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.  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]].
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==
===Accessory Pathway===
===Accessory Pathway===
*Individuals with WPW have a congenital [[accessory pathway]] that communicates between the [[atria]] and the [[ventricles]], in addition to the [[AV node]].
* Individuals with WPW have a congenital [[accessory pathway]] that communicates between the [[atria]] and the [[ventricles]], in addition to the [[AV node]].
*This [[accessory pathway]] is known as the [[bundle of Kent]].
* This [[accessory pathway]] is known as the [[bundle of Kent]].
*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> 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>
* 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>  
* 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>


The accessory pathway:<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>
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>
* Conducts electrical stimulus faster than the [[AV node]]
* Conducting  electrical stimulus faster than the [[AV node]]
* Has a longer refractory period compared to the [[AV node]]
* Longer refractory period compared to the [[AV node]]
* Is most commonly characterized by a non-decremental conduction in response to an increased paced rates
* A non-decremental conduction in response to an increased paced rates


===Electrical Activity===
===Electrical Activity===
====Normal 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]].  
* 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.
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]]
[[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 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.
* 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 ventricles), which is usually shortened to less than 120 milliseconds in duration.
* 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====
====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, [[tachycardia]] may therefore result.
* 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 heart versus that in the presence of an accessory pathway.
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]]
[[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:
* 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]])
* 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 retrogarde (less common)
* Only antegrade (least common)
* Only antegrade (least common)


When arrhythmia occurs in a patient with an accessory pathway, the patient is said to have WPW syndrome. The most common type of tachycardia associated with WPW is [[atrioventricular reciprocating tachycardia]] ([[AVRT]]). AVRT in WPW can be one of two types:
* When [[arrhythmia]] occurs in a patient with an [[accessory pathway]], it defines as [[WPW syndrome]].  
* Orthodromic (~95%): the antegrade electrical signal moves from the [[atria]] to the [[ventricle]]s through the [[AV node]], whereas the retrograde electrical signal moves from the [[ventricle]]s to the [[atria]] through the accessory pathway.
* The most common type of tachycardia associated with [[WPW]] is [[atrioventricular reciprocating tachycardia]] ([[AVRT]]).  
* 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]].
** [[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]].


Shown below are two images depicting the difference in the antegrade and retrograde conduction of the electrical signals in orthodromic and antidromic AVRT.


<center>
{|
| [[File:Orthodromic AVRT.png|300px|The antegrade electrical signal moves from the [[atria]] to the [[ventricle]]s through the [[AV node]], whereas the retrograde electrical signal moves from the [[ventricle]]s to the [[atria]] through the accessory pathway.]] || [[File:Antidromic AVRT.png|300px|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]].]]
|}
</center>


Other arrhythmia can 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. However, since 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 cardiac [[arrhythmia]] can trigger [[ventricular fibrillation]], a leading cause of [[sudden cardiac death]]. For instance, 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.
* 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.  
===Genetics===
* 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]].
* Most cases of Wolff-Parkinson-White syndrome occur in people with no apparent family history of the condition. These cases are described as sporadic and are not inherited.
* 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]].
* Familial Wolff-Parkinson-White syndrome accounts for only a small percentage of all cases of this condition.  The familial form of the disorder typically has an [[autosomal dominant]] pattern of inheritance, which means one copy of the altered gene in each cell is sufficient to cause the condition.  In most cases, a person with familial Wolff-Parkinson-White syndrome has inherited the condition from an affected parent.<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>
* 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>
 
* While the cause of Wolff-Parkinson-White syndrome is unknown in most cases, a small percentage of all cases of Wolff-Parkinson-White syndrome are caused by [[mutations]] in the PRKAG2 gene. Some people with these mutations also have features of [[hypertrophic cardiomyopathy]].  The PRKAG2 gene encodes the protein AMP-activated protein kinase (AMPK) gamma-2 subunit.  This enzyme helps sense and responds to energy demands within cells.  It is likely involved in the development of the heart before birth, although its role in this process is unknown.<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>
 
* Researchers are uncertain how PRKAG2 mutations lead to the development of Wolff-Parkinson-White syndrome and related heart abnormalities.  Research suggests that these mutations alter the activity of AMP-activated protein [[kinase]] in the heart, although it is unclear whether the genetic changes overactivate the enzyme or reduce its activity.  Studies indicate that changes in AMP-activated protein kinase activity allow [[glycogen]] to build up abnormally within cardiac muscle cells.  It has been reported that patients with familial WPW usually have increased amounts of [[glycogen]] in the myocardial tissue.  Other studies have found that altered AMP-activated protein kinase activity is related to changes in the regulation of certain [[ion channels]] in the heart.  These channels, which transport positively charged atoms (ions) into and out of cardiac muscle cells, play critical roles in maintaining the heart's normal rhythm.<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><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>


===Associated Conditions===
===Associated Conditions===

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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