpitation|Palpitations]]
*[[QRS complex alternans|QRS Alternans]] – phasic variation in QRS amplitude associated with AVNRT and AVRT, distinguished from electrical altrens by a normal QRS amplitude
**[[Dizziness]] or [[lightheadedness]]
*T wave inversion common
**[[Dyspnea|Shortness of breath]]
*[[ST segment depression]]
**[[Chest pain]]
**[[Fatigue]]
**[[Anxiety]]
**[[Fainting]]
**[[Difficulty breathing]]


<br />
==Treatment==
====2) AVRT with Antidromic Conduction====
===Medical Treatment===
In this, the anterograde conduction occurs via the accessory pathway and retrograde conduction via the AV node. Occurring only in-app. 5% of patients with WPW.


ECG features are:
*'''[[Hemodynamically unstable|HEMODYNAMICALLY UNSTABLE]] [[Patient|PATIENT]]''' --  [[Direct-current cardioversion|DIRECT SYNCHRONIZED CARDIOVERSION]], [[Biphasic|BIPHASIC]] (INITIAL 100 [[Joule|J]],  LATER ON- 200[[Joule|J]] OR 360[[Joule|J]]).
*'''[[Hemodynamically|HEMODYNAMICALLY]] [[Stability|STABLE]] [[Patient|PATIENT]]'''  -- THE FOLLOWING [[Protocols|PROTOCOL]] SHOULD BE FOLLOWED:


*Rate usually 200 – 300 bpm.
====GENERAL PROTOCOL====
*[[Wide QRS complexes]] due to abnormal accessory pathway ventricular depolarisation.
General [[Protocols|protocol]] includes the following:<ref name="pmid30056397">{{cite journal |vauthors=Stasiak A, Niewiadomska-Jarosik K, Kędziora P |title=Clinical course and treatment of children and adolescents with the preexcitation syndrome - own studies |journal=Dev Period Med |volume=22 |issue=2 |pages=113–122 |date=2018 |pmid=30056397 |doi= |url=}}</ref>
*Due to wide complex, Commonly mistaken for [[Ventricular tachycardia|Ventricular Tachycardia.]]


<br />
*[[Antiarrhythmic drug|'''Antiarrhythmic drug''']]
====3) Atrial Fib/Atrial Flutter in WPW====
**Helps in slowing the [[accessory pathway]] [[conduction]] and thus plays a major role in the [[Acute|acute events.]]
*'''[[Atrioventricular block|AV Nodal blocking]] agents should NOT be used'''
**As they aggravate [[WPW]] by increasing the [[conduction]] through the [[accessory pathway]].
*'''Address the underlying [[Causes|cause]] [[Trigger|triggering]] [[dysrhythmias]] which may include:'''
**[[Coronary artery disease]]
**[[Cardiomyopathy]]
**[[Electrolyte abnormalities|Electrolyte derangement]]
**[[Anemia]]
**[[Thyroid disease]]


*In 20% of the patients WPW Atrial fibrillation can occur and in approx 7% of patients with [[Wolff-Parkinson-White syndrome|WPW]] [[atrial flutter]] can occur. Accessory pathways plays major role by allowing the rapid conduction of impulses directly to the ventricles without involving [[Atrioventricular node|AV node]], in extreme cases may lead to VT or VF.
====IN CASE OF [[ACUTE]] [[AVRT]]/[[AVNRT]]====


ECG features are:
*[[Treatment|Treated]] by [[Blocking (statistics)|blocking]] the [[AV nodal]] [[conduction]]
**Help in [[Blocking (statistics)|blocking]] the [[Pathways Health and Research Centre|pathways]] responsible for causing [[dysrhythmias]] through the involvement of the [[AV node]] ([[AV reentrant tachycardia|AVRT]]/[[AV nodal reentrant tachycardia|AVNRT]]).
**[[Vagal maneuvers|Vagal Maneuvers]] - [[Valsalva maneuver]], immersing the face in [[cold water]] or [[ice water]], [[carotid sinus massage]]
**[[IV]] [[Adenosine]]- very short [[half-life]] and commonly used in [[dose]] around 6-12 mg
**[[IV]] [[Verapamil]]- this is a [[calcium]] [[channel blocker]] and commonly used as 5-10 mg.


*Rate > 200 bpm
====[[ATRIAL FLUTTER]]/[[FIBRILLATION]]====
*[[Irregular rhythm]]
*Wide QRS complexes due to abnormal ventricular depolarisation via an accessory pathway
*QRS Complexes change in shape and morphology
*Axis remains stable unlike [[Ventricular tachycardia classification|Polymorphic VT]]
*[[Atrial flutter|Atrial Flutter]] presents with same features as atrial fibrillation in WPW except rhythm is regular and commonly mistaken for VT


<br />
*If [[wide complex]] [[tachycardia]] is present:<ref name="pmid23545139">{{cite journal |vauthors=Wann LS, Curtis AB, Ellenbogen KA, Estes NA, Ezekowitz MD, Jackman WM, January CT, Lowe JE, Page RL, Slotwiner DJ, Stevenson WG, Tracy CM, Fuster V, Rydén LE, Cannom DS, Crijns HJ, Curtis AB, Ellenbogen KA, Halperin JL, Le Heuzey J, Kay GN, Lowe JE, Olsson SB, Prystowsky EN, Tamargo JL, Wann LS |title=Management of patients with atrial fibrillation (compilation of 2006 ACCF/AHA/ESC and 2011 ACCF/AHA/HRS recommendations): a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines |journal=Circulation |volume=127 |issue=18 |pages=1916–26 |date=May 2013 |pmid=23545139 |doi=10.1161/CIR.0b013e318290826d |url=}}</ref>
==Treatment==
**Use IV [[Amiodarone]] or [[Procainamide|Procainamaide]]


===Medical Treatment===
====[[Radiofrequency ablation|RADIOFREQUENCY ABLATION]]====


====Orthodromic AVRT====
*This [[modality]] has replaced [[drug therapy]] and other [[Surgery operation|surgical treatment]] options by showing promising [[Result|results]]. The best [[Result|results]] have been found when it is used in [[Conjunction introduction|conjunction]] with [[cryoblation]] (commonly used for [[accessory pathway|septal accessory pathways]] and for [[accessory pathways]] near small [[coronary arteries]]).<ref name="pmid22579340">{{cite journal |vauthors=Cohen MI, Triedman JK, Cannon BC, Davis AM, Drago F, Janousek J, Klein GJ, Law IH, Morady FJ, Paul T, Perry JC, Sanatani S, Tanel RE |title=PACES/HRS expert consensus statement on the management of the asymptomatic young patient with a Wolff-Parkinson-White (WPW, ventricular preexcitation) electrocardiographic pattern: developed in partnership between the Pediatric and Congenital Electrophysiology Society (PACES) and the Heart Rhythm Society (HRS). Endorsed by the governing bodies of PACES, HRS, the American College of Cardiology Foundation (ACCF), the American Heart Association (AHA), the American Academy of Pediatrics (AAP), and the Canadian Heart Rhythm Society (CHRS) |journal=Heart Rhythm |volume=9 |issue=6 |pages=1006–24 |date=June 2012 |pmid=22579340 |doi=10.1016/j.hrthm.2012.03.050 |url=}}</ref>
*This technique is used widely with best [[Result|results]] in:
**[[Patients]] with [[AVRT]] showing [[symptoms]] of [[dysrhythmias]]
**[[Patients]] with impaired functional [[Activities of daily living|daily activities]] having no [[symptoms]] with ventricular pre-excitation
**[[Patients]] with [[Wolff-Parkinson-White syndrome|WPW]] and [[family history]] of [[sudden cardiac death]] in first or [[second]]-degree relatives.
**[[Patients]] with [[AVRT]] OR [[Atrial fibrillation|A.FIB]] with RVR
**[[Patients]] with H/O pre-excited [[Atrial fibrillation|A.FIB]]
*[[Patients]] who are not willing to undergo [[radiofrequency]] [[ablation]] can be managed on [[medical]] management with the use of [[anti-arrhythmic]]. Though its role in the [[prevention]] of future episodes of [[arrhythmias]] is limited, still this is the most commonly used [[modality]] of choice.
*Class 3 [[Antiarrhythmics]] and class IC [[drugs]] are used with [[Atrioventricular block|AV nodal blocking]] agents in [[patients]] with a history of [[atrial flutter]] or [[Atrial fibrillation|A.Fib]].
*[[Sotalol]] and [[Flecainide]] are safe options to use in [[pregnancy]].


*Hemodynamically Unstable patients (Low BP, Altered mental state, pulmonary edema)- Synchronized DC Cardioversion.
===Surgical management===
*Hemodynamically stable- Vagal maneuvers, Adenosine, CCB, and DC cardioversion as a last resort only if the patient not responding to medical therapy.


=====Antidromic AVRT=====
*[[Surgery|Surgical]] management includes the following options:
**'''[[Endocardial|ENDOCARDIAL]] [[Surgery|SURGICAL]] [[APPROACH]]'''
**'''[[Epicardial|EPICARDIAL]] [[Surgery|SURGICAL]] [[APPROACH]]'''
**Due to the [[continuing]] advancement in [[medical]] [[science]], [[radiofrequency catheter ablation]] is widely used as a preferred [[treatment]] option.
**Role of the [[Surgery|surgical]] approach is limited to:
***[[Patients]] who are undergoing [[cardiac surgery]] due to other [[causes]].
***[[Patients]] in whom [[catheter ablation]] is tried but failed in the past.
***[[Patients]] with multiple [[Area|areas]] or [[foci]] [[Generation|generating]] the [[impulses]] usually requires a [[surgical]] approach for best [[Outcome|outcomes]].


*Hemodynamically unstable patients:- Urgent synchronized DC cardioversion.
*Hemodynamically stable patients:- Amiodarone, procainamide, or ibutilide.
======AF with WPW======
*Hemodynamically unstable patients: Urgent synchronized DC cardioversion
*Hemodynamically stable patients:- Procainamide or ibutilide.
*<u>'''Caution''':</u> Adenosine, CCB, Beta blockers enhances conduction via accessory pathway resulting in worsening & possible degeneration into VT or VF
===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].
<br />
==Prevention==
==Prevention==
For preventing the recurrence of episodes major options available are


*[[Radiofrequency ablation|Radio frequency ablation]]
*The most common [[preventive]] measures used against [[WPW]] are [[radiofrequency catheter ablation]].
**Ablation of [[Accessory pathway|accessory pathway tracts]]
**This [[helps]] in [[preventing]] future [[Attack rate|attacks]] by [[Ablation|ablating]] the [[accessory pathways]] with a success [[rate]] of >95%.
**cures 95% of the time
*Although the success [[rate]] for the [[surgical]] approach is 100%, still the [[catheter ablation]] is preferred as it is less [[invasive]] and [[Association (statistics)|associated]] with lower [[complication]] [[rates]].
*Surgery.  
*General [[Measure (mathematics)|measures]] that help in [[preventing]] the [[episodes]] such as [[valsalva maneuvers]] should be taught to the [[patient]] so that [[tachycardia]] can be relieved during an [[acute episode]].
**Success rate for surgical ablation is around 100 percent along with lower complication rates. Radiofrequency ablation is a less invasive option and preferred over surgery.
*Although [[medicines]]/[[antiarrhythmic]] can help [[Prevention|prevent]] [[recurrent]] [[episodes]], this is only preferred in [[Patient|patients]] who are not the candidates for [[catheter]] [[ablation]] or [[surgical]] approach.
**Surgery can be considered if a patient is undergoing cardiac surgery for other reasons such as [[Coronary artery bypass surgery|CABG]] or other heart valve surgery.
*Medications
**Although Medications can prevent recurrent episodes of tachycardia they are only used on patients who are not the candidates for ablation or surgery.
**These patients must be taught to perform Valsalva maneuvers that can relieve tachycardia during the episodes.<br />


==References==
==References==
<references />
{{Reflist|2}}
 
[[Category:Cardiology]]
[[Category:Up TO Date]]

Latest revision as of 13:04, 15 April 2021

Pre-excitation syndrome Microchapters

Overview

Historical Perspective

Classification

Pathophysiology

Differentiating Pre-excitation Syndrome from other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications, and Prognosis

Diagnosis

Treatment

Prevention

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2] Associate Editor(s)-in-Chief: Shivam Singla, M.D.[3]

Synonyms and keywords: Pre Excitation Syndromes; Lown-Ganong-Levine Syndrome; Pre-Excitation, Mahaim-Type Pre-excitation; Wolff-Parkinson-White Syndrome

Overview

Pre-excitation syndrome is a condition in which the ventricles of heart depolarize earlier than expected via some accessory pathway conduction, leading to a premature contraction. Normally, atria and ventricles are interconnected with each other via the AV node (atrioventricular node). However, in all the pre-excitation syndromes, an accessory pathway is present that conducts impulses to ventricles besides the AV node. The accessory pathway passes the electrical impulses to the ventricles before the normal impulse of depolarization passes through the AV node. The phenomenon of depolarizing ventricles through the accessory pathway earlier than the usual depolarization is supposed to happen through the AV node is referred to as "Pre- Excitation". WPW syndrome was described in 1930 and named after John Parkinson, Paul Dudley White, and Louis Wolff. The accessory pathways are named depending upon the regions of atria and ventricles they are connecting such as Bundle of His, Mahaim fibers, and James fibers. The typical ECG findings associated with WPW syndrome are shortened PR interval, widened QRS complex and Delta wave which is a slurring in the upstroke of QRS complex due to preexcitation of ventricles via the accessory pathway. ECG findings along with symptomatic tachyarrhythmias are referred to as Wolff-Parkinson-White syndrome. Although it is more common in adults, males have an incidence rate of 0.1-0.3 %, WPW can be considered as a congenital anomaly in some cases where it is usually present since the birth and in others, it is considered as a developmental anomaly. Studies have proven its lower prevalence in children aged between 6-13 than those in the age group of 14-15 years of age. Hemodynamically unstable patients should be managed with a direct cardioversion. For the stable patients, medical management should be used first before using acceptable options of catheter ablation or surgical intervention. Although catheter ablation has widely replaced the surgical option, as it is a less invasive technique with better outcomes, in cases where catheter ablation cannot be done or doesn't prove to be effective, the surgical option is worth considering with a curative rate of nearly 100%.

Historical Perspective

WPW Syndrome was given its name in 1930 by Wolf, Parkinson, and White. Source: Ecgpedia.org

Classification

Type Conduction pathway QRS interval PR interval Delta wave
Wolff-Parkinson-White syndrome Bundle of Kent Wide/long Usually short Yes
Lown-Ganong-Levine syndrome "James bundle" (atria to bundle of His) Normal/Unaffected Short No
Mahaim-type Pre-excitation Mahaim fibers Long Normal No

Pathophysiology

Normal electrical conduction pathway of heart

Pre-excitation pathway

Differentiating Pre-excitation Syndrome from other Diseases

Arrhythmia Rhythm Rate P wave PR Interval QRS Complex Response to Maneuvers Epidemiology Co-existing Conditions
Atrial Fibrillation (AFib)[6][7]
  • Absent
Atrial Flutter[8]
  • Varies depending upon the magnitude of the block, but is short
Atrioventricular nodal reentry tachycardia (AVNRT)[9][10][11]
  • Regular
Multifocal Atrial Tachycardia[12][13]
Paroxysmal Supraventricular Tachycardia
  • Regular
  • 150 and 240 bpm
  • Absent
  • Hidden in QRS
  • Absent
Premature Atrial Contractrions (PAC)[14][15]
  • Upright
  • Usually narrow (< 0.12 s)
Wolff-Parkinson-White Syndrome[16][17]
  • Regular
Ventricular Fibrillation (VF)[18][19][20]
  • Absent
  • Absent
  • Absent (R on T phenomenon in the setting of ischemia)
Ventricular Tachycardia[21][22]
  • Regular
  • > 100 bpm (150-200 bpm common)
  • Absent

Epidemiology and Demographics

Risk Factors

Natural History, Complications, and Prognosis

Natural History

Complications

Prognosis

Diagnosis

WPW Syndrome

WPW ECG changes with significant 1) Delta wave 2) PR interval shortening 3) Wide QRS complexes. [1]

Lown-Ganong-Levine (LGL) Syndrome

Mahaim-Type Pre-excitation

History and Symptoms

Treatment

Medical Treatment

GENERAL PROTOCOL

General protocol includes the following:[26]

IN CASE OF ACUTE AVRT/AVNRT

ATRIAL FLUTTER/FIBRILLATION

RADIOFREQUENCY ABLATION

Surgical management

Prevention

References

  1. ↑ https://doi.org/10.1016/j.eupc.2004.09.005
  2. ↑ Lowe KG, Emslie-Smith D, Ward C, Watson H (January 1975). "Classification of ventricular pre-excitation. Vectorcardiographic study". Br Heart J. 37 (1): 9–19. doi:10.1136/hrt.37.1.9. PMC 484149. PMID 1111564.
  3. ↑ Blomström-Lundqvist C, Scheinman MM, Aliot EM, Alpert JS, Calkins H, Camm AJ; et al. (2003). "ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias--executive summary. a report of the American college of cardiology/American heart association task force on practice guidelines and the European society of cardiology committee for practice guidelines (writing committee to develop guidelines for the management of patients with supraventricular arrhythmias) developed in collaboration with NASPE-Heart Rhythm Society". J Am Coll Cardiol. 42 (8): 1493–531. PMID 14563598.
  4. ↑ Kuramoto K, Matsushita S (August 1972). "[Classification and interpretation of WPW syndrome]". Nippon Rinsho (in Japanese). 30 (8): 1770–8. PMID 4561817.
  5. ↑ Moskowitz A, Chen KP, Cooper AZ, Chahin A, Ghassemi MM, Celi LA (October 2017). "Management of Atrial Fibrillation with Rapid Ventricular Response in the Intensive Care Unit: A Secondary Analysis of Electronic Health Record Data". Shock. 48 (4): 436–440. doi:10.1097/SHK.0000000000000869. PMC 5603354. PMID 28328711.
  6. ↑ 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.
  7. ↑ 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.
  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. ↑ 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.
  10. ↑ 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.
  11. ↑ 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.
  12. ↑ 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.
  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. ↑ 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.
  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. ↑ 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.
  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. ↑ 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.
  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. ↑ Levis JT (2011). "ECG Diagnosis: Monomorphic Ventricular Tachycardia". Perm J. 15 (1): 65. doi:10.7812/tpp/10-130. PMC 3048638. PMID 21505622.
  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. ↑ 23.0 23.1 Cohen MI, Triedman JK, Cannon BC, Davis AM, Drago F, Janousek J, Klein GJ, Law IH, Morady FJ, Paul T, Perry JC, Sanatani S, Tanel RE (June 2012). "PACES/HRS expert consensus statement on the management of the asymptomatic young patient with a Wolff-Parkinson-White (WPW, ventricular preexcitation) electrocardiographic pattern: developed in partnership between the Pediatric and Congenital Electrophysiology Society (PACES) and the Heart Rhythm Society (HRS). Endorsed by the governing bodies of PACES, HRS, the American College of Cardiology Foundation (ACCF), the American Heart Association (AHA), the American Academy of Pediatrics (AAP), and the Canadian Heart Rhythm Society (CHRS)". Heart Rhythm. 9 (6): 1006–24. doi:10.1016/j.hrthm.2012.03.050. PMID 22579340.
  24. ↑ 24.0 24.1 Obeyesekere MN, Leong-Sit P, Massel D, Manlucu J, Modi S, Krahn AD, Skanes AC, Yee R, Gula LJ, Klein GJ (May 2012). "Risk of arrhythmia and sudden death in patients with asymptomatic preexcitation: a meta-analysis". Circulation. 125 (19): 2308–15. doi:10.1161/CIRCULATIONAHA.111.055350. PMID 22532593.
  25. ↑ Sternick EB, Timmermans C, Sosa E, Cruz FE, Rodriguez LM, Fagundes MA, Gerken LM, Wellens HJ (October 2004). "The electrocardiogram during sinus rhythm and tachycardia in patients with Mahaim fibers: the importance of an "rS" pattern in lead III". J. Am. Coll. Cardiol. 44 (8): 1626–35. doi:10.1016/j.jacc.2004.07.035. PMID 15489095.
  26. ↑ Stasiak A, Niewiadomska-Jarosik K, Kędziora P (2018). "Clinical course and treatment of children and adolescents with the preexcitation syndrome - own studies". Dev Period Med. 22 (2): 113–122. PMID 30056397.
  27. ↑ Wann LS, Curtis AB, Ellenbogen KA, Estes NA, Ezekowitz MD, Jackman WM, January CT, Lowe JE, Page RL, Slotwiner DJ, Stevenson WG, Tracy CM, Fuster V, Rydén LE, Cannom DS, Crijns HJ, Curtis AB, Ellenbogen KA, Halperin JL, Le Heuzey J, Kay GN, Lowe JE, Olsson SB, Prystowsky EN, Tamargo JL, Wann LS (May 2013). "Management of patients with atrial fibrillation (compilation of 2006 ACCF/AHA/ESC and 2011 ACCF/AHA/HRS recommendations): a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines". Circulation. 127 (18): 1916–26. doi:10.1161/CIR.0b013e318290826d. PMID 23545139.
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