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Wolff-Parkinson-White pattern(WPW)

MedGen UID:
12162
Concept ID:
C0043202
Disease or Syndrome
Synonyms: Anomalous ventricular excitation syndrome; Auriculoventricular accessory pathway syndrome; False bundle branch block syndrome; Wolff-Parkinson-White Syndrome; WPW syndrome
SNOMED CT: Ventricular pre-excitation with arrhythmia (74390002); Wolff Parkinson White syndrome (74390002); Wolff-Parkinson-White pattern (74390002); WPW - Wolff-Parkinson-White pattern (74390002); WPW - Wolff-Parkinson-White syndrome (74390002)
 
Gene (location): PRKAG2 (7q36.1)
 
HPO: HP:0001716
Monarch Initiative: MONDO:0008685
OMIM®: 194200
Orphanet: ORPHA907

Definition

Wolff-Parkinson-White syndrome is a condition characterized by abnormal electrical pathways in the heart that cause a disruption of the heart's normal rhythm (arrhythmia).

The heartbeat is controlled by electrical signals that move through the heart in a highly coordinated way. A specialized cluster of cells called the atrioventricular node conducts electrical impulses from the heart's upper chambers (the atria) to the lower chambers (the ventricles). Impulses move through the atrioventricular node during each heartbeat, stimulating the ventricles to contract slightly later than the atria.

People with Wolff-Parkinson-White syndrome are born with an extra connection in the heart, called an accessory pathway, that allows electrical signals to bypass the atrioventricular node and move from the atria to the ventricles faster than usual. The accessory pathway may also transmit electrical impulses abnormally from the ventricles back to the atria. This extra connection can disrupt the coordinated movement of electrical signals through the heart, leading to an abnormally fast heartbeat (tachycardia) and other changes in heart rhythm. Resulting symptoms include dizziness, a sensation of fluttering or pounding in the chest (palpitations), shortness of breath, and fainting (syncope). In rare cases, arrhythmias associated with Wolff-Parkinson-White syndrome can lead to cardiac arrest and sudden death. The most common arrhythmia associated with Wolff-Parkinson-White syndrome is called paroxysmal supraventricular tachycardia.

Complications of Wolff-Parkinson-White syndrome can occur at any age, although some individuals born with an accessory pathway in the heart never experience any health problems associated with the condition.

Wolff-Parkinson-White syndrome often occurs with other structural abnormalities of the heart or underlying heart disease. The most common heart defect associated with the condition is Ebstein anomaly, which affects the valve that allows blood to flow from the right atrium to the right ventricle (the tricuspid valve). Additionally, the heart rhythm problems associated with Wolff-Parkinson-White syndrome can be a component of several other genetic syndromes, including hypokalemic periodic paralysis (a condition that causes episodes of extreme muscle weakness), Pompe disease (a disorder characterized by the storage of excess glycogen), Danon disease (a condition that weakens the heart and skeletal muscles and causes intellectual disability), and tuberous sclerosis complex (a condition that results in the growth of noncancerous tumors in many parts of the body). [from MedlinePlus Genetics]

Clinical features

From HPO
Sudden cardiac death
MedGen UID:
38841
Concept ID:
C0085298
Pathologic Function
The heart suddenly and unexpectedly stops beating resulting in death within a short time period (generally within 1 h of symptom onset).
Atrial flutter
MedGen UID:
13955
Concept ID:
C0004239
Pathologic Function
A type of atrial arrhythmia characterized by atrial rates of between 240 and 400 beats per minute and some degree of atrioventricular node conduction block. Typically, the ventricular rate is half the atrial rate. In the EKG; atrial flutter waves are observed as sawtooth-like atrial activity. Pathophysiologically, atrial flutter is a form of atrial reentry in which there is a premature electrical impulse creates a self-propagating circuit.
Palpitations
MedGen UID:
14579
Concept ID:
C0030252
Finding
A sensation that the heart is pounding or racing, which is a non-specific sign but may be a manifestation of arrhythmia.
Syncope
MedGen UID:
21443
Concept ID:
C0039070
Sign or Symptom
Syncope refers to a generalized weakness of muscles with loss of postural tone, inability to stand upright, and loss of consciousness. Once the patient is in a horizontal position, blood flow to the brain is no longer hindered by gravitation and consciousness is regained. Unconsciousness usually lasts for seconds to minutes. Headache and drowsiness (which usually follow seizures) do not follow a syncopal attack. Syncope results from a sudden impairment of brain metabolism usually due to a reduction in cerebral blood flow.
Wolff-Parkinson-White pattern
MedGen UID:
12162
Concept ID:
C0043202
Disease or Syndrome
Wolff-Parkinson-White syndrome is a condition characterized by abnormal electrical pathways in the heart that cause a disruption of the heart's normal rhythm (arrhythmia).\n\nThe heartbeat is controlled by electrical signals that move through the heart in a highly coordinated way. A specialized cluster of cells called the atrioventricular node conducts electrical impulses from the heart's upper chambers (the atria) to the lower chambers (the ventricles). Impulses move through the atrioventricular node during each heartbeat, stimulating the ventricles to contract slightly later than the atria.\n\nPeople with Wolff-Parkinson-White syndrome are born with an extra connection in the heart, called an accessory pathway, that allows electrical signals to bypass the atrioventricular node and move from the atria to the ventricles faster than usual. The accessory pathway may also transmit electrical impulses abnormally from the ventricles back to the atria. This extra connection can disrupt the coordinated movement of electrical signals through the heart, leading to an abnormally fast heartbeat (tachycardia) and other changes in heart rhythm. Resulting symptoms include dizziness, a sensation of fluttering or pounding in the chest (palpitations), shortness of breath, and fainting (syncope). In rare cases, arrhythmias associated with Wolff-Parkinson-White syndrome can lead to cardiac arrest and sudden death. The most common arrhythmia associated with Wolff-Parkinson-White syndrome is called paroxysmal supraventricular tachycardia.\n\nComplications of Wolff-Parkinson-White syndrome can occur at any age, although some individuals born with an accessory pathway in the heart never experience any health problems associated with the condition.\n\nWolff-Parkinson-White syndrome often occurs with other structural abnormalities of the heart or underlying heart disease. The most common heart defect associated with the condition is Ebstein anomaly, which affects the valve that allows blood to flow from the right atrium to the right ventricle (the tricuspid valve). Additionally, the heart rhythm problems associated with Wolff-Parkinson-White syndrome can be a component of several other genetic syndromes, including hypokalemic periodic paralysis (a condition that causes episodes of extreme muscle weakness), Pompe disease (a disorder characterized by the storage of excess glycogen), Danon disease (a condition that weakens the heart and skeletal muscles and causes intellectual disability), and tuberous sclerosis complex (a condition that results in the growth of noncancerous tumors in many parts of the body).
Prolonged QRS complex
MedGen UID:
489828
Concept ID:
C0235475
Finding
Increased time for the complex comprised of the Q wave, R wave, and S wave as measured by the electrocardiogram (EKG).. In adults, normal values are 0.06 - 0.10 sec.
Paroxysmal atrial fibrillation
MedGen UID:
115990
Concept ID:
C0235480
Disease or Syndrome
Episodes of atrial fibrillation that typically last for several hours up to one day and terminate spontaneously.
Shortened PR interval
MedGen UID:
105466
Concept ID:
C0520878
Finding
Reduced time for the PR interval (beginning of the P wave to the beginning of the QRS complex). In adults, normal values are 120 to 200 ms long.
Ventricular preexcitation
MedGen UID:
107848
Concept ID:
C0559106
Disease or Syndrome
An abnormality in which the cardiac ventricles depolarize too early as a result of an abnormality of cardiac conduction pathways such as an accessory pathway.
Ventricular preexcitation with multiple accessory pathways
MedGen UID:
870556
Concept ID:
C4025004
Finding
A form of ventricular preexcitation due to the presence of multiple accessory pathways for cardiac conduction.

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • CROGVWolff-Parkinson-White pattern

Conditions with this feature

Glycogen storage disease, type II
MedGen UID:
5340
Concept ID:
C0017921
Disease or Syndrome
Pompe disease is classified by age of onset, organ involvement, severity, and rate of progression. Infantile-onset Pompe disease (IOPD; individuals with onset before age 12 months with cardiomyopathy) may be apparent in utero but more typically onset is at the median age of four months with hypotonia, generalized muscle weakness, feeding difficulties, failure to thrive, respiratory distress, and hypertrophic cardiomyopathy. Without treatment by enzyme replacement therapy (ERT), IOPD commonly results in death by age two years from progressive left ventricular outflow obstruction and respiratory insufficiency. Late-onset Pompe disease (LOPD; including: (a) individuals with onset before age 12 months without cardiomyopathy; and (b) all individuals with onset after age 12 months) is characterized by proximal muscle weakness and respiratory insufficiency; clinically significant cardiac involvement is uncommon.
Wolff-Parkinson-White pattern
MedGen UID:
12162
Concept ID:
C0043202
Disease or Syndrome
Wolff-Parkinson-White syndrome is a condition characterized by abnormal electrical pathways in the heart that cause a disruption of the heart's normal rhythm (arrhythmia).\n\nThe heartbeat is controlled by electrical signals that move through the heart in a highly coordinated way. A specialized cluster of cells called the atrioventricular node conducts electrical impulses from the heart's upper chambers (the atria) to the lower chambers (the ventricles). Impulses move through the atrioventricular node during each heartbeat, stimulating the ventricles to contract slightly later than the atria.\n\nPeople with Wolff-Parkinson-White syndrome are born with an extra connection in the heart, called an accessory pathway, that allows electrical signals to bypass the atrioventricular node and move from the atria to the ventricles faster than usual. The accessory pathway may also transmit electrical impulses abnormally from the ventricles back to the atria. This extra connection can disrupt the coordinated movement of electrical signals through the heart, leading to an abnormally fast heartbeat (tachycardia) and other changes in heart rhythm. Resulting symptoms include dizziness, a sensation of fluttering or pounding in the chest (palpitations), shortness of breath, and fainting (syncope). In rare cases, arrhythmias associated with Wolff-Parkinson-White syndrome can lead to cardiac arrest and sudden death. The most common arrhythmia associated with Wolff-Parkinson-White syndrome is called paroxysmal supraventricular tachycardia.\n\nComplications of Wolff-Parkinson-White syndrome can occur at any age, although some individuals born with an accessory pathway in the heart never experience any health problems associated with the condition.\n\nWolff-Parkinson-White syndrome often occurs with other structural abnormalities of the heart or underlying heart disease. The most common heart defect associated with the condition is Ebstein anomaly, which affects the valve that allows blood to flow from the right atrium to the right ventricle (the tricuspid valve). Additionally, the heart rhythm problems associated with Wolff-Parkinson-White syndrome can be a component of several other genetic syndromes, including hypokalemic periodic paralysis (a condition that causes episodes of extreme muscle weakness), Pompe disease (a disorder characterized by the storage of excess glycogen), Danon disease (a condition that weakens the heart and skeletal muscles and causes intellectual disability), and tuberous sclerosis complex (a condition that results in the growth of noncancerous tumors in many parts of the body).
Juvenile myopathy, encephalopathy, lactic acidosis AND stroke
MedGen UID:
56485
Concept ID:
C0162671
Disease or Syndrome
MELAS (mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes) is a multisystem disorder with protean manifestations. The vast majority of affected individuals develop signs and symptoms of MELAS between ages two and 40 years. Common clinical manifestations include stroke-like episodes, encephalopathy with seizures and/or dementia, muscle weakness and exercise intolerance, normal early psychomotor development, recurrent headaches, recurrent vomiting, hearing impairment, peripheral neuropathy, learning disability, and short stature. During the stroke-like episodes neuroimaging shows increased T2-weighted signal areas that do not correspond to the classic vascular distribution (hence the term "stroke-like"). Lactic acidemia is very common and muscle biopsies typically show ragged red fibers.
Danon disease
MedGen UID:
209235
Concept ID:
C0878677
Disease or Syndrome
Danon disease is a multisystem condition with predominant involvement of the heart, skeletal muscles, and retina, with overlying cognitive dysfunction. Males are typically more severely affected than females. Males usually present with childhood onset concentric hypertrophic cardiomyopathy that is progressive and often requires heart transplantation. Rarely, hypertrophic cardiomyopathy can evolve to resemble dilated cardiomyopathy. Most affected males also have cardiac conduction abnormalities. Skeletal muscle weakness may lead to delayed acquisition of motor milestones. Learning disability and intellectual disability, most often in the mild range, are common. Additionally, affected males can develop retinopathy with subsequent visual impairment. The clinical features in females are broader and more variable. Females are more likely to have dilated cardiomyopathy, with a smaller proportion requiring heart transplantation compared to affected males. Cardiac conduction abnormalities, skeletal muscle weakness, mild cognitive impairment, and pigmentary retinopathy are variably seen in affected females.
Cerebellar ataxia-areflexia-pes cavus-optic atrophy-sensorineural hearing loss syndrome
MedGen UID:
318633
Concept ID:
C1832466
Disease or Syndrome
ATP1A3-related neurologic disorders represent a clinical continuum in which at least three distinct phenotypes have been delineated: rapid-onset dystonia-parkinsonism (RDP); alternating hemiplegia of childhood (ACH); and cerebellar ataxia, areflexia, pes cavus, optic atrophy, and sensorineural hearing loss (CAPOS). However, some affected individuals have intermediate phenotypes or only a few features that do not fit well into one of these major phenotypes. RDP has been characterized by: abrupt onset of dystonia over days to weeks with parkinsonism (primarily bradykinesia and postural instability); common bulbar involvement; and absence or minimal response to an adequate trial of L-dopa therapy, with few exceptions. Often fever, physiologic stress, or alcoholic binges trigger the onset of symptoms. After their initial appearance, symptoms often stabilize with little improvement; occasionally second episodes occur with abrupt worsening of symptoms. Rarely, affected individuals have reported a more gradual onset of symptoms over weeks to months. Anxiety, depression, and seizures have been reported. Age of onset ranges from four to 55 years, although a childhood variation of RDP with onset between ages nine and 14 months has been reported. AHC is a complex neurodevelopmental syndrome most frequently manifesting in infancy or early childhood with paroxysmal episodic neurologic dysfunction including alternating hemiparesis or dystonia, quadriparesis, seizure-like episodes, and oculomotor abnormalities. Episodes can last for minutes, hours, days, or even weeks. Remission of symptoms occurs with sleep and immediately after awakening. Over time, persistent neurologic deficits including oculomotor apraxia, ataxia, choreoathetosis, dystonia, parkinsonism, and cognitive and behavioral dysfunction develop in the majority of those affected; more than 50% develop epilepsy in addition to their episodic movement disorder phenotype. CAPOS (cerebellar ataxia, areflexia, pes cavus, optic atrophy, and sensorineural hearing loss) syndrome is characterized by episodes of ataxic encephalopathy and/or weakness during and after a febrile illness. Onset is between ages six months and four years. Some acute symptoms resolve; progression of sensory losses and severity vary.
Hypertrophic cardiomyopathy 6
MedGen UID:
331466
Concept ID:
C1833236
Disease or Syndrome
Mutations in the PRKAG2 gene (602743) give rise to a moderate, essentially heart-specific, nonlysosomal glycogenosis with clinical onset typically in late adolescence or in the third decade of life, ventricular pre-excitation predisposing to supraventricular arrhythmias, mild to severe cardiac hypertrophy, enhanced risk of sudden cardiac death in midlife, and autosomal dominant inheritance with full penetrance (summary by Burwinkel et al., 2005).
Tuberous sclerosis 1
MedGen UID:
344288
Concept ID:
C1854465
Disease or Syndrome
Tuberous sclerosis complex (TSC) involves abnormalities of the skin (hypomelanotic macules, confetti skin lesions, facial angiofibromas, shagreen patches, fibrous cephalic plaques, ungual fibromas); brain (subependymal nodules, cortical tubers, and subependymal giant cell astrocytomas [SEGAs], seizures, intellectual disability / developmental delay, psychiatric illness); kidney (angiomyolipomas, cysts, renal cell carcinomas); heart (rhabdomyomas, arrhythmias); and lungs (lymphangioleiomyomatosis [LAM], multifocal micronodular pneumonocyte hyperplasia). Central nervous system tumors are the leading cause of morbidity and mortality; renal disease is the second leading cause of early death.
Tuberous sclerosis 2
MedGen UID:
348170
Concept ID:
C1860707
Disease or Syndrome
Tuberous sclerosis complex (TSC) involves abnormalities of the skin (hypomelanotic macules, confetti skin lesions, facial angiofibromas, shagreen patches, fibrous cephalic plaques, ungual fibromas); brain (subependymal nodules, cortical tubers, and subependymal giant cell astrocytomas [SEGAs], seizures, intellectual disability / developmental delay, psychiatric illness); kidney (angiomyolipomas, cysts, renal cell carcinomas); heart (rhabdomyomas, arrhythmias); and lungs (lymphangioleiomyomatosis [LAM], multifocal micronodular pneumonocyte hyperplasia). Central nervous system tumors are the leading cause of morbidity and mortality; renal disease is the second leading cause of early death.
Hypertrophic cardiomyopathy 7
MedGen UID:
348695
Concept ID:
C1860752
Disease or Syndrome
Hypertrophic cardiomyopathy is a heart condition characterized by thickening (hypertrophy) of the heart (cardiac) muscle. When multiple members of a family have the condition, it is known as familial hypertrophic cardiomyopathy. Hypertrophic cardiomyopathy also occurs in people with no family history; these cases are considered nonfamilial hypertrophic cardiomyopathy. \n\nIn familial hypertrophic cardiomyopathy, cardiac thickening usually occurs in the interventricular septum, which is the muscular wall that separates the lower left chamber of the heart (the left ventricle) from the lower right chamber (the right ventricle). In some people, thickening of the interventricular septum impedes the flow of oxygen-rich blood from the heart, which may lead to an abnormal heart sound during a heartbeat (heart murmur) and other signs and symptoms of the condition. Other affected individuals do not have physical obstruction of blood flow, but the pumping of blood is less efficient, which can also lead to symptoms of the condition. Familial hypertrophic cardiomyopathy often begins in adolescence or young adulthood, although it can develop at any time throughout life.\n\nNonfamilial hypertrophic cardiomyopathy tends to be milder. This form typically begins later in life than familial hypertrophic cardiomyopathy, and affected individuals have a lower risk of serious cardiac events and sudden death than people with the familial form.\n\nThe symptoms of familial hypertrophic cardiomyopathy are variable, even within the same family. Many affected individuals have no symptoms. Other people with familial hypertrophic cardiomyopathy may experience chest pain; shortness of breath, especially with physical exertion; a sensation of fluttering or pounding in the chest (palpitations); lightheadedness; dizziness; and fainting.\n\nWhile most people with familial hypertrophic cardiomyopathy are symptom-free or have only mild symptoms, this condition can have serious consequences. It can cause abnormal heart rhythms (arrhythmias) that may be life threatening. People with familial hypertrophic cardiomyopathy have an increased risk of sudden death, even if they have no other symptoms of the condition. A small number of affected individuals develop potentially fatal heart failure, which may require heart transplantation.
Hypertrophic cardiomyopathy 25
MedGen UID:
895360
Concept ID:
C4225408
Disease or Syndrome
Any hypertrophic cardiomyopathy in which the cause of the disease is a mutation in the TCAP gene.
Combined oxidative phosphorylation defect type 15
MedGen UID:
1646555
Concept ID:
C4706313
Disease or Syndrome
A rare mitochondrial disease due to a defect in mitochondrial protein synthesis with onset in infancy or early childhood of muscular hypotonia, gait ataxia, mild bilateral pyramidal tract signs, developmental delay (affecting mostly speech and coordination) and subsequent intellectual disability. Short stature, obesity, microcephaly, strabismus, nystagmus, reduced visual acuity, lactic acidosis, and a brain neuropathology consistent with Leigh syndrome are also reported. Caused by homozygous or compound heterozygous mutation in the MTFMT gene on chromosome 15q22.
Mitochondrial complex 1 deficiency, nuclear type 11
MedGen UID:
1648356
Concept ID:
C4748769
Disease or Syndrome
Combined oxidative phosphorylation deficiency 38
MedGen UID:
1682102
Concept ID:
C5193064
Disease or Syndrome
Muscular dystrophy, limb-girdle, autosomal recessive 27
MedGen UID:
1794212
Concept ID:
C5562002
Disease or Syndrome
Autosomal recessive limb-girdle muscular dystrophy-27 (LGMDR27) is characterized by progressive muscle weakness primarily affecting the lower limbs and resulting in walking difficulty or loss of ambulation. The age at onset is highly variable, from infancy to young adulthood. Patients with infantile onset may have a more severe disease course with rapid progression. Upper limb involvement and distal muscle weakness may also occur. Additional more variable features include neck muscle weakness, scoliosis, and joint contractures. Less common features include impaired intellectual development or speech delay, cardiomyopathy, and cardiac arrhythmia. Muscle biopsy shows nonspecific dystrophic changes (Coppens et al., 2021). For a discussion of genetic heterogeneity of autosomal recessive limb-girdle muscular dystrophy, see LGMDR1 (253600).
Chromosome 1p36 deletion syndrome, proximal
MedGen UID:
1794324
Concept ID:
C5562114
Disease or Syndrome
Proximal 1p36 deletion syndrome is a multisystem developmental disorder characterized by global developmental delay with impaired intellectual development, poor overall growth with microcephaly, axial hypotonia, and dysmorphic facial features. Most patients have congenital cardiac malformations or cardiac dysfunction. Additional more variable features may include distal skeletal anomalies, seizures, and cleft palate. The phenotype shows some overlap with distal chromosome 1p36 deletion syndrome (summary by Kang et al., 2007).
Immunodeficiency 93 and hypertrophic cardiomyopathy
MedGen UID:
1804175
Concept ID:
C5676899
Disease or Syndrome
Immunodeficiency-93 and hypertrophic cardiomyopathy (IMD93) is an autosomal recessive disorder characterized by onset of recurrent viral and bacterial infections, particularly with encapsulated bacteria, and hypertrophic cardiomyopathy in the first months or years of life. Immunologic workup typically shows decreased circulating B cells and hypo- or agammaglobulinemia, sometimes with neutropenia or T-cell lymphocytosis, although laboratory findings may be variable among patients. Ig replacement therapy is beneficial. Cardiac involvement can also include atrial septal defect, valvular insufficiency, and pre-excitation syndrome. Rare myopathic or neurologic involvement has been reported, but these features are not consistently part of the disorder and may be related to other genetic defects (summary by Niehues et al., 2020 and Saettini et al., 2021).

Professional guidelines

PubMed

Chubb H, Campbell RM, Motonaga KS, Ceresnak SR, Dubin AM
J Pediatr 2019 Oct;213:88-95.e1. Epub 2019 Jun 22 doi: 10.1016/j.jpeds.2019.05.058. PMID: 31235382
Raposo D, António N, Andrade H, Sousa P, Pires A, Gonçalves L
Pediatr Cardiol 2019 Jun;40(5):892-900. Epub 2019 May 8 doi: 10.1007/s00246-019-02110-6. PMID: 31069431
Dores H, Dinis P, Fernandes R, Barra S, Ferreira S, Silveira MC, Rocha E, Cardoso J, Monge J
Mil Med 2017 Nov;182(11):e2041-e2045. doi: 10.7205/MILMED-D-16-00443. PMID: 29087878

Recent clinical studies

Etiology

Pærregaard MM, Hartmann J, Sillesen AS, Pihl C, Dannesbo S, Kock TO, Pietersen A, Raja AA, Iversen KK, Bundgaard H, Christensen AH
Europace 2023 Jul 4;25(7) doi: 10.1093/europace/euad165. PMID: 37465966Free PMC Article
Raposo D, António N, Andrade H, Sousa P, Pires A, Gonçalves L
Pediatr Cardiol 2019 Jun;40(5):892-900. Epub 2019 May 8 doi: 10.1007/s00246-019-02110-6. PMID: 31069431
Kim SS, Knight BP
Trends Cardiovasc Med 2017 May;27(4):260-268. Epub 2016 Dec 5 doi: 10.1016/j.tcm.2016.12.001. PMID: 28108086
Benson DW, Cohen MI
Cardiol Young 2017 Jan;27(S1):S62-S67. doi: 10.1017/S1047951116002250. PMID: 28084962
Davenport ED, Rupp KA, Palileo E, Haynes J
Aerosp Med Hum Perform 2017 Jan 1;88(1):56-60. doi: 10.3357/AMHP.4569.2017. PMID: 28061924

Diagnosis

Pærregaard MM, Hartmann J, Sillesen AS, Pihl C, Dannesbo S, Kock TO, Pietersen A, Raja AA, Iversen KK, Bundgaard H, Christensen AH
Europace 2023 Jul 4;25(7) doi: 10.1093/europace/euad165. PMID: 37465966Free PMC Article
Chubb H, Campbell RM, Motonaga KS, Ceresnak SR, Dubin AM
J Pediatr 2019 Oct;213:88-95.e1. Epub 2019 Jun 22 doi: 10.1016/j.jpeds.2019.05.058. PMID: 31235382
Raposo D, António N, Andrade H, Sousa P, Pires A, Gonçalves L
Pediatr Cardiol 2019 Jun;40(5):892-900. Epub 2019 May 8 doi: 10.1007/s00246-019-02110-6. PMID: 31069431
Koca S, Pac FA, Kavurt AV, Cay S, Mihcioglu A, Aras D, Topaloglu S
Pacing Clin Electrophysiol 2017 Jul;40(7):808-814. Epub 2017 Jun 1 doi: 10.1111/pace.13100. PMID: 28436586
Kim SS, Knight BP
Trends Cardiovasc Med 2017 May;27(4):260-268. Epub 2016 Dec 5 doi: 10.1016/j.tcm.2016.12.001. PMID: 28108086

Therapy

Pærregaard MM, Hartmann J, Sillesen AS, Pihl C, Dannesbo S, Kock TO, Pietersen A, Raja AA, Iversen KK, Bundgaard H, Christensen AH
Europace 2023 Jul 4;25(7) doi: 10.1093/europace/euad165. PMID: 37465966Free PMC Article
Benson DW, Cohen MI
Cardiol Young 2017 Jan;27(S1):S62-S67. doi: 10.1017/S1047951116002250. PMID: 28084962
Skanes AC, Obeyesekere M, Klein GJ
Card Electrophysiol Clin 2015 Sep;7(3):377-83. Epub 2015 Jul 7 doi: 10.1016/j.ccep.2015.05.002. PMID: 26304516
Kubuš P, Vít P, Gebauer RA, Materna O, Janoušek J
Circ Arrhythm Electrophysiol 2014 Apr;7(2):218-23. Epub 2014 Jan 31 doi: 10.1161/CIRCEP.113.000930. PMID: 24488978
Deal BJ, Keane JF, Gillette PC, Garson A Jr
J Am Coll Cardiol 1985 Jan;5(1):130-5. doi: 10.1016/s0735-1097(85)80095-4. PMID: 3964800

Prognosis

Pærregaard MM, Hartmann J, Sillesen AS, Pihl C, Dannesbo S, Kock TO, Pietersen A, Raja AA, Iversen KK, Bundgaard H, Christensen AH
Europace 2023 Jul 4;25(7) doi: 10.1093/europace/euad165. PMID: 37465966Free PMC Article
Raposo D, António N, Andrade H, Sousa P, Pires A, Gonçalves L
Pediatr Cardiol 2019 Jun;40(5):892-900. Epub 2019 May 8 doi: 10.1007/s00246-019-02110-6. PMID: 31069431
Koca S, Pac FA, Kavurt AV, Cay S, Mihcioglu A, Aras D, Topaloglu S
Pacing Clin Electrophysiol 2017 Jul;40(7):808-814. Epub 2017 Jun 1 doi: 10.1111/pace.13100. PMID: 28436586
Kim SS, Knight BP
Trends Cardiovasc Med 2017 May;27(4):260-268. Epub 2016 Dec 5 doi: 10.1016/j.tcm.2016.12.001. PMID: 28108086
Benson DW, Cohen MI
Cardiol Young 2017 Jan;27(S1):S62-S67. doi: 10.1017/S1047951116002250. PMID: 28084962

Clinical prediction guides

Pærregaard MM, Hartmann J, Sillesen AS, Pihl C, Dannesbo S, Kock TO, Pietersen A, Raja AA, Iversen KK, Bundgaard H, Christensen AH
Europace 2023 Jul 4;25(7) doi: 10.1093/europace/euad165. PMID: 37465966Free PMC Article
Raposo D, António N, Andrade H, Sousa P, Pires A, Gonçalves L
Pediatr Cardiol 2019 Jun;40(5):892-900. Epub 2019 May 8 doi: 10.1007/s00246-019-02110-6. PMID: 31069431
Kim SS, Knight BP
Trends Cardiovasc Med 2017 May;27(4):260-268. Epub 2016 Dec 5 doi: 10.1016/j.tcm.2016.12.001. PMID: 28108086
Benson DW, Cohen MI
Cardiol Young 2017 Jan;27(S1):S62-S67. doi: 10.1017/S1047951116002250. PMID: 28084962
Davenport ED, Rupp KA, Palileo E, Haynes J
Aerosp Med Hum Perform 2017 Jan 1;88(1):56-60. doi: 10.3357/AMHP.4569.2017. PMID: 28061924

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