Brugada Syndrome: Difference between revisions

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{{authors|
{{authors|
|mainauthor= [[user:Pgpostema|P.G. Postema, MD]]
|mainauthor= [[user:Pgpostema|P.G. Postema, MD]]
|superauthor=
|supervisor=
|coauthor=
|coauthor= [[user:Drj|J.S.S.G. de Jong, MD]]
|moderator= [[user:Pgpostema|P.G. Postema, MD]]
|moderator= [[user:Pgpostema|P.G. Postema, MD]]
|editor= [[user:Drj|J.S.S.G. de Jong, MD]]
|editor=  
}}
}}
[[Image:Brugada.png|thumb|Typical ECG abnormalities in Brugada syndrome: ST elevation in V1-V3, without ischemia.]]
[[Image:Brugada_ecg_characteristics.svg|thumb| Typical ECG abnormalities in Brugada syndrome]]
[[Image:brugada.jpg|thumb| Dr. Pedro Brugada. Pedro and Josep Brugada described in 1992 a landmark publication with a case-series of 8 patients with sudden cardiac death. <cite>Brugada</cite> Currently, three brothers of the Brugada family (Pedro, Josep and Ramon Brugada) conduct research in the syndrome that has been named after them.]]
[[Image:scn5a.jpg|thumb| The SCN5a gen is located on the short arm (p) of chromosome 3]]


==Wat is het Brugada syndroom?==
[[Afbeelding:Brugada.png|thumb|Typische afwijkingen op het ECG passend bij Brugada: ST elevatie in V1-V3]]
[[Afbeelding:scn5a.jpg|thumb| De plaats waar het SCN5a gen zich bevindt: op de korte arm (p) van chromosoom 3]]
[[Afbeelding:brugada.jpg|thumb| Dr. Pedro Brugada. Pedro en Josep Brugada beschreven in 1992 een case-serie van 8 patiënten met acute hartdood. <cite>Brugada</cite> Inmiddels zijn er vier artsen uit de familie Brugada bezig met onderzoek naar het syndroom. Overigens was het ECG patroon al in 1953 beschreven<cite>osher</cite>, maar Brugada was de eerste die de link legde met het optreden van acute hartdood.]]


'''Het Brugada syndroom is een erfelijke aandoening die een verhoogde kans geeft op plotselinge hartdood'''. Het wordt gekarakteriseerd door de typische 'handtekening' op het ECG: ST segment elevatie in de rechts precordiale leads (V1 - V3) al dan niet samen met ventriculaire tachyarrhythmien (ventrikelfibrilleren).  
The '''Brugada syndrome is an hereditary disease that is associated with high risk of sudden cardiac death'''. It is characterized by typical ECG abnormalities: '''ST segment elevation in the precordial leads (V1 - V3)'''.


'''Het Brugada syndroom is een [[w:Autosomal_dominant|autosomaal dominante]] aandoening''', wat betekent dat wanneer een van de ouders het heeft, de kans 50/50 is dat ieder van zijn of haar kinderen het overerft. Ook is het zeer waarschijnlijk dat 1 van zijn of haar ouders het heeft doorgegeven aan hem of haar en is de kans dus ook 50/50 dat de broers en zussen van de ouder ook Brugada syndroom hebben. De incidentie varieert van 5-50 per 10 000 inwoners. De incidentie is hoger in Oost/Zuidoost Azie waar Brugada syndroom de 2e doodsoorzaak overall is tussen jonge mannen (na auto ongelukken). In Azie is Brugada syndroom de basis van het 'Sudden Unexpected Death Syndrome' (SUDS). SUDS is al heel lang bekend in Azie en is in verschillende landen bekend met een eigen naam: in de Philipijnen bijvoorbeeld als ''bangungut'' (to rise and moan in sleep) en in Thailand als ''lai tai'' (death during sleep). In 1992 is de ziekte voor het eerst beschreven door de broers en cardiologen Brugada, in de jaren daarna heeft het hun naam gekregen. In een artikel uit 1953 wordt echter ook al een typisch Brugada ECG besproken waarover men toen alleen maar kon speculeren.<cite>osher</cite>
==Characteristics of the Brugada syndrome:==
*Inheritable arrhythmia syndrome with [[w:Autosomal_dominant|autosomal dominant]] inheritance. If one of the two parents is affected, each child (both males and females) has a 50% chance of inheriting the disease.
*Males are more often symptomatic than females, probably by the influence of sex hormones on cardiac arrhythmias and/or ion channels, and a different distribution of ion channels across the heart in males versus females.
*The arrhythmias usually occur in patients between 30 and 40 years of age. (range 1-77 yrs) and often during rest or while sleeping (high vagal tone).
*In only about 30% of patients, genetic defects can be detected in the ([http://ghr.nlm.nih.gov/gene=scn5a SCN5A]) gene which encodes the cardiac sodium channel (loss-of-function mutation). In much smaller quantities, mutations may be found in the GPD1L gene (which probably influences cardiac sodium channel function) or in cardiac calcium channel encoding genes (CACNxxx). In the remaining patients, the disease is probably multi-genetic or caused by yet unknown genetic defects.
*The right ventricle is most affected in Brugada syndrome, and particularly (but not specifically) the right ventricular outflow tract .  
*The prevalence varies between 5-50:10.000, largely depending on geographic location. In some southeast Asian countries the disease is considered endemic and believed to be the second cause of death among young men (after car accidents). In these countries Brugada syndrome is believed to underly (in part) the 'Sudden Unexpected Death Syndrome' (SUDS). This relation has, however, not been thoroughly investigated and there are almost no epidemiological studies into Brugada syndrome ECGs (apart from Japan). In different Asian countries, different names have been given to SUDS: in the Phillipines it is called ''bangungut'' (to rise and moan in sleep) and in Thailand ''lai tai'' (death during sleep).  


Het kan zo zijn dat iemand met de genetische afwijking de ziekte (hartritmestoornissen) niet krijgt (en dus drager is); mannen zijn vaker aangedaan dan vrouwen (wat te maken lijkt te hebben met testosteron). De ritmeproblemen manifesteren zich gemiddeld rond het 30e tot 40e levensjaar (range 1-77 jaar), vaak in rust, tijdens de slaap.
The Brugada brothers were the first to describe the characteristic ECG findings and link them to sudden death. Before that, the characteristic ECG findings, were often mistaken for a [[Right_Ventricle_MI|right ventricle myocardial infarction]] and already in 1953, a publication mentions that the ECG findings were not associated with ischemia as people often expected.<cite>osher</cite>


Het enige gen met een bewezen invloed is het SCN5A gen ([http://ghr.nlm.nih.gov/gene=scn5a GHR]), welke codeert voor het cardiale Natrium kanaal. Echter, in slechts 20 tot 30% van de aangedane personen is er een dergelijke SCN5A mutatie te vinden, wat zeer waarschijnlijk betekent dat er nog andere genen een rol spelen maar dat die 'simpelweg' nog niet bekend zijn. De mutatie zorgt ervoor dat het Natrium kanaal minder goed functioneert, dit leidt tot een verandering van de electrische stromen in het hart, en dan met name in de rechter ventrikel outflow tract (RVOT). Wat nu precies deze 'verandering van electrische stromen' veroorzaakt is nog niet geheel duidelijk. Enerzijds zou het kunnen zijn dat door het ontbreken van de Natriumstroom (in fase 1 van de actiepotentiaal) er in de RVOT een gradient ontstaat tussen epi- en endocard omdat een 'tegenwerkende' stroom (Ito) daar in een ongelijke mate is vertegenwoordigd. Deze gradient kan dan zorgen voor een re-entry fenomeen waarna VF zou kunnen ontstaan. Anderzijds zou het zo kunnen zijn dat door de verminderde werking van het Natriumkanaal er geleidingsvertraging optreedt in de RVOT waardoor eveneens een gradient ontstaat en er re-entry en eventueel VF kan optreden.
==Diagnosis and treatment==


Brugada syndroom kan in speciale gevallen (families) optreden in combinatie met andere electrische hartziekten zoals het Lange QT syndroom. Ook kunnen bepaalde mutaties van het SCN5A gen aanleiding geven tot hele andere hartritmestoornissen zoals 'atrial standstill' of andere (mogelijk zeer uitgebreide) geleidingsstoornissen.
*Patients who are symptomatic (unexplained syncopes, ventricular tachycardias or aborted sudden cardiac death) may have a symptom recurrence risk of 2 to 10% per year. In these patients an [[:w:nl:Internal_Cardiac_Defibrillator|ICD]] implant is advisable. Further, life-style advice is given (see below).
{{clr}}
*Some groups advise an electrophysiological investigation (inducibility of ventricular fibrillation) for risk assessment in Brugada patients,<cite>brug2</cite><cite>brug3</cite> but others could not reproduce the predictive value of these tests,<cite>priori</cite><cite>eckhardt</cite> so the value of inducibility is controversial.
*In large studies familial sudden death did not appear to be a risk factor for sudden death in siblings.
*In asymptomatic patients in whom the Brugada ECG characteristics are present (either spontaneously or provoked by fever or sodium channel blockers like ajmaline, procainimde or flecainide) life style advice is given. This advice includes:
**A number of medications should not be taken (including sodium channel blockers and certain anti-depressants and anti-arrhythmics, see [http://www.brugadadrugs.org www.BrugadaDrugs.org])
**Rigorous treatment of fever with paracetamol/Tylenol, as fever may elicit a Brugada ECG and arrhythmias in some patients.
* Spontaneous Type I ECGs do appear to be more prevalent in patients who experienced symptoms.


==Symptomen==
For a full list of the diagnostic criteria, see <cite>Wilde</cite>


Blackouts (collaps), hartkloppingen en plotselinge hartdood. Een belangrijk 'symptoom' is de aanwezigheid van plotseling en jong overleden familieleden (net zoals bij Lange QT syndroom of bv catecholaminerge polymorfe VT (CPVT))
==Electrocardiographic criteria==
[[Image:Brugada_lead_placement.png|thumb|Changed lead positions of leads V3 and V5 to increase the sensitiviy to 'catch' a Brugada pattern on the ECG]]
Three ECG repolarization patterns in the right precordial leads are recognized in the diagnosis of Brugada syndrome.


'''Type I''' is the only ECG criterion that is diagnostic of Brugada syndrome. The type I ECG is characterized by a J elevation >=2 mm (0.2 mV) a coved type ST segment followed by a negative T wave (see figure). Brugada syndrome is definitively diagnosed when a type 1 ST-segment is observed in >1 right precordial lead (V1 to V3) in the presence or absence of a sodium channel–blocking agent, and in conjunction with one of the following:
*documented ventricular fibrillation (VF)
*polymorphic ventricular tachycardia (VT)
*a family history of sudden cardiac death at <45 years old
*coved-type ECGs in family members
*inducibility of VT with programmed electrical stimulation
*syncope
*nocturnal agonal respiration.
The sensitivity of the ECG for Brugada syndrome can be increased with placement of ECG leads in the intercostal space above V1 and V2 (V1ic3 and V2ic3)


==Diagnose en behandeling==
Electrocardiograms of Brugada patients can change over time from type I to type II and/or normal ECGs and back.
A type III ECG is rather common and is considered a normal variant, but also the Type II is a normal variant (albeit suggestive of Brugada syndrome).


Sommige centra in de wereld gebruiken een electrisch fysiologisch onderzoek (EFO) om het Brugada syndroom te provoceren, de resultaten hiervan en de interpretatie daarvan met betrekking tot het risico op hartritmestoornissen is betwist.  
A recent study suggests that''' fractionation of the QRS complex''' is a marker of a worse prognosis in Brugada syndrome.<cite>Morita</cite>


Symptomatische patiënten hebben een mortaliteit van 10% per jaar. Omdat niet bekend is wat precies de VF veroorzaakt is men voor de behandeling aangewezen op een [[:w:nl:Internal_Cardiac_Defibrillator|ICD]]. Het is echter lang niet altijd nodig om een ICD te implanteren. Wanneer iemand geen symptomen heeft en geen spontaan Brugada ECG, wordt hier in de meeste gevallen vanaf gezien omdat het risico op hartritme stoornissen niet lijkt te zijn verhoogd en ook een ICD een complicaties kan geven. Wel wordt iedereen met een spontaan of opwekbaar Brugada ECG / Brugada syndroom ontraden om bepaalde geneesmiddelen te gebruiken waarvan nu bekend is dat ze ook aanleiding kunnen geven (of de 'druppel' kunnen zijn) tot het manifest worden van Brugada syndroom; waaronder klasse I antiarrhythmica maar ook bepaalde antidepressiva en lidocaine bijvoorbeeld. Ook zijn er bepaalde typen van het Brugada syndroom temperatuur gevoelig; ritmestoornissen treden dan op bij koorts. In die gevallen wordt geadviseerd om de koorts te onderdrukken (met paracetamol).
{| class="wikitable" font-size="90%"
De diagnostische criteria zijn uitstekend beschreven door Wilde et al. <cite>Wilde</cite>
|- style="text-align:center;background-color:#6EB4EB;"
|+'''ST segment abnormalities in the different types of Brugada syndrome'''<cite>Wilde2</cite>
|-
!
!Type I
!Type II
!Type III
|-
!J wave amplitude
|>= 2mm
|>= 2mm
|>= 2mm
|-
!T wave
|Negative
|Positive or biphasis
|Positive
|-
!ST-T configuration
|Coved type
|Saddleback
|Saddleback
|-
!ST segment (terminal portion)
|Gradually descending
|Elevated >= 1mm
|Elevated < 1mm
|-
|}


Als het ECG geen afwijkingen vertoond kan er toch sprake zijn van Brugada-syndroom. Om in zo'n geval de diagnose te stellen kan een flecaïnide of ajmaline test gedaan worden. Deze medicijnen (natrium-kanaalblokkers) vertragen de geleiding en kunnen de typische ECG afwijkingen uitlokken. Op die manier kan toch de diagnose gesteld worden. Dit wordt wel gedaan bij familieleden van patiënten of bij patiënten met onverklaarde collaps.


==Externe links==
<gallery caption="Examples of Brugada syndrome type I">
*Cardiogenetica website van het AMC [http://www.cardiogenetica.nl cardiogentica.nl]
Image:Brugada_syndrome_type1_example1.png
Image:Brugada_syndrome_type1_example2.png
Image:Brugada_syndrome_type1_example3.png
Image:Brugada_syndrome_type1_example4.png
Image:Brugada_syndrome_type1_example5.png
Image:Brugada_syndrome_type1_example6.jpg|Brugada ECG during ajmaline testing
</gallery>
<gallery caption="Examples of Brugada syndrome type II">
Image:Brugada_syndrome_type2_example1.png
Image:Brugada_syndrome_type2_example2.jpg
</gallery>
 
==External links==
*Cardiogenetics website of the AMC [http://www.cardiogenetica.nl cardiogentica.nl]
*[http://www.brugada.org Brugada.org ]
*[http://www.brugada.org Brugada.org ]
*[http://www.genereviews.org/servlet/access?id=8888891&key=ghdBRjkdNXE6y&gry=INSERTGRY&fcn=y&fw=E0gK&filename=/profiles/brugada/index.html Genereview Brugada]
*[http://www.genereviews.org/servlet/access?id=8888891&key=ghdBRjkdNXE6y&gry=INSERTGRY&fcn=y&fw=E0gK&filename=/profiles/brugada/index.html Genereview Brugada]
 
*[http://www.brugadadrugs.org Brugada drugs contains lists of medications that should be avoided in patients with Brugada syndrome and medication that can be used to diagnose the syndrome]
==Referenties==
==References==
<biblio>
<biblio>
#Wilde pmid=15898165
#Wilde pmid=15898165
#Brugada pmid=1309182
#Brugada pmid=1309182
#osher pmid=13104407
#osher pmid=13104407
#brug2 pmid=11772879
#brug3 pmid=12776858
#priori pmid=11901046
#Wilde2 pmid=12417552
#Morita pmid=18838563
#eckhardt pmid=15642768
</biblio>
</biblio>
<analytics uacct="UA-807577-6"></analytics>

Latest revision as of 05:54, 22 May 2013

Author(s) P.G. Postema, MD
Moderator P.G. Postema, MD
Supervisor
some notes about authorship
Typical ECG abnormalities in Brugada syndrome: ST elevation in V1-V3, without ischemia.
Typical ECG abnormalities in Brugada syndrome
Dr. Pedro Brugada. Pedro and Josep Brugada described in 1992 a landmark publication with a case-series of 8 patients with sudden cardiac death. [1] Currently, three brothers of the Brugada family (Pedro, Josep and Ramon Brugada) conduct research in the syndrome that has been named after them.
The SCN5a gen is located on the short arm (p) of chromosome 3


The Brugada syndrome is an hereditary disease that is associated with high risk of sudden cardiac death. It is characterized by typical ECG abnormalities: ST segment elevation in the precordial leads (V1 - V3).

Characteristics of the Brugada syndrome:

  • Inheritable arrhythmia syndrome with autosomal dominant inheritance. If one of the two parents is affected, each child (both males and females) has a 50% chance of inheriting the disease.
  • Males are more often symptomatic than females, probably by the influence of sex hormones on cardiac arrhythmias and/or ion channels, and a different distribution of ion channels across the heart in males versus females.
  • The arrhythmias usually occur in patients between 30 and 40 years of age. (range 1-77 yrs) and often during rest or while sleeping (high vagal tone).
  • In only about 30% of patients, genetic defects can be detected in the (SCN5A) gene which encodes the cardiac sodium channel (loss-of-function mutation). In much smaller quantities, mutations may be found in the GPD1L gene (which probably influences cardiac sodium channel function) or in cardiac calcium channel encoding genes (CACNxxx). In the remaining patients, the disease is probably multi-genetic or caused by yet unknown genetic defects.
  • The right ventricle is most affected in Brugada syndrome, and particularly (but not specifically) the right ventricular outflow tract .
  • The prevalence varies between 5-50:10.000, largely depending on geographic location. In some southeast Asian countries the disease is considered endemic and believed to be the second cause of death among young men (after car accidents). In these countries Brugada syndrome is believed to underly (in part) the 'Sudden Unexpected Death Syndrome' (SUDS). This relation has, however, not been thoroughly investigated and there are almost no epidemiological studies into Brugada syndrome ECGs (apart from Japan). In different Asian countries, different names have been given to SUDS: in the Phillipines it is called bangungut (to rise and moan in sleep) and in Thailand lai tai (death during sleep).

The Brugada brothers were the first to describe the characteristic ECG findings and link them to sudden death. Before that, the characteristic ECG findings, were often mistaken for a right ventricle myocardial infarction and already in 1953, a publication mentions that the ECG findings were not associated with ischemia as people often expected.[2]

Diagnosis and treatment

  • Patients who are symptomatic (unexplained syncopes, ventricular tachycardias or aborted sudden cardiac death) may have a symptom recurrence risk of 2 to 10% per year. In these patients an ICD implant is advisable. Further, life-style advice is given (see below).
  • Some groups advise an electrophysiological investigation (inducibility of ventricular fibrillation) for risk assessment in Brugada patients,[3][4] but others could not reproduce the predictive value of these tests,[5][6] so the value of inducibility is controversial.
  • In large studies familial sudden death did not appear to be a risk factor for sudden death in siblings.
  • In asymptomatic patients in whom the Brugada ECG characteristics are present (either spontaneously or provoked by fever or sodium channel blockers like ajmaline, procainimde or flecainide) life style advice is given. This advice includes:
    • A number of medications should not be taken (including sodium channel blockers and certain anti-depressants and anti-arrhythmics, see www.BrugadaDrugs.org)
    • Rigorous treatment of fever with paracetamol/Tylenol, as fever may elicit a Brugada ECG and arrhythmias in some patients.
  • Spontaneous Type I ECGs do appear to be more prevalent in patients who experienced symptoms.

For a full list of the diagnostic criteria, see [7]

Electrocardiographic criteria

Changed lead positions of leads V3 and V5 to increase the sensitiviy to 'catch' a Brugada pattern on the ECG

Three ECG repolarization patterns in the right precordial leads are recognized in the diagnosis of Brugada syndrome.

Type I is the only ECG criterion that is diagnostic of Brugada syndrome. The type I ECG is characterized by a J elevation >=2 mm (0.2 mV) a coved type ST segment followed by a negative T wave (see figure). Brugada syndrome is definitively diagnosed when a type 1 ST-segment is observed in >1 right precordial lead (V1 to V3) in the presence or absence of a sodium channel–blocking agent, and in conjunction with one of the following:

  • documented ventricular fibrillation (VF)
  • polymorphic ventricular tachycardia (VT)
  • a family history of sudden cardiac death at <45 years old
  • coved-type ECGs in family members
  • inducibility of VT with programmed electrical stimulation
  • syncope
  • nocturnal agonal respiration.

The sensitivity of the ECG for Brugada syndrome can be increased with placement of ECG leads in the intercostal space above V1 and V2 (V1ic3 and V2ic3)

Electrocardiograms of Brugada patients can change over time from type I to type II and/or normal ECGs and back. A type III ECG is rather common and is considered a normal variant, but also the Type II is a normal variant (albeit suggestive of Brugada syndrome).

A recent study suggests that fractionation of the QRS complex is a marker of a worse prognosis in Brugada syndrome.[8]

ST segment abnormalities in the different types of Brugada syndrome[9]
Type I Type II Type III
J wave amplitude >= 2mm >= 2mm >= 2mm
T wave Negative Positive or biphasis Positive
ST-T configuration Coved type Saddleback Saddleback
ST segment (terminal portion) Gradually descending Elevated >= 1mm Elevated < 1mm


External links

References

  1. Brugada P and Brugada J. Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome. A multicenter report. J Am Coll Cardiol. 1992 Nov 15;20(6):1391-6. DOI:10.1016/0735-1097(92)90253-j | PubMed ID:1309182 | HubMed [Brugada]
  2. OSHER HL and WOLFF L. Electrocardiographic pattern simulating acute myocardial injury. Am J Med Sci. 1953 Nov;226(5):541-5. PubMed ID:13104407 | HubMed [osher]
  3. Brugada J, Brugada R, Antzelevitch C, Towbin J, Nademanee K, and Brugada P. Long-term follow-up of individuals with the electrocardiographic pattern of right bundle-branch block and ST-segment elevation in precordial leads V1 to V3. Circulation. 2002 Jan 1;105(1):73-8. DOI:10.1161/hc0102.101354 | PubMed ID:11772879 | HubMed [brug2]
  4. Brugada P, Brugada R, Mont L, Rivero M, Geelen P, and Brugada J. Natural history of Brugada syndrome: the prognostic value of programmed electrical stimulation of the heart. J Cardiovasc Electrophysiol. 2003 May;14(5):455-7. DOI:10.1046/j.1540-8167.2003.02517.x | PubMed ID:12776858 | HubMed [brug3]
  5. Priori SG, Napolitano C, Gasparini M, Pappone C, Della Bella P, Giordano U, Bloise R, Giustetto C, De Nardis R, Grillo M, Ronchetti E, Faggiano G, and Nastoli J. Natural history of Brugada syndrome: insights for risk stratification and management. Circulation. 2002 Mar 19;105(11):1342-7. DOI:10.1161/hc1102.105288 | PubMed ID:11901046 | HubMed [priori]
  6. Eckardt L, Probst V, Smits JP, Bahr ES, Wolpert C, Schimpf R, Wichter T, Boisseau P, Heinecke A, Breithardt G, Borggrefe M, LeMarec H, Böcker D, and Wilde AA. Long-term prognosis of individuals with right precordial ST-segment-elevation Brugada syndrome. Circulation. 2005 Jan 25;111(3):257-63. DOI:10.1161/01.CIR.0000153267.21278.8D | PubMed ID:15642768 | HubMed [eckhardt]
  7. Antzelevitch C, Brugada P, Borggrefe M, Brugada J, Brugada R, Corrado D, Gussak I, LeMarec H, Nademanee K, Perez Riera AR, Shimizu W, Schulze-Bahr E, Tan H, and Wilde A. Brugada syndrome: report of the second consensus conference. Heart Rhythm. 2005 Apr;2(4):429-40. DOI:10.1016/j.hrthm.2005.01.005 | PubMed ID:15898165 | HubMed [Wilde]
  8. Morita H, Kusano KF, Miura D, Nagase S, Nakamura K, Morita ST, Ohe T, Zipes DP, and Wu J. Fragmented QRS as a marker of conduction abnormality and a predictor of prognosis of Brugada syndrome. Circulation. 2008 Oct 21;118(17):1697-704. DOI:10.1161/CIRCULATIONAHA.108.770917 | PubMed ID:18838563 | HubMed [Morita]
  9. Wilde AA, Antzelevitch C, Borggrefe M, Brugada J, Brugada R, Brugada P, Corrado D, Hauer RN, Kass RS, Nademanee K, Priori SG, Towbin JA, and Study Group on the Molecular Basis of Arrhythmias of the European Society of Cardiology. Proposed diagnostic criteria for the Brugada syndrome: consensus report. Circulation. 2002 Nov 5;106(19):2514-9. DOI:10.1161/01.cir.0000034169.45752.4a | PubMed ID:12417552 | HubMed [Wilde2]

All Medline abstracts: PubMed | HubMed