Wolff-Parkinson-White syndrome pathophysiology: Difference between revisions

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{{Wolff-Parkinson-White syndrome}}
{{Wolff-Parkinson-White syndrome}}
{{CMG}}; {{AE}} {{CZ}}
{{CMG}}; {{AE}} {{Sara.Zand}}  {{CZ}}


==Overview==
==Overview==
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]]).
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. Individuals with [[Wolf-parkinson-White]] ([[WPW]]) have an [[accessory pathway]], known as the [[bundle of Kent]], that communicates between the [[atria]] and the [[ventricles]].  The conduction through the accessory pathway can be bidirectional (most commonly), only retrogarde (less common), or only antegrade (least common).  The most common type of tachycardia associated with WPW is [[atrioventricular reciprocating tachycardia]] ([[AVRT]]).  The accessory pathway does not share the rate-slowing properties of the [[AV node]]; therefore, the combination of an accessory pathway and cardiac [[arrhythmia]] can trigger [[ventricular fibrillation]], a leading cause of [[sudden cardiac death]].


==Pathophysiology==
==Pathophysiology==
*The AV node slows the conduction of the impulses coming from the [[SA node]], in that way the atrial contraction is completed before the ventricular contraction begins.<ref>{{Cite book  | last1 = Silverthorn | first1 = Dee Unglaub | last2 = Johnson | first2 = Bruce R. | last3 = Ober | first3 = William C. | last4 = Garrison | first4 = Claire W. | last5 = Silverthorn | first5 = Andrew C. | title = Human physiology : an integrated approac | date = 2013 | publisher = Pearson Education | location = Boston | isbn = 978-0-321-75007-5 | pages = }}</ref>
===Accessory Pathway===
*In that way, if the impulses form the SA node increases (as in [[atrial fibrillation]] or [[atrial flutter]]) the [[AV node]] will slow the conduction to the [[ventricles]]. With this property of th [[AV node]], if the atrium has a frequency of 300 beats per minute, only half of the impulses will reach the [[ventricles]] generating a [[heart rate]] of 150 beats per minute.<ref>{{Cite book  | last1 = Silverthorn | first1 = Dee Unglaub | last2 = Johnson | first2 = Bruce R. | last3 = Ober | first3 = William C. | last4 = Garrison | first4 = Claire W. | last5 = Silverthorn | first5 = Andrew C. | title = Human physiology : an integrated approac | date = 2013 | publisher = Pearson Education | location = Boston | isbn = 978-0-321-75007-5 | pages = }}</ref>
* Individuals with WPW have a congenital [[accessory pathway]] that communicates between the [[atria]] and the [[ventricles]], in addition to the [[AV node]].
*The passage of the impulses through the [[AV node]] is manifested on the [[electrocardiogram|ECG]] as the PR interval; the period of time between the contraction of the [[atria]] and the contraction of the [[ventricles]].<ref>{{Cite book  | last1 = Silverthorn | first1 = Dee Unglaub | last2 = Johnson | first2 = Bruce R. | last3 = Ober | first3 = William C. | last4 = Garrison | first4 = Claire W. | last5 = Silverthorn | first5 = Andrew C. | title = Human physiology : an integrated approac | date = 2013 | publisher = Pearson Education | location = Boston | isbn = 978-0-321-75007-5 | pages =  }}</ref>
* This [[accessory pathway]] is known as the [[bundle of Kent]].
*In patients with WPW, an accessory pathway connects the [[atria]] and the [[ventricles]] in addition to the [[AV node]], this accessory pathway is known as the [[bundle of Kent]].  This accessory pathway serves as a by-pass to the [[AV node]] as it does not have the capacity of of slowing the impulse that the [[AV node]] has, therefore it transmits impulses at higher rates.<ref name="Sethi-2007">{{Cite journal  | last1 = Sethi | first1 = KK. | last2 = Dhall | first2 = A. | last3 = Chadha | first3 = DS. | last4 = Garg | first4 = S. | last5 = Malani | first5 = SK. | last6 = Mathew | first6 = OP. | title = WPW and preexcitation syndromes. | journal = J Assoc Physicians India | volume = 55 Suppl | issue =  | pages = 10-5 | month = Apr | year = 2007 | doi =  | PMID = 18368860 }}</ref>  
* The [[bundle of Kent]] is an abnormal extra or [[accessory pathway|accessory conduction pathway]] between the atria and ventricles that is present in a small percentage (between 0.1% and 0.3%) of the general population.<ref name=Sorbo1995>{{cite journal|author=Sorbo MD, Buja GF, Miorelli M, Nistri S, Perrone C, Manca S, Grasso F, Giordano GM, Nava A|title=The prevalence of the Wolff–Parkinson–White syndrome in a population of 116,542 young males|journal=Giornale Italiano di Cardiologia|volume=25|issue=6|year=1995|pages=681–7|pmid=7649416|language=Italian}}</ref><ref name=Munger1993>{{cite journal|author=Munger TM, Packer DL, Hammill SC, Feldman BJ, Bailey KR, Ballard DJ, Holmes DR Jr, Gersh BJ|title=A population study of the natural history of Wolff–Parkinson–White syndrome in Olmsted County, Minnesota, 1953–1989|journal=Circulation.|volume=87|issue=3|year=1993|pages=866–73|pmid=8443907|doi=10.1161/01.CIR.87.3.866}}</ref>  
*Using the example above, a patient with an atrial rate of 300 beats per minute with an accessory bundle may conduct all the electrical impulses with the ability of generating a ventricular rate of 300 beats per minute.
* This pathway may communicate between the [[left atrium]] and the [[left ventricle]], in which case it is termed a "type A pre-excitation", or between the [[right atrium]] and the [[right ventricle]], in which case it is termed a "type B pre-excitation".<ref name=americanheart>[http://www.americanheart.org/presenter.jhtml?identifier=563 americanheart.org Atrial and Ventricular Depolarization Changes] Last updated 11/24/2008.</ref>
[[Image:WPW.png|thumb|center|300px|A atrioventricular tachycardia through the accessory bundle. The electrical signal travels from the ventricles via the accessory bundle to the atria and returns to the ventricles via the AV node]]


===Genetics===
The accessory pathway is characterized by:<ref name="pmid9717020">{{cite journal| author=Obel OA, Camm AJ| title=Accessory pathway reciprocating tachycardia. | journal=Eur Heart J | year= 1998 | volume= 19 Suppl E | issue=  | pages= E13-24, E50-1 | pmid=9717020 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9717020  }} </ref>
WPW syndrome has been identified in to have a genetic backgournd as 0.55% of degree relatives of patients with WPW presents the disease. Missgene mutations (single nucelotide changes) in the gene PAKAG2 have been found in families with WPW. PAKAG2 encodes for the protein AMP-activated protein kinase (AMPK) gamma-2 subunit. AMPK, among other physiological functions, decreases glycogen synthesis, glycogen is abundant in the hearts conduction system, therefore an excesive acumulation of glycogen will prevent the accessory pathway to close. It has been reported that patients with familial WPW usualy have increased amounts of glycogen in the myocardial tissue. Patients with this disease, along with the preexcitations, they present [[myocardial hypertrophy]] and [[AV block]]. Nevertheless, WPW syndrome is usualy sporadic in origin and a small percentage from all csases have familial origin which presents as an autosomal dominant form.<ref name="Sidhu-2003">{{Cite journal | last1 = Sidhu | first1 = J. | last2 = Roberts | first2 = R. | title = Genetic basis and pathogenesis of familial WPW syndrome. | journal = Indian Pacing Electrophysiol J | volume = 3 | issue = 4 | pages = 197-201 | month = | year = 2003 | doi = | PMID = 16943919 }}</ref>
* Conducting  electrical stimulus faster than the [[AV node]]
* Longer refractory period compared to the [[AV node]]
* A non-decremental conduction in response to an increased paced rates
 
===Electrical Activity===
====Normal Electrical Activity====
* The electrical activity in the normal human [[heart]] is initiated when a cardiac [[action potential]] arises in the [[SA node|sinoatrial]] (SA) node, which is located in the [[right atrium]].
* From there, the electrical stimulus is transmitted via internodal pathways to the [[AV node|atrioventricular]] (AV) node.
* After a brief delay at the [[AV node]], the stimulus is conducted through the [[bundle of His]] to the left and [[right bundle branches]] and then to the [[Purkinje fibers]] and the [[endocardium]] at the apex of the[[ heart]], then finally to the [[ventricular]] [[myocardium]].
 
Shown below is an image depicting the conduction system in the normal [[heart]].
 
[[File:Conduction system in the heart.png|400px|center|The conduction system in the normal heart]]
 
* The [[AV node]] serves an important function as a "gatekeeper", limiting the [[ electrical activity]] that reaches the [[ventricle]]s.  
* In situations where the [[atria]] generate excessively rapid electrical activity (such as [[atrial fibrillation]] or [[atrial flutter]]), the [[AV node]] limits the number of signals conducted to the ventricles.  
* For example, if the [[atria]] are electrically activated at 300 beats per minute, half those electrical impulses may be blocked by the [[AV node]], so that the [[ventricle]]s are stimulated at only 150 beats per minute—resulting in a pulse of 150 beats per minute.
 
 
* Another important property of the [[AV node]] is that it slows down individual electrical impulses.
* This is manifested on the [[electrocardiogram]] as the [[PR interval]] (the time from electrical activation of the atria to electrical activation of the[[ ventricle]]s), which is usually shortened to less than 120 milliseconds in duration.
 
====Electrical Activity in WPW====
 
* The accessory pathway communicates between the [[atria]] and [[ventricle]]. 
* The accessory pathway can remain a bystander; however, problems may arise when this pathway creates an [[Electrical network|electrical circuit]] that bypasses the [[AV node]].  When an aberrant electrical connection occurs via the [[bundle of Kent]], [[tachyarrhythmia]] may therefore result.
 
Shown below is an image depicting the normal conduction of electrical signals in the [[ heart]] versus that in the presence of an [[accessory pathway]].
 
[[File: Abnormal [[electrical pathway]] in [[WPW]].jpeg|center| The normal conduction of electrical signals in the normal[[ heart]] versus that in the presence of an [[accessory pathway]]
 
* The conduction through the accessory pathway can be:
* Bidirectional (most commonly): retrogarde (also known as concealed) as well as antegrade (also known as manifest, responsible for the [[ ECG]] findings of [[delta wave]] and short [[PR interval]])
* Only retrogarde (less common)
* Only antegrade (least common)
 
* When [[arrhythmia]] occurs in a patient with an [[accessory pathway]], it defines as [[WPW syndrome]].
* The most common type of tachycardia associated with [[WPW]] is [[atrioventricular reciprocating tachycardia]] ([[AVRT]]).
** [[AVRT]] in [[ WPW]] can be derived as follows:
* [[Orthodromic]] (~95%): the antegrade electrical signal moves from the [[atria]] to the [[ventricles]] through the [[AV node]], whereas the retrograde electrical signal moves from the [[ventricle]]s to the [[atria]] through the [[accessory pathway]].
* [[Antidromic]] (~5%): the antegrade electrical signal moves from the [[atria]] to the [[ventricle]]s through the [[accessory pathway]], whereas the retrograde electrical signal moves from the [[ventricle]]s to the [[atria]] through either the [[AV node]] or a second [[accessory pathway]].
 
 
 
* Other [[ supraventricular tachyarrhythmia]] may occur in patients with [[ WPW]], such as [[atrial tachycardia]], [[atrial flutter]], [[atrial fibrillation]],[[AVNRT]].
* In these [[arrhythmia]], the [[accessory pathway]] may act as a bystander.
* 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]].
* The combination of an [[accessory pathway]] and [[tachyarrhythmia]] can trigger [[ventricular fibrillation]] and [[sudden cardiac death]].
* 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 contract at 300 beats per minute. Extremely rapid [[heart rates]] such as this may result in [[hemodynamic instability]] or [[cardiogenic shock]].
* The [[missense Mutation]] in PKRAG2 has been associated with the development of familiar [[ WPW syndrome]] and [[cardiac hypertrophy]] , involving the gamma-2 subunit of AMPK pathway<ref name="pmid16943919">{{cite journal |vauthors=Sidhu J, Roberts R |title=Genetic basis and pathogenesis of familial WPW syndrome |journal=Indian Pacing Electrophysiol J |volume=3 |issue=4 |pages=197–201 |date=October 2003 |pmid=16943919 |pmc=1502052 |doi= |url=}}</ref>


===Associated Conditions===
===Associated Conditions===
Associated disorders when present are most commonly associated with right-sided accessory pathway than left-sided pathways.  WPW syndrome is associated with the following disorders:
WPW syndrome is associated with the following disorders:
* [[Ebstein's anomaly]]<ref name="pmid21570234">{{cite journal |author=Rao MP, Panduranga P, Al-Mukhaini M, Al-Jufaili M |title=Ebstein anomaly in an adult presenting with wide QRS tachycardia: diagnostic and therapeutic dilemmas |journal=Am J Emerg Med |volume=30 |issue=5 |pages=834.e1–4 |year=2012 |month=June |pmid=21570234 |doi=10.1016/j.ajem.2011.03.001 |url=}}</ref><ref name="pmid20150013">{{cite journal |author=Bayar N, Canbay A, Uçar O, Aydoğdu S, Diker E |title=[Association of Gerbode-type defect and Wolff-Parkinson-White syndrome with Ebstein's anomaly] |language=Turkish |journal=Anadolu Kardiyol Derg |volume=10 |issue=1 |pages=88–90 |year=2010 |month=February |pmid=20150013 |doi= |url=}}</ref><ref name="pmid20924185">{{cite journal |author=Legius B, Van De Bruaene A, Van Deyk K, ''et al.'' |title=Behavior of Ebstein's anomaly: single-center experience and midterm follow-up |journal=Cardiology |volume=117 |issue=2 |pages=90–5 |year=2010 |pmid=20924185 |doi=10.1159/000318041 |url=}}</ref>
* [[Ebstein's anomaly]]<ref name="pmid21570234">{{cite journal |author=Rao MP, Panduranga P, Al-Mukhaini M, Al-Jufaili M |title=Ebstein anomaly in an adult presenting with wide QRS tachycardia: diagnostic and therapeutic dilemmas |journal=Am J Emerg Med |volume=30 |issue=5 |pages=834.e1–4 |year=2012 |month=June |pmid=21570234 |doi=10.1016/j.ajem.2011.03.001 |url=}}</ref><ref name="pmid20150013">{{cite journal |author=Bayar N, Canbay A, Uçar O, Aydoğdu S, Diker E |title=[Association of Gerbode-type defect and Wolff-Parkinson-White syndrome with Ebstein's anomaly] |language=Turkish |journal=Anadolu Kardiyol Derg |volume=10 |issue=1 |pages=88–90 |year=2010 |month=February |pmid=20150013 |doi= |url=}}</ref><ref name="pmid20924185">{{cite journal |author=Legius B, Van De Bruaene A, Van Deyk K, ''et al.'' |title=Behavior of Ebstein's anomaly: single-center experience and midterm follow-up |journal=Cardiology |volume=117 |issue=2 |pages=90–5 |year=2010 |pmid=20924185 |doi=10.1159/000318041 |url=}}</ref>
* [[Mitral valve prolapse]]: This cardiac disorder, if present, is associated with left-sided accessory pathways<ref name="pmid7970027">{{cite journal |author=Savini E, Capone PL |title=[Wolff-Parkinson-White, a study on the prevalence of the site of accessory pathways: relations between stability of pre-excitation, symptoms, cardiac arrhythmias and association of mitral valve prolapse with localization of pre-excitation] |language=Italian |journal=Minerva Cardioangiol |volume=42 |issue=7-8 |pages=339–43 |year=1994 |pmid=7970027 |doi= |url=}}</ref>.
* [[Mitral valve prolapse]]: This cardiac disorder, if present, is associated with left-sided accessory pathways.<ref name="pmid7970027">{{cite journal |author=Savini E, Capone PL |title=[Wolff-Parkinson-White, a study on the prevalence of the site of accessory pathways: relations between stability of pre-excitation, symptoms, cardiac arrhythmias and association of mitral valve prolapse with localization of pre-excitation] |language=Italian |journal=Minerva Cardioangiol |volume=42 |issue=7-8 |pages=339–43 |year=1994 |pmid=7970027 |doi= |url=}}</ref>
* [[Hypertrophic cardiomyopathy]]: This disorder is associated with familial/inherited form of WPW syndrome<ref name="pmid22839583">{{cite journal |author=Kruchina TK, Vasichkina ES, Egorov DF, Tatarskiĭ BA |title=[Asymptomatic ventricular pre-excitation in children: a 17 year follow-up study] |language=Russian |journal=Kardiologiia |volume=52 |issue=5 |pages=30–6 |year=2012 |pmid=22839583 |doi= |url=}}</ref>.
* [[Hypertrophic cardiomyopathy]]: This disorder is associated with familial/inherited form of WPW syndrome.<ref name="pmid22839583">{{cite journal |author=Kruchina TK, Vasichkina ES, Egorov DF, Tatarskiĭ BA |title=[Asymptomatic ventricular pre-excitation in children: a 17 year follow-up study] |language=Russian |journal=Kardiologiia |volume=52 |issue=5 |pages=30–6 |year=2012 |pmid=22839583 |doi= |url=}}</ref>
* [[Hypokalemic periodic paralysis]]<ref name="nlm">{{Cite web  | last =  | first =  | title = Wolff-Parkinson-White syndrome - Genetics Home Reference | url = http://ghr.nlm.nih.gov/condition/wolff-parkinson-white-syndrome | publisher =  | date =  | accessdate = 15 April 2014 }}</ref>
* [[Pompe disease]]<ref name="nlm">{{Cite web  | last =  | first =  | title = Wolff-Parkinson-White syndrome - Genetics Home Reference | url = http://ghr.nlm.nih.gov/condition/wolff-parkinson-white-syndrome | publisher =  | date =  | accessdate = 15 April 2014 }}</ref>
* [[Tuberous sclerosis]]<ref name="nlm">{{Cite web  | last =  | first =  | title = Wolff-Parkinson-White syndrome - Genetics Home Reference | url = http://ghr.nlm.nih.gov/condition/wolff-parkinson-white-syndrome | publisher =  | date =  | accessdate = 15 April 2014 }}</ref>


==References==
==References==

Latest revision as of 19:40, 9 November 2020

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Cafer Zorkun, M.D., Ph.D. [3]

Overview

In normal individuals, electrical activity in the heart is initiated in the sinoatrial (SA) node (located in the right atrium), propagates to the atrioventricular (AV) node, and then through the bundle of His to the ventricles of the heart. Individuals with Wolf-parkinson-White (WPW) have an accessory pathway, known as the bundle of Kent, that communicates between the atria and the ventricles. The conduction through the accessory pathway can be bidirectional (most commonly), only retrogarde (less common), or only antegrade (least common). The most common type of tachycardia associated with WPW is atrioventricular reciprocating tachycardia (AVRT). The accessory pathway does not share the rate-slowing properties of the AV node; therefore, the combination of an accessory pathway and cardiac arrhythmia can trigger ventricular fibrillation, a leading cause of sudden cardiac death.

Pathophysiology

Accessory Pathway

The accessory pathway is characterized by:[4]

  • Conducting electrical stimulus faster than the AV node
  • Longer refractory period compared to the AV node
  • A non-decremental conduction in response to an increased paced rates

Electrical Activity

Normal Electrical Activity

Shown below is an image depicting the conduction system in the normal heart.

The conduction system in the normal heart
The conduction system in the normal heart
  • The AV node serves an important function as a "gatekeeper", limiting the electrical activity that reaches the ventricles.
  • In situations where the atria generate excessively rapid electrical activity (such as atrial fibrillation or atrial flutter), the AV node limits the number of signals conducted to the ventricles.
  • For example, if the atria are electrically activated at 300 beats per minute, half those electrical impulses may be blocked by the AV node, so that the ventricles are stimulated at only 150 beats per minute—resulting in a pulse of 150 beats per minute.


  • Another important property of the AV node is that it slows down individual electrical impulses.
  • This is manifested on the electrocardiogram as the PR interval (the time from electrical activation of the atria to electrical activation of theventricles), which is usually shortened to less than 120 milliseconds in duration.

Electrical Activity in WPW

Shown below is an image depicting the normal conduction of electrical signals in the heart versus that in the presence of an accessory pathway.

[[File: Abnormal electrical pathway in WPW.jpeg|center| The normal conduction of electrical signals in the normalheart versus that in the presence of an accessory pathway

  • The conduction through the accessory pathway can be:
  • Bidirectional (most commonly): retrogarde (also known as concealed) as well as antegrade (also known as manifest, responsible for the ECG findings of delta wave and short PR interval)
  • Only retrogarde (less common)
  • Only antegrade (least common)


Associated Conditions

WPW syndrome is associated with the following disorders:

References

  1. ↑ Sorbo MD, Buja GF, Miorelli M, Nistri S, Perrone C, Manca S, Grasso F, Giordano GM, Nava A (1995). "The prevalence of the Wolff–Parkinson–White syndrome in a population of 116,542 young males". Giornale Italiano di Cardiologia (in Italian). 25 (6): 681–7. PMID 7649416.
  2. ↑ Munger TM, Packer DL, Hammill SC, Feldman BJ, Bailey KR, Ballard DJ, Holmes DR Jr, Gersh BJ (1993). "A population study of the natural history of Wolff–Parkinson–White syndrome in Olmsted County, Minnesota, 1953–1989". Circulation. 87 (3): 866–73. doi:10.1161/01.CIR.87.3.866. PMID 8443907.
  3. ↑ americanheart.org Atrial and Ventricular Depolarization Changes Last updated 11/24/2008.
  4. ↑ Obel OA, Camm AJ (1998). "Accessory pathway reciprocating tachycardia". Eur Heart J. 19 Suppl E: E13–24, E50–1. PMID 9717020.
  5. ↑ Sidhu J, Roberts R (October 2003). "Genetic basis and pathogenesis of familial WPW syndrome". Indian Pacing Electrophysiol J. 3 (4): 197–201. PMC 1502052. PMID 16943919.
  6. ↑ Rao MP, Panduranga P, Al-Mukhaini M, Al-Jufaili M (2012). "Ebstein anomaly in an adult presenting with wide QRS tachycardia: diagnostic and therapeutic dilemmas". Am J Emerg Med. 30 (5): 834.e1–4. doi:10.1016/j.ajem.2011.03.001. PMID 21570234. Unknown parameter |month= ignored (help)
  7. ↑ Bayar N, Canbay A, Uçar O, Aydoğdu S, Diker E (2010). "[Association of Gerbode-type defect and Wolff-Parkinson-White syndrome with Ebstein's anomaly]". Anadolu Kardiyol Derg (in Turkish). 10 (1): 88–90. PMID 20150013. Unknown parameter |month= ignored (help)
  8. ↑ Legius B, Van De Bruaene A, Van Deyk K; et al. (2010). "Behavior of Ebstein's anomaly: single-center experience and midterm follow-up". Cardiology. 117 (2): 90–5. doi:10.1159/000318041. PMID 20924185.
  9. ↑ Savini E, Capone PL (1994). "[Wolff-Parkinson-White, a study on the prevalence of the site of accessory pathways: relations between stability of pre-excitation, symptoms, cardiac arrhythmias and association of mitral valve prolapse with localization of pre-excitation]". Minerva Cardioangiol (in Italian). 42 (7–8): 339–43. PMID 7970027.
  10. ↑ Kruchina TK, Vasichkina ES, Egorov DF, Tatarskiĭ BA (2012). "[Asymptomatic ventricular pre-excitation in children: a 17 year follow-up study]". Kardiologiia (in Russian). 52 (5): 30–6. PMID 22839583.
  11. ↑ 11.0 11.1 11.2 "Wolff-Parkinson-White syndrome - Genetics Home Reference". Retrieved 15 April 2014.

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