https://en.ecgpedia.org/api.php?action=feedcontributions&user=145.117.40.234&feedformat=atomECGpedia - User contributions [en]2024-03-28T18:29:25ZUser contributionsMediaWiki 1.39.5https://en.ecgpedia.org/index.php?title=De_Voogt_ECG_Archive&diff=8303De Voogt ECG Archive2008-08-08T08:21:54Z<p>145.117.40.234: </p>
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<div>Below you will fine the ''De Voogt ECG Archive'' which contains > 2000 ECGs. This archive was collected by W.G. de Voogt, MD, PhD and is available under a creative commons license.<br />
<br />
{|width="85%" align="center" cellspacing="3" style="border: 1px solid #C0C090; background-color: #F8EABA; margin-bottom: 3px;"<br />
|align="center"|'''This archive is currently being developed and in a testing phase'''. <br />
|<br />
|}<br />
<br />
* Arrhythmias<br />
** Supraventricular<br />
*** [[De Voogt ECG Archive - Supraventricular Rhythms - AF|atrial fibrillation]]<br />
*** [[De Voogt ECG Archive - Supraventricular Rhythms - Atrial flutter|atrial flutter]]<br />
*** [[De Voogt ECG Archive - Supraventricular Rhythms - Atrial rhythm|atrial rhythm]]<br />
*** [[De Voogt ECG Archive - Supraventricular Rhythms - Atrial tachycardia|atrial tachycardia]]<br />
*** [[De Voogt ECG Archive - Supraventricular Rhythms - AVNRT|AVNRT]]<br />
*** [[De Voogt ECG Archive - Supraventricular Rhythms - AVRT|AVRT]]<br />
*** [[De Voogt ECG Archive - Supraventricular Rhythms - Holter|Holter]]<br />
*** [[De Voogt ECG Archive - Supraventricular Rhythms - Parasystole|parasystole]]<br />
*** [[De Voogt ECG Archive - Supraventricular Rhythms - SSS|sick sinus syndrome]]<br />
*** [[De Voogt ECG Archive - Supraventricular Rhythms - WPW|WPW]]<br />
** [[De Voogt ECG Archive - Pre-exitation|pre-exitation]]<br />
** [[De Voogt ECG Archive - Junctional Tachycardias|junctional]]<br />
** [[De Voogt ECG Archive - Ventricular Arrhythmias|ventricular]]<br />
** [[De Voogt ECG Archive - Genetic Arrhythmias|genetic]]<br />
** [[De Voogt ECG Archive - Ectopic Beats|ectopic beats]]<br />
* [[De Voogt ECG Archive - AV Conduction|AV Conduction]]<br />
* [[De Voogt ECG Archive - Intraventricular Conduction|Intraventricular Conduction]]<br />
* Myocardial Infarction<br />
** [[De Voogt ECG Archive - Myocardial Infarction - Anterior|Anterior MI]]<br />
** [[De Voogt ECG Archive - Myocardial Infarction - Atrial|Atrial MI]]<br />
** [[De Voogt ECG Archive - Myocardial Infarction - Inferior|Inferior MI]]<br />
** [[De Voogt ECG Archive - Myocardial Infarction - Pseudo|Pseudo MI]]<br />
** [[De Voogt ECG Archive - Myocardial Infarction - in LBBB|MI in LBBB]]<br />
* [[De Voogt ECG Archive - Chamber Hypertrophy and Enlargment|Chamber Hypertrophy]]<br />
* [[De Voogt ECG Archive - Clinical Disorders|Clinical Disorders]]<br />
* [[De Voogt ECG Archive - Electrolyte Disorders|Electrolyte Disorders]]<br />
* Devices<br />
** [[De Voogt ECG Archive - Pacemaker|Pacemaker]]<br />
** [[De Voogt ECG Archive - ICD|ICD]]<br />
* [[De Voogt ECG Archive - Technical Problems|Technical Problems]]<br />
* [[De Voogt ECG Archive - Cases|Cases]]<br />
<br />
==The Comprehensive Archive on a Single Page==<br />
[[Comprehensive De Voogt ECG Archive]]</div>145.117.40.234https://en.ecgpedia.org/index.php?title=Arrhythmogenic_Right_Ventricular_Cardiomyopathy&diff=6009Arrhythmogenic Right Ventricular Cardiomyopathy2008-06-10T13:23:47Z<p>145.117.40.234: </p>
<hr />
<div>{{authors|<br />
|mainauthor= [[user:Drj|J.S.S.G. de Jong, MD]]<br />
|advisor=<br />
|coauthor=<br />
|moderator= [[user:Drj|J.S.S.G. de Jong, MD]]<br />
|editor= P.G. Postema, MD<br />
}}<br />
[[Image:epsilon_wave.png|thumb|ECG with an epsilon wave in V1]]<br />
[[Image:arvdhart.png|thumb| A section throught the heart of a ARVC patient. (A) Transmural fatty replacement of the right ventricular free wall. (B) Myocardial atrophy is confined to the right ventricle and substantially spares the interventricular septum as well as the left ventricular free wall. <cite>Corrado</cite> Reproduced with permission from BMJ Publishing Group Ltd. ]]<br />
[[Image:arvd_ecg1.jpg|thumb]]<br />
[[Image:arvd_ecg2.jpg|thumb]]<br />
[[Image:arvd_ecg3.jpg|thumb]]<br />
<br />
'''Arrythmogenic Right Ventricular Cardiomyopathy''', (ARVC, or ARVD: Arrythmogenic Right Ventricular Disease) is characterized by fatty replacement and fibrosis of the heart. Especially the right ventricle apex and outflow tract are involved. However the left ventricle can be affected to.<br />
<br />
As a result of the fatty replacement and fibrosis, ventricular arrhythmias are common in this disease and can lead to palpitations, syncope and sudden death. At older age right ventricular pump failure can occur.<br />
<br />
The diagnosis is based on major and minor criteria, as published by the European Society of Cardiology.<cite>McKenna1994</cite><br />
<br />
ARVC is a progressive disease. The '''incidence''' is estimated to be 1:3.000-1:10.000. Manifestations is usually during teenage. Although the diagnosis is more often made in athletes, sports are not thought to have a causative relationship with the disease. ARVD can occur in families; more than 9 different chromosomal defects have been described, most often with autosomal dominant inheritance. <br />
<br />
One unique form of ARVD, called Naxos disease (after the Greek island where it was first diagnosed), has an autosomal recessive pattern of inheritance. <br />
<br />
'''Diagnosis''' ARVC is a difficult diagnosis to make. Therefore, the European Society of Cardiology has created a list of diagnositc criteria for the diagnosis of ARVC<cite>#McKenna1994</cite> (see table).<br />
{| class="wikitable" align="left" width="400px"<br />
!Major diagnostic criteria for Aritmogenic Right Ventricular Cardiomyopathy<cite>McKenna1994</cite><br />
|-<br />
|<ul><li>Familial disease confirmed at necroscopy or surgery</li><br />
<li>Severe dilatation and reduciton of right ventricular ejection fraction with no (or only mild) LV impairment</li><br />
<li>Localised irhgt ventricular aneurysms (akinetic or diskinetic areas with diastolic bulging)</li><br />
<li>Severe segmental dilataion of the right ventricle</li><br />
<li>Fibrofatty replacement of myocardium on endomyocardial biopsy</li><br />
</ul><br />
|-<br />
!Diagnostic criteria that can be diagnosed on the ECG<br />
|-<br />
|<ul><br />
<li>(major) Epsilon wave or localised prolongation (>110ms) of the QRS complex in right precordial leads (V1-V3)</li><br />
<li>(minor) Inverted T waves in right precordial leads (V2 and V3) (people aged more than 12 yr; in absence of [[RBBB]]</li><br />
<li>(minor) [[Late potentials]] ([[SAECG|signal averaged ECG]])</li><br />
<li>(minor) Left bundle branch block type [[Ventricular Tachycardia|ventricular tachycardia]] (sutained and non-sustained) (ECG, [[Holter]], [[Exercise Testing|exercise testing]]</li><br />
<li>(minor) Frequent [[Ventricular Premature Beats|ventricular extrasystoles]] (more than 1000/24h) ([[Holter]])</li><br />
</ul><br />
|}<br />
<br />
{{clr}}<br />
'''Treatment''' focuses on avoiding complications.<cite>ACC2006</cite><br />
*Medication: <br />
**anti-arrithmics: Sotalol better than Amiodarone.<br />
**ACE-inhibitors to prevent cardiac remodelling<br />
*[[ICD]] implantation is recommended for the prevention of sudden cardiac death in patients with ARVC with documented sustained VT or VF who are receiving chronic optimal medical therapy.<br />
*[[ICD]]] implantation can be considered for the prevention of sudden cardiac death in patients with ARVC with extensive disease, including those with left ventricular involvement, 1 or more affected family member with SCD, or undiagnosed syncope when [[Ventricular Tachycardia|ventricular tachycardia]] or [[Ventricular Fibrillation|ventricular Fibrillation]] has not been excluded as the cause of syncope, who are receiving chronic optimal medical therapy, and who have reasonable expectation of survival with a good functional status for more than 1 y.<br />
*Radiofrequency [[ablation]] can be useful as adjunctive therapy in management of patients with ARVC with recurrent [[Ventricular Tachycardia|ventricular tachycardia]], despite optimal antiarrhythmic drug therapy.<br />
<br />
==Referenties==<br />
<biblio><br />
#McKenna1994 pmid=8142187<br />
#Corrado pmid=10768917<br />
#ACC2006 pmid=16949478<br />
</biblio></div>145.117.40.234https://en.ecgpedia.org/index.php?title=ECGs_in_Athletes&diff=5889ECGs in Athletes2008-04-03T20:20:30Z<p>145.117.40.234: /* Prevalence of ECG abnormalities in athletes */</p>
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<div>Corrado et al. have published an ESC consensus document on the screening of athletes for competitive sports.<cite>Corrado</cite> Besides a good medical history and examination, a 12 lead ECG is also part of the screening. They have set up special ECG criteria for participants in competitive sports (table 1). If one of the described findings are present on the ECG, the ECG is considered 'positive' and further evaluation is mandatory which can include echocardiography, 24-h ambulatory Holter monitoring, and exercise testing. ECG Features of cardiac diseases detectable at pre-participation screening in young competitive athletes are shown in table 2.<br />
<br />
Prevalence of ECG abnormalities in competitive athletes has been studied by Pellicia et al.<cite>Pellicia</cite>(see table below). ECG abnormalities in their study increased with age and level of exercise. In young amateur athletes they found ECG abnormalities in about 7%, a number that rised to 40% in "adult elite athletes". Especially [[RBBB]] and [[lvh|left ventricular hypertrophy]] were often seen.<br />
<br />
Recently fierce debate has been going on about whether an ECG should be part of the screening of apparently healthy young sporters. In Italy this screening is compulsory by law and this country is a strong advocate of the use of an ECG as part of this screening. However, others<cite>Chaitman</cite> have stated that costs are too high for the yield (expressed in dollars per prevented sudden cardiac death) and an ECG is not included in the screening protocol of the American Heart Association.<cite>Maron</cite><cite>Myerburg</cite><br />
==Criteria for a positive ECG==<br />
{| class="wikitable" style="font-size:90%;"<br />
|- <br />
|+'''Table 1: Criteria for a positive 12-lead ECG'''<br />
|-<br />
!P wave<br />
|<br />
<ul><br />
<li>left atrial enlargement: negative portion of the P wave in lead V1 ≥ 0.1 mV in depth and ≥ 0.04 s in duration</li><br />
<li>right atrial enlargement: peaked P wave in leads II and III or V1 ≥ 0.25 mV in amplitude</li><br />
</ul><br />
|-<br />
!QRS complex<br />
|<br />
<ul><br />
<li>frontal plane axis deviation: right ≥ +120° or left –30° to –90°;</li><br />
<li>increased voltage: amplitude of R or S wave in in a standard lead ≥2 mV, S wave in lead V1 or V2 ≥ 3 mV, or R wave in lead V5 or V6 ≥ 3 mV;</li><br />
<li>abnormal Q waves ≥ 0.04 s in duration or ≥ 25% of the height of the ensuing R wave or QS pattern in<br />
two or more leads;</li><br />
<li>right or left bundle branch block with QRS duration ≥ 0.12 s;</li><br />
<li>R or R' wave in lead V1 ≥ 0.5 mV in amplitude and R/S ratio ≥ 1.</li><br />
</ul><br />
|-<br />
!ST-segment, T-waves, and QT interval<br />
|<br />
<ul><br />
<li>ST-segment depression or T-wave flattening or inversion in two or more leads;</li><br />
<li>prolongation of heart rate corrected QT interval (QTc) > 0.44 s in males and > 0.46 s in females.</li><br />
</ul><br />
|-<br />
!Rhythm and conduction abnormalities<br />
|<br />
<ul><br />
<li>premature ventricular beats or more severe ventricular arrhythmias;</li><br />
<li>supraventricular tachycardias, atrial flutter, or atrial fibrillation;</li><br />
<li>short PR interval (< 0.12 s) with or without ‘delta’ wave;</li><br />
<li>sinus bradycardia with resting heart rate ≤ 40 beats/min;<sup>a</sup></li><br />
<li>first (PR ≥ 0.21 s<sup>b</sup>), second or third degree atrioventricular block.</li><br />
</ul><br />
|- <br />
| colspan="2" style="text-align:left;" font-size="80%"|<br />
<sup>a</sup>Increasing less than 100 beats/min during limited exercise test.<br />
<sup>b</sup>Not shortening with hyperventilation or limited exercise test.<br />
|-<br />
|}<br />
==Cardiac diseases and their ECG features==<br />
{| class="wikitable" style="font-size:90%;"<br />
|- <br />
|+'''Table 2: ECG Features of cardiac diseases detectable at pre-participation screening in young competitive athletes'''<br />
! Disease<br />
! QTc interval<br />
! P wave<br />
! PR interval<br />
! QRS complex<br />
! ST interval<br />
! T wave<br />
! Arrhythmias<br />
|-<br />
! [[Clinical_Disorders#Hypertrophic_Obstructive_Cardiomyopathy|HCM]]<br />
| Normal<br />
| (left atrial enlargement)<br />
| Normal<br />
| Increased voltages in mid-left precordial leads; abnormal Q waves in inferior and / or lateral leads; (LAD, LBBB); (delta wave)<br />
| Down-sloping (up-sloping)<br />
| Inverted in mid-left precordial leads; (giant and negative in the apical variant)<br />
| (Atrial fibrillation); (PVB); (VT)<br />
|-<br />
! [[arvd|Arrhythmogenic right ventricular cardiomyopathy / dysplasia]]<br />
| Normal<br />
| Normal<br />
| Normal<br />
| Prolonged > 110 ms in right precordial leads; epsilon wave in right precordial leads; reduced voltages <= 0.5 mV in frontal leads; (RBBB)<br />
| (Up-sloping in right precordial leads)<br />
| Inverted in right precordial leads<br />
| PVB with a LBBB pattern; (VT with a LBBB pattern)<br />
|-<br />
! Dilated cardiomyopathy<br />
| Normal<br />
| (Left atrial enlargement)<br />
| (Prolonged >= 0.21s)<br />
| LBBB<br />
| Down-sloping (up-sloping)<br />
| Inverted in inferior and / or lateral leads<br />
| PVB; (VT)<br />
|-<br />
! [[lqts|Long QT syndrome]]<br />
| Prolonged<br />
*> 440ms in males<br />
*> 460ms in females<br />
| Normal<br />
| Normal<br />
| Normal<br />
| Normal<br />
| Bifid or biphasic in all leads<br />
| (PVB); (torsade de pointes)<br />
|-<br />
! [[Brugada Syndrome]]<br />
| Normal<br />
|<br />
| Prolonged >= 0.21s<br />
| S1S2S3 pattern; (RBBB/LAD)<br />
| Up-sloping coved-type in right precordial leads<br />
| Inverted in right precordial leads<br />
| (Polymorphic VT); (atrial fibrillation) (sinus tachycardia)<br />
|-<br />
! Lenègre disease<br />
| Normal<br />
| Normal<br />
| Prolonged >= 0.21s<br />
| RBBB; RBBB/LAD; LBBB<br />
| Normal<br />
| Secondary changes<br />
| (2nd or 3rd degree AV block)<br />
|-<br />
! [[Short QT Syndrome]]<br />
| Shortened < 300 ms<br />
| Normal<br />
| Normal<br />
| Normal<br />
| Normal<br />
| Normal<br />
| Atrial fibrillation (polymorphic VT)<br />
|-<br />
! [[WPW|Pre-excitation syndrome (WPW)]]<br />
| Normal<br />
| Normal<br />
| Shortened < 0.12s<br />
| Delta wave<br />
| Secondary changes<br />
| Secondary changes<br />
| Supraventricular tachycardia; (atrial fibrillation)<br />
|-<br />
! Coronary artery diseases<sup>a</sup><br />
| (Prolonged)<br />
| Normal<br />
| Normal<br />
| (Abnormal Q waves)<sup>b</sup><br />
| (Down-or up-sloping)<br />
| Inverted in >= 2 leads<br />
| PVB; (VT);<br />
|- <br />
| colspan="8" style="text-align:left;" font-size="80%"|<br />
*Less common or uncommon ECG findings are reported in brackets. <br />
*[[QTc]]: QT interval corrected for heart rate by Bazett’s formula. [[LBBB]]: left bundle branch block. [[RBBB]]: right bundle branch block. LAD: left axis deviation of –30 degrees or more. [[PVB]]: either single or coupled premature ventricular beats. [[VT]]: either non-sustained or sustained ventricular tachycardia.<br />
*<sup>a</sup>Coronary artery diseases: either premature coronary atherosclerosis or congenital coronary anomalies.<br />
*<sup>b</sup>Abnormal Q waves (table 1)<br />
|-<br />
|}<br />
<br />
==Prevalence of ECG abnormalities in athletes==<br />
{| class="wikitable" style="font-size:90%;"<br />
|- <br />
|+Table 3: Prevalence of ECG abnormalities in an unselected population of 32 652 young individuals undergoing the pre-participation cardiovascular screening'''<br />
! ECG abnormalities<br />
! Athletes, ''n'' (%)<br />
|-<br />
! Negative T-waves in precordial/standard leads<br />
| align="left" valign="top" | 751 (2.3)<br />
|-<br />
! [[RBBB]]<br />
| align="left" valign="top" | 351 (1.0)<br />
|-<br />
! Increased R/S wave voltages (suggestive of LVH)<br />
| align="left" valign="top" | 247 (0.8)<br />
|-<br />
! [[Left anterior fascicular block]]<br />
| align="left" valign="top" | 162 (0.5)<br />
|-<br />
! [[wpw|Pre-excitation pattern]]<br />
| align="left" valign="top" | 42 (0.1)<br />
|-<br />
! [[LBBB]]<br />
| align="left" valign="top" | 19 (0.1)<br />
|-<br />
! Prolonged corrected QT interval<br />
| align="left" valign="top" | 1 (0.003)<br />
|-<br />
! Others (incomplete [[RBBB]], prolonged PR interval, early repolarization pattern)<br />
| align="left" valign="top" | 2280 (7.0)<br />
|-<br />
! Total<br />
| align="left" valign="top" | 3853 (11.8)<br />
|-<br />
| colspan="2" style="text-align:left;" font-size="80%"|<br />
*RBBB, right bundle branch block; LVH, left ventricular hypertrophy; LBBB, left bundle branch block.<cite>Pellicia</cite><br />
|-<br />
|}<br />
<br />
==References==<br />
<biblio><br />
#Corrado pmid=15689345<br />
#Pellicia pmid=17623682<br />
#Maron pmid=17353433<br />
#Myerburg pmid=18040041<br />
#Chaitman pmid=18040040<br />
</bilbio></div>145.117.40.234https://en.ecgpedia.org/index.php?title=Supraventricular_Rhythms&diff=5783Supraventricular Rhythms2008-01-06T22:54:30Z<p>145.117.40.234: /* Also read: */</p>
<hr />
<div>{{authors|<br />
|mainauthor= [[user:Drj|J.S.S.G. de Jong]]<br />
|moderator= [[user:Drj|J.S.S.G. de jong]]<br />
|supervisor= <br />
}}<br />
===An overview of supraventricular tachycardias===<br />
{| class="wikitable" font-size="90%"<br />
|- style="text-align:center;background-color:#6EB4EB;"<br />
|+'''An overview of supraventricular tachycardias'''<br />
|-<br />
!<br />
!example<br />
!regularity<br />
!atrial frequency<br />
!ventricular frequency<br />
!origin (SVT/VT)<br />
!p-wave<br />
!effect of adenosine<br />
|- <br />
| colspan="8" style="text-align:left;background-color:#cfefcf;" | '''Narrow complex (QRS<0.12)'''<br />
|-<br />
! [[Sinustachycardia]]<br />
| [[Image:sinustachy_small.svg|200px]]<br />
| regular<br />
| 100-180 bpm<br />
| 100-180 bpm<br />
| sinusnode (SVT)<br />
| precedes every QRS complex<br />
| gradual slowing<br />
|-<br />
! [[Atrial Fibrillation]]<br />
| [[Image:afib_small.svg|200px]]<br />
| grossly irregular<br />
| 400-600 bpm <br />
| 75-175 bpm <br />
| atria (SVT)<br />
| absent<br />
| slows down rate; irregularity remains<br />
|-<br />
! [[Atrial Flutter]]<br />
| [[Image:aflutt_small.svg|200px]]<br />
| regular (sometimes alternating block) <br />
| 250-350 bpm <br />
| 75-150 bpm (3:1 or 2:1 block is most common) <br />
| atria (SVT)<br />
| negative sawtooth in lead II <br />
| temporary reduced conduction (e.g. 4:1)<br />
|-<br />
! [[AVNRT]] <br />
| [[Image:avnrt_small.svg|200px]]<br />
| regular <br />
| 180-250 bpm<br />
| 180-250 bpm <br />
| AV-node (SVT)<br />
| in QRS complex (R') <br />
| stops<br />
|-<br />
! [[Atrial Tachycardia]]<br />
| [[Image:atrialtachy_small.svg|200px]]<br />
| regular<br />
| 120-250 bpm <br />
| 75-200 bpm<br />
| atria<br />
| precedes QRS, p wave differs from sinus-p <br />
| temporary AV-block<br />
|-<br />
! [[AVRT|Atrio-Ventricular Reentry Tachycardia (AVRT)- orthodromic]]<br />
| [[Image:avrt_small.svg|200px]]<br />
| regular <br />
| 150-250 bpm<br />
| 150-250 bpm<br />
| circle: av-node - ventricles - bypass - atria<br />
| RP < PR <br />
| stops<br />
|-<br />
! [[AVJT|AV junctional tachycardia]]<br />
| [[Image:avnodal_small.svg|200px]]<br />
| regular <br />
| 60-100 bpm<br />
| 70-130 bpm<br />
| AV node<br />
| RP < PR <br />
| reduces rate<br />
|- <br />
| colspan="8" style="text-align:left;background-color:#cfefcf;" | '''Wide complex (QRS>0.12)'''<br />
|-<br />
! [[Supraventricular tachycardia with block]]<br />
| [[Image:atrial_tachy_with_LBBB_leadII.svg|200px]]<br />
| (ir)regular depending on SVT<br />
| 150-250 bpm<br />
| 75-200 bpm<br />
| atria (SVT)<br />
| absent<br />
| temporary increased AV-block (eg 4:1)<br />
|-<br />
! [[AVRT|Atrio-ventricular Reentry Tachycardia (AVRT) - antidrome]]<br />
| <br />
| regular <br />
| 150-250 bpm<br />
| 150-250 bpm<br />
| circular: bypass - atria - av-node - ventricles<br />
| RP < PR <br />
| stops<br />
|-<br />
|}<br />
<br />
===Supraventricular [[Ectopic Beats|ectopic beats]]===<br />
*[[Atrial Premature Complexes]]<br />
*[[Wandering Pacemaker]]<br />
*[[AV-nodal complexes]]<br />
<br />
===Also read===<br />
*Flowchart: [[Media:narrow_tachycardia_flow.png|Approach to the Narrow Complex Tachycardia]] Adapted from <cite>ESCnarrowQRS</cite>.<br />
*[[Introduction to Arrhythmias]]<br />
*[[Mechanisms of Arrhythmias]]<br />
*[[Sinus node rhythms and arrhythmias]]<br />
*[[Junctional Tachycardias]]<br />
*[[Ventricular Arrhythmias]]<br />
<br />
==References==<br />
<biblio><br />
#ESCnarrowQRS pmid=14563598<br />
</biblio></div>145.117.40.234https://en.ecgpedia.org/index.php?title=Pacemaker&diff=5559Pacemaker2007-12-20T09:53:58Z<p>145.117.40.234: /* References */</p>
<hr />
<div>{{authors|<br />
|mainauthor= [[user:Drj|J.S.S.G. de Jong]]<br />
|moderator= [[user:Drj|J.S.S.G. de jong]]<br />
|supervisor= <br />
}}<br />
[[Image:picture_pacemaker.jpg|thumb|A (used) DDDr pacemaker]]<br />
[[Image:paced2.gif|thumb| Ventricular paced rhythm shows ventricular pacemaker spikes]]<br />
[[Image:Pacemaker2.jpg |thumb| VVI pacemaker rhythm. Note the LBBB morphology with left axis deviation indicating the pacing lead in the right ventricular apex.]]<br />
<br />
<br />
A pacemaker is indicated when the electrical impulse conduction or formation is dangerously disturbed. The paced '''pacemaker rhythm''' can easily be recognized on the ECG as it shows '''pacemaker spikes''': vertical signals that represent the electrical activity of the pacemaker.<br />
<br />
In the first example image, the atria are being paced, but not the ventricles, resulting in a '''atrial paced rhythm'''. Accordingly the ventricular beat is delayed until the atrial signal has passed the AV node. In the second image the ventricles are paced directly, resulting in '''ventricular paced rhythm'''. As ventricular pacing occurs exclusively in the right ventricle the ECG shows a left bundle branch pattern. An exception to this rule is left ventricular pacing in patients with congenital anomalies and patients with an epicardial pacemaker that has been placed during surgery.<br />
<br />
===Pacemaker Coding===<br />
Pacemakers can be categorized according to the NASPE coding system, that usually consists of 3-5 letters. <br />
* The first letter represents the chamber where the signal is "sensed": O=none, A=atria, V=ventricle, D=dual (atrial and / or ventricle)<br />
* The second letter represents the chamber that is being paced: A=atria, V=ventricle, D=dual (atria and / or ventricle)<br />
* The third letter represents the action that follows the sensed signal: O = none, T = triggered, I = inhibited (i.e. if the heart beats by itself, the pacemaker is silent) and D = dual (T + I). <br />
* The fourth letter denotes whether the pacemaker has a fixed rate (0 = none) or has rate modulation (R).<br />
* The fifth letter indicates whether the pacemaker can pace both the atria and right chamber. This letter is seldomly used.<br />
<br />
===Commonly Used Pacemakers===<br />
The most often used codes are:<br />
* '''AAI''': the atria are paced, when the intrinsic atrial rhythm falls below the pacemakers threshold<br />
* '''VVI''': the ventricles are paced, when the intrinsic ventricular rhythm falls below the pacemakers threshold<br />
* '''DDD''': the pacemaker records both the atrial and ventricular rate and can pace one of each chambers when needed.<br />
* '''DDDR''': as above, but the pacemaker has a sensor that records a demand for higher cardiac output and can adjust the heart rate accordingly.<br />
* Biventricular pacemakers ('''CRT-D'''): leads in both ventricles are present to synchronize contraction. This cardiac synchronization therapy can improve symptoms and survival in some heart failure patients. <br />
* '''[[ICD]]''' (Internal Cardioversion Device): this device can detect and treat [[Ventricular Tachycardia]] and [[Ventricular Fibrillation]]. Usually the first treatment is anti-tachy pacing (pacing at a rate +- 10% above the ventricular rate in ventricular tachycardia, which can convert the rhythm to sinus rhythm). If this is not effective an defibrillator shock is delivered, usually with 16-36 Joules of energy. ICDs can save lives in patients who have a high risk of ventricular arrhythmias. All ICDs have optional pacemaker activity to treat bradycardias. New biventricular ICDs have 3 leads: an atrial lead, a left ventricular lead and a right ventricular lead.<br />
<br />
===Pacemaker Indications===<br />
A full list of pacemaker indications can be read in the ESC guidelines on cardiac pacing <cite>Vardas</cite>. A selection of class I indications are: chronic symptomatic third- or second degree (Mobtiz I or II) atrioventricular block. Syncope with sinus node disease. Alternating bundle branch block. Persisting AV block after surgery.<br />
<br />
===ICD Indications===<br />
<br />
===Atrial-sensed ventricular-paced rhythm===<br />
===AV dual-paced rhythm===<br />
===Pacemaker Malfunction===<br />
to be filled in ...<br />
====Failure of appropriate capture, atrial====<br />
====Failure of appropriate capture, ventricular====<br />
====Failure of appropriate inhibition, atrial====<br />
====Failure of appropriate inhibition, ventricular====<br />
====Failure of appropriate pacemaker firing====<br />
====Retrograde atrial activation====<br />
====Pacemaker mediated tachycardia====<br />
<br />
==External Links==<br />
[http://www.hrsonline.org/swPositionStatementFiles/ps101036428.asp Heart Rhytm Society]<br />
<br />
<br />
==References==<br />
<biblio><br />
#Vardas pmid=17726042<br />
#Gregoratos pmid=12379588<br />
</biblio><br />
<br />
{{clr}}</div>145.117.40.234https://en.ecgpedia.org/index.php?title=Short_coupled_Torsades_de_Pointes&diff=5534Short coupled Torsades de Pointes2007-12-17T11:22:52Z<p>145.117.40.234: </p>
<hr />
<div>Short coupled Torsades de Pointes <cite>Leenhardt</cite><br />
[[Image:shortcoupled_tdp1.jpg|thumb|Arrhythmias in a patient with short coupled torsades de pointes]]<br />
[[Image:shortcoupled_tdp2.jpg|thumb|Arrhythmias in a patient with short coupled torsades de pointes degenerating in [[ventricular fibrillation]]]]<br />
[[Image:shortcoupled_tdp3.jpg|thumb|Arrhythmias in a patient with short coupled torsades de pointes: frequent short coupled extrasystoles]]<br />
==References==<br />
<biblio><br />
#Leenhardt pmid=8281648<br />
</biblio></div>145.117.40.234https://en.ecgpedia.org/index.php?title=Short_coupled_Torsades_de_Pointes&diff=5533Short coupled Torsades de Pointes2007-12-17T11:20:29Z<p>145.117.40.234: </p>
<hr />
<div>Short coupled Torsades de Pointes <cite>Leenhardt</cite><br />
[[Image:shortcoupled_tdp1.jpg|thumb]]<br />
[[Image:shortcoupled_tdp2.jpg|thumb]]<br />
[[Image:shortcoupled_tdp3.jpg|thumb]]<br />
==References==<br />
<biblio><br />
#Leenhardt pmid=8281648<br />
</biblio></div>145.117.40.234https://en.ecgpedia.org/index.php?title=Brugada_Syndrome&diff=5488Brugada Syndrome2007-11-29T16:53:26Z<p>145.117.40.234: </p>
<hr />
<div>{{authors|<br />
|mainauthor= [[user:Pgpostema|P.G. Postema, MD]]<br />
|supervisor=<br />
|coauthor= [[user:Drj|J.S.S.G. de Jong, MD]]<br />
|moderator= [[user:Pgpostema|P.G. Postema, MD]]<br />
|editor= <br />
}}<br />
[[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 four members of the Brugada family conduct research after the syndrome that has been named after them.]]<br />
[[Image:Brugada.png|thumb|Typical ECG abnormalities in Brugada syndrome: ST elevation in V1-V3, without ischemia.]]<br />
[[Image:scn5a.jpg|thumb| The SCN5a gen is located on the short arm (p) of chromosome 3]]<br />
<br />
<br />
The '''Brugada syndrome is an hereditary disease that is associated with higher risk of sudden cardiac death'''. It is characterized by typical ECG abnormalities: '''ST segment elevation in the precordial leads (V1 - V3)'''.<br />
<br />
==Characteristics of the Brugada syndrome:==<br />
*[[w:Autosomal_dominant|autosomal dominant]] inheritance. If one of both parents are affected, their children have a 50% chance of inheriting the disease.<br />
*Man are more often symptomatic than women, probably by the influence of sex hormones on cardiac arrhythmias. <br />
*The arrhythmias usually occur between 30 and 40 years of age. (range 1-77 yrs) and often during rest or while sleeping.<br />
*Only in about 30% of patients, genetic defects can be detected in the ([http://ghr.nlm.nih.gov/gene=scn5a SCN5A]) gen. In the other patients the disease is probably multi-genetic or caused by yet unknown genetic defects.<br />
*The right ventricular outflow tract (right before the pulmonary valve) is most affected in the Brugada syndrome. <br />
*The prevalence varies between 5-50:10.000, largely depending on geographic location. In some south-east Asian countries the disease is endemic and sometimes considered the second cause of death amongst young men (after car accidents). There it is called 'Sudden Unexpected Death Syndrome' (SUDS). In different Asian countries, different names have been given to the syndrome: in the Phillipines it is called ''bangungut'' (to rise and moan in sleep) and in Thailand ''lai tai'' (death during sleep)<br />
<br />
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><br />
<br />
==Diagnosis and treatment==<br />
*Patients who are symptomatic (syncope, ventricular tachycardias or survivors of sudden cardiac death) have a mortality risk of up to 10% per year. In these patients an [[:w:nl:Internal_Cardiac_Defibrillator|ICD]] should be implanted. <br />
*Some groups advice an electrofysiologic investigation for risk assessment in Brugada patients,<cite>brug2</cite><cite>brug3</cite> but others could not reproduce the predicive value of these tests,<cite>priori</cite><cite>eckhardt</cite> so this is still controversial.<br />
*In large studies familiar sudden death is not a risk factor for sudden death in siblings.<br />
*In asymptomatic patients in whom the Brugada ECG characteristics are present either spontaneously or provoked by fever or sodium channel blockers (ajmaline, flecainide) life style advices are given, which include:<br />
**A number of medications should not be taken (amongst others beta-blockers, and sodium channel blockers such as certain anti-depressants and anti-arrhythmics)<br />
**Rigorous treatment of fever with paracetamol / Tylenol<br />
<br />
For a full list of the diagnostic criteria, see <cite>Wilde</cite><br />
<br />
==Electrocardiographic criteria==<br />
Three ECG repolarization patterns in the right precordial leads are recognized in the diagnosis of Brugada syndrome.<br />
<br />
'''Type I''' is the only ECG criterium that is diagnostic of Brugada syndrome. Type I repolarization is characterized by a coved ST-segment elevation >=2 mm (0.2 mV) followed by a negative T wave (see figure). Brugada syndrome is definitively diagnosed when a type 1 ST-segment elevation 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: <br />
*documented ventricular fibrillation (VF)<br />
*polymorphic ventricular tachycardia (VT)<br />
*a family history of sudden cardiac death at <45 years old<br />
*coved-type ECGs in family members<br />
*inducibility of VT with programmed electrical stimulation<br />
*syncope<br />
*nocturnal agonal respiration.<br />
<br />
Electrocardiograms of Brugada patients can change over time from type I to type II ECGs and back.<br />
A type III ECG is rather common and is concidered a normal variant.<br />
<br />
{| class="wikitable" font-size="90%"<br />
|- style="text-align:center;background-color:#6EB4EB;"<br />
|+'''ST segment abnormalities in the different types of Brugada syndrome'''<cite>Wilde2</cite><br />
|-<br />
!<br />
!Type I<br />
!Type II<br />
!Type III<br />
|- <br />
!J wave amplitude<br />
|>= 2mm<br />
|>= 2mm<br />
|>= 2mm<br />
|-<br />
!T wave<br />
|negative<br />
|positive or biphasis<br />
|positive<br />
|-<br />
!ST-T configuration<br />
|coved type<br />
|saddleback<br />
|saddleback<br />
|-<br />
!ST segment (terminal portion)<br />
|gradually descending<br />
|elevated >= 1mm<br />
|elevated < 1mm<br />
|-<br />
|}<br />
<br />
<br />
<gallery caption="Examples of Brugada syndrome type I"><br />
Image:Brugada_syndrome_type1_example1.png<br />
Image:Brugada_syndrome_type1_example2.png<br />
Image:Brugada_syndrome_type1_example3.png<br />
Image:Brugada_syndrome_type1_example4.png<br />
Image:Brugada_syndrome_type1_example5.png<br />
</gallery><br />
<gallery caption="Examples of Brugada syndrome type II"><br />
Image:Brugada_syndrome_type2_example1.png<br />
</gallery><br />
<br />
==External links==<br />
*Cardiogenetics website of the AMC [http://www.cardiogenetica.nl cardiogentica.nl]<br />
*[http://www.brugada.org Brugada.org ]<br />
*[http://www.genereviews.org/servlet/access?id=8888891&key=ghdBRjkdNXE6y&gry=INSERTGRY&fcn=y&fw=E0gK&filename=/profiles/brugada/index.html Genereview Brugada]<br />
<br />
==Referenties==<br />
<biblio><br />
#Wilde pmid=15898165<br />
#Brugada pmid=1309182<br />
#osher pmid=13104407<br />
#brug2 pmid=11772879 <br />
#brug3 pmid=12776858<br />
#priori pmid=11901046<br />
#eckhardt pmid=15642768<br />
#Wilde2 pmid=12417552<br />
</biblio></div>145.117.40.234https://en.ecgpedia.org/index.php?title=Brugada_Syndrome&diff=5487Brugada Syndrome2007-11-29T16:52:36Z<p>145.117.40.234: /* Electrocardiographic criteria */</p>
<hr />
<div>{{authors|<br />
|mainauthor= [[user:Pgpostema|P.G. Postema, MD]]<br />
|advisor=<br />
|coauthor= [[user:Drj|J.S.S.G. de Jong, MD]]<br />
|moderator= [[user:Pgpostema|P.G. Postema, MD]]<br />
|editor= <br />
}}<br />
[[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 four members of the Brugada family conduct research after the syndrome that has been named after them.]]<br />
[[Image:Brugada.png|thumb|Typical ECG abnormalities in Brugada syndrome: ST elevation in V1-V3, without ischemia.]]<br />
[[Image:scn5a.jpg|thumb| The SCN5a gen is located on the short arm (p) of chromosome 3]]<br />
<br />
<br />
The '''Brugada syndrome is an hereditary disease that is associated with higher risk of sudden cardiac death'''. It is characterized by typical ECG abnormalities: '''ST segment elevation in the precordial leads (V1 - V3)'''.<br />
<br />
==Characteristics of the Brugada syndrome:==<br />
*[[w:Autosomal_dominant|autosomal dominant]] inheritance. If one of both parents are affected, their children have a 50% chance of inheriting the disease.<br />
*Man are more often symptomatic than women, probably by the influence of sex hormones on cardiac arrhythmias. <br />
*The arrhythmias usually occur between 30 and 40 years of age. (range 1-77 yrs) and often during rest or while sleeping.<br />
*Only in about 30% of patients, genetic defects can be detected in the ([http://ghr.nlm.nih.gov/gene=scn5a SCN5A]) gen. In the other patients the disease is probably multi-genetic or caused by yet unknown genetic defects.<br />
*The right ventricular outflow tract (right before the pulmonary valve) is most affected in the Brugada syndrome. <br />
*The prevalence varies between 5-50:10.000, largely depending on geographic location. In some south-east Asian countries the disease is endemic and sometimes considered the second cause of death amongst young men (after car accidents). There it is called 'Sudden Unexpected Death Syndrome' (SUDS). In different Asian countries, different names have been given to the syndrome: in the Phillipines it is called ''bangungut'' (to rise and moan in sleep) and in Thailand ''lai tai'' (death during sleep)<br />
<br />
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><br />
<br />
==Diagnosis and treatment==<br />
*Patients who are symptomatic (syncope, ventricular tachycardias or survivors of sudden cardiac death) have a mortality risk of up to 10% per year. In these patients an [[:w:nl:Internal_Cardiac_Defibrillator|ICD]] should be implanted. <br />
*Some groups advice an electrofysiologic investigation for risk assessment in Brugada patients,<cite>brug2</cite><cite>brug3</cite> but others could not reproduce the predicive value of these tests,<cite>priori</cite><cite>eckhardt</cite> so this is still controversial.<br />
*In large studies familiar sudden death is not a risk factor for sudden death in siblings.<br />
*In asymptomatic patients in whom the Brugada ECG characteristics are present either spontaneously or provoked by fever or sodium channel blockers (ajmaline, flecainide) life style advices are given, which include:<br />
**A number of medications should not be taken (amongst others beta-blockers, and sodium channel blockers such as certain anti-depressants and anti-arrhythmics)<br />
**Rigorous treatment of fever with paracetamol / Tylenol<br />
<br />
For a full list of the diagnostic criteria, see <cite>Wilde</cite><br />
<br />
==Electrocardiographic criteria==<br />
Three ECG repolarization patterns in the right precordial leads are recognized in the diagnosis of Brugada syndrome.<br />
<br />
'''Type I''' is the only ECG criterium that is diagnostic of Brugada syndrome. Type I repolarization is characterized by a coved ST-segment elevation >=2 mm (0.2 mV) followed by a negative T wave (see figure). Brugada syndrome is definitively diagnosed when a type 1 ST-segment elevation 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: <br />
*documented ventricular fibrillation (VF)<br />
*polymorphic ventricular tachycardia (VT)<br />
*a family history of sudden cardiac death at <45 years old<br />
*coved-type ECGs in family members<br />
*inducibility of VT with programmed electrical stimulation<br />
*syncope<br />
*nocturnal agonal respiration.<br />
<br />
Electrocardiograms of Brugada patients can change over time from type I to type II ECGs and back.<br />
A type III ECG is rather common and is concidered a normal variant.<br />
<br />
{| class="wikitable" font-size="90%"<br />
|- style="text-align:center;background-color:#6EB4EB;"<br />
|+'''ST segment abnormalities in the different types of Brugada syndrome'''<cite>Wilde2</cite><br />
|-<br />
!<br />
!Type I<br />
!Type II<br />
!Type III<br />
|- <br />
!J wave amplitude<br />
|>= 2mm<br />
|>= 2mm<br />
|>= 2mm<br />
|-<br />
!T wave<br />
|negative<br />
|positive or biphasis<br />
|positive<br />
|-<br />
!ST-T configuration<br />
|coved type<br />
|saddleback<br />
|saddleback<br />
|-<br />
!ST segment (terminal portion)<br />
|gradually descending<br />
|elevated >= 1mm<br />
|elevated < 1mm<br />
|-<br />
|}<br />
<br />
<br />
<gallery caption="Examples of Brugada syndrome type I"><br />
Image:Brugada_syndrome_type1_example1.png<br />
Image:Brugada_syndrome_type1_example2.png<br />
Image:Brugada_syndrome_type1_example3.png<br />
Image:Brugada_syndrome_type1_example4.png<br />
Image:Brugada_syndrome_type1_example5.png<br />
</gallery><br />
<gallery caption="Examples of Brugada syndrome type II"><br />
Image:Brugada_syndrome_type2_example1.png<br />
</gallery><br />
<br />
==External links==<br />
*Cardiogenetics website of the AMC [http://www.cardiogenetica.nl cardiogentica.nl]<br />
*[http://www.brugada.org Brugada.org ]<br />
*[http://www.genereviews.org/servlet/access?id=8888891&key=ghdBRjkdNXE6y&gry=INSERTGRY&fcn=y&fw=E0gK&filename=/profiles/brugada/index.html Genereview Brugada]<br />
<br />
==Referenties==<br />
<biblio><br />
#Wilde pmid=15898165<br />
#Brugada pmid=1309182<br />
#osher pmid=13104407<br />
#brug2 pmid=11772879 <br />
#brug3 pmid=12776858<br />
#priori pmid=11901046<br />
#eckhardt pmid=15642768<br />
#Wilde2 pmid=12417552<br />
</biblio></div>145.117.40.234https://en.ecgpedia.org/index.php?title=Brugada_Syndrome&diff=5486Brugada Syndrome2007-11-29T16:48:58Z<p>145.117.40.234: /* Electrocardiographic criteria */</p>
<hr />
<div>{{authors|<br />
|mainauthor= [[user:Pgpostema|P.G. Postema, MD]]<br />
|advisor=<br />
|coauthor= [[user:Drj|J.S.S.G. de Jong, MD]]<br />
|moderator= [[user:Pgpostema|P.G. Postema, MD]]<br />
|editor= <br />
}}<br />
[[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 four members of the Brugada family conduct research after the syndrome that has been named after them.]]<br />
[[Image:Brugada.png|thumb|Typical ECG abnormalities in Brugada syndrome: ST elevation in V1-V3, without ischemia.]]<br />
[[Image:scn5a.jpg|thumb| The SCN5a gen is located on the short arm (p) of chromosome 3]]<br />
<br />
<br />
The '''Brugada syndrome is an hereditary disease that is associated with higher risk of sudden cardiac death'''. It is characterized by typical ECG abnormalities: '''ST segment elevation in the precordial leads (V1 - V3)'''.<br />
<br />
==Characteristics of the Brugada syndrome:==<br />
*[[w:Autosomal_dominant|autosomal dominant]] inheritance. If one of both parents are affected, their children have a 50% chance of inheriting the disease.<br />
*Man are more often symptomatic than women, probably by the influence of sex hormones on cardiac arrhythmias. <br />
*The arrhythmias usually occur between 30 and 40 years of age. (range 1-77 yrs) and often during rest or while sleeping.<br />
*Only in about 30% of patients, genetic defects can be detected in the ([http://ghr.nlm.nih.gov/gene=scn5a SCN5A]) gen. In the other patients the disease is probably multi-genetic or caused by yet unknown genetic defects.<br />
*The right ventricular outflow tract (right before the pulmonary valve) is most affected in the Brugada syndrome. <br />
*The prevalence varies between 5-50:10.000, largely depending on geographic location. In some south-east Asian countries the disease is endemic and sometimes considered the second cause of death amongst young men (after car accidents). There it is called 'Sudden Unexpected Death Syndrome' (SUDS). In different Asian countries, different names have been given to the syndrome: in the Phillipines it is called ''bangungut'' (to rise and moan in sleep) and in Thailand ''lai tai'' (death during sleep)<br />
<br />
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><br />
<br />
==Diagnosis and treatment==<br />
*Patients who are symptomatic (syncope, ventricular tachycardias or survivors of sudden cardiac death) have a mortality risk of up to 10% per year. In these patients an [[:w:nl:Internal_Cardiac_Defibrillator|ICD]] should be implanted. <br />
*Some groups advice an electrofysiologic investigation for risk assessment in Brugada patients,<cite>brug2</cite><cite>brug3</cite> but others could not reproduce the predicive value of these tests,<cite>priori</cite><cite>eckhardt</cite> so this is still controversial.<br />
*In large studies familiar sudden death is not a risk factor for sudden death in siblings.<br />
*In asymptomatic patients in whom the Brugada ECG characteristics are present either spontaneously or provoked by fever or sodium channel blockers (ajmaline, flecainide) life style advices are given, which include:<br />
**A number of medications should not be taken (amongst others beta-blockers, and sodium channel blockers such as certain anti-depressants and anti-arrhythmics)<br />
**Rigorous treatment of fever with paracetamol / Tylenol<br />
<br />
For a full list of the diagnostic criteria, see <cite>Wilde</cite><br />
<br />
==Electrocardiographic criteria==<br />
Three ECG repolarization patterns in the right precordial leads are recognized in the diagnosis of Brugada syndrome.<br />
<br />
'''Type I''' is the only ECG criterium that is diagnostic of Brugada syndrome. Type I repolarization is characterized by a coved ST-segment elevation >=2 mm (0.2 mV) followed by a negative T wave (see figure). Brugada syndrome is definitively diagnosed when a type 1 ST-segment elevation 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, or nocturnal agonal respiration.<br />
<br />
{| class="wikitable" font-size="90%"<br />
|- style="text-align:center;background-color:#6EB4EB;"<br />
|+'''ST segment abnormalities in the different types of Brugada syndrome'''<cite>Wilde2</cite><br />
|-<br />
!<br />
!Type I<br />
!Type II<br />
!Type III<br />
|- <br />
!J wave amplitude<br />
|>= 2mm<br />
|>= 2mm<br />
|>= 2mm<br />
|-<br />
!T wave<br />
|negative<br />
|positive or biphasis<br />
|positive<br />
|-<br />
!ST-T configuration<br />
|coved type<br />
|saddleback<br />
|saddleback<br />
|-<br />
!ST segment (terminal portion)<br />
|gradually descending<br />
|elevated >= 1mm<br />
|elevated < 1mm<br />
|-<br />
|}<br />
<br />
<br />
<gallery caption="Examples of Brugada syndrome type I"><br />
Image:Brugada_syndrome_type1_example1.png<br />
Image:Brugada_syndrome_type1_example2.png<br />
Image:Brugada_syndrome_type1_example3.png<br />
Image:Brugada_syndrome_type1_example4.png<br />
Image:Brugada_syndrome_type1_example5.png<br />
</gallery><br />
<gallery caption="Examples of Brugada syndrome type II"><br />
Image:Brugada_syndrome_type2_example1.png<br />
</gallery><br />
<br />
==External links==<br />
*Cardiogenetics website of the AMC [http://www.cardiogenetica.nl cardiogentica.nl]<br />
*[http://www.brugada.org Brugada.org ]<br />
*[http://www.genereviews.org/servlet/access?id=8888891&key=ghdBRjkdNXE6y&gry=INSERTGRY&fcn=y&fw=E0gK&filename=/profiles/brugada/index.html Genereview Brugada]<br />
<br />
==Referenties==<br />
<biblio><br />
#Wilde pmid=15898165<br />
#Brugada pmid=1309182<br />
#osher pmid=13104407<br />
#brug2 pmid=11772879 <br />
#brug3 pmid=12776858<br />
#priori pmid=11901046<br />
#eckhardt pmid=15642768<br />
#Wilde2 pmid=12417552<br />
</biblio></div>145.117.40.234https://en.ecgpedia.org/index.php?title=Brugada_Syndrome&diff=5485Brugada Syndrome2007-11-29T16:43:14Z<p>145.117.40.234: /* Referenties */</p>
<hr />
<div>{{authors|<br />
|mainauthor= [[user:Pgpostema|P.G. Postema, MD]]<br />
|advisor=<br />
|coauthor= [[user:Drj|J.S.S.G. de Jong, MD]]<br />
|moderator= [[user:Pgpostema|P.G. Postema, MD]]<br />
|editor= <br />
}}<br />
[[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 four members of the Brugada family conduct research after the syndrome that has been named after them.]]<br />
[[Image:Brugada.png|thumb|Typical ECG abnormalities in Brugada syndrome: ST elevation in V1-V3, without ischemia.]]<br />
[[Image:scn5a.jpg|thumb| The SCN5a gen is located on the short arm (p) of chromosome 3]]<br />
<br />
<br />
The '''Brugada syndrome is an hereditary disease that is associated with higher risk of sudden cardiac death'''. It is characterized by typical ECG abnormalities: '''ST segment elevation in the precordial leads (V1 - V3)'''.<br />
<br />
==Characteristics of the Brugada syndrome:==<br />
*[[w:Autosomal_dominant|autosomal dominant]] inheritance. If one of both parents are affected, their children have a 50% chance of inheriting the disease.<br />
*Man are more often symptomatic than women, probably by the influence of sex hormones on cardiac arrhythmias. <br />
*The arrhythmias usually occur between 30 and 40 years of age. (range 1-77 yrs) and often during rest or while sleeping.<br />
*Only in about 30% of patients, genetic defects can be detected in the ([http://ghr.nlm.nih.gov/gene=scn5a SCN5A]) gen. In the other patients the disease is probably multi-genetic or caused by yet unknown genetic defects.<br />
*The right ventricular outflow tract (right before the pulmonary valve) is most affected in the Brugada syndrome. <br />
*The prevalence varies between 5-50:10.000, largely depending on geographic location. In some south-east Asian countries the disease is endemic and sometimes considered the second cause of death amongst young men (after car accidents). There it is called 'Sudden Unexpected Death Syndrome' (SUDS). In different Asian countries, different names have been given to the syndrome: in the Phillipines it is called ''bangungut'' (to rise and moan in sleep) and in Thailand ''lai tai'' (death during sleep)<br />
<br />
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><br />
<br />
==Diagnosis and treatment==<br />
*Patients who are symptomatic (syncope, ventricular tachycardias or survivors of sudden cardiac death) have a mortality risk of up to 10% per year. In these patients an [[:w:nl:Internal_Cardiac_Defibrillator|ICD]] should be implanted. <br />
*Some groups advice an electrofysiologic investigation for risk assessment in Brugada patients,<cite>brug2</cite><cite>brug3</cite> but others could not reproduce the predicive value of these tests,<cite>priori</cite><cite>eckhardt</cite> so this is still controversial.<br />
*In large studies familiar sudden death is not a risk factor for sudden death in siblings.<br />
*In asymptomatic patients in whom the Brugada ECG characteristics are present either spontaneously or provoked by fever or sodium channel blockers (ajmaline, flecainide) life style advices are given, which include:<br />
**A number of medications should not be taken (amongst others beta-blockers, and sodium channel blockers such as certain anti-depressants and anti-arrhythmics)<br />
**Rigorous treatment of fever with paracetamol / Tylenol<br />
<br />
For a full list of the diagnostic criteria, see <cite>Wilde</cite><br />
<br />
==Electrocardiographic criteria==<br />
Three ECG repolarization patterns in the right precordial leads are recognized in the diagnosis of Brugada syndrome.<br />
<br />
'''Type I''' is the only ECG criterium that is diagnostic of Brugada syndrome. Type I repolarization is characterized by a coved ST-segment elevation >=2 mm (0.2 mV) followed by a negative T wave (see figure). Brugada syndrome is definitively diagnosed when a type 1 ST-segment elevation 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, or nocturnal agonal respiration.<br />
<br />
{| class="wikitable" font-size="90%"<br />
|- style="text-align:center;background-color:#6EB4EB;"<br />
|+'''ST segment abnormalities in the different types of Brugada syndrome'''<cite>Wilde2</cite><br />
|-<br />
!<br />
!Type I<br />
!Type II<br />
!Type III<br />
|- <br />
!J wave amplitude<br />
|>= 2mm<br />
|>= 2mm<br />
|>= 2mm<br />
|-<br />
!T wave<br />
|negative<br />
|positive or biphasis<br />
|positive<br />
|-<br />
!ST-T configuration<br />
|coved type<br />
|saddleback<br />
|saddleback<br />
|-<br />
!ST segment (terminal portion)<br />
|gradually descending<br />
|elevated >= 1mm<br />
|elevated < 1mm<br />
|-<br />
|}<br />
<br />
<br />
<gallery><br />
Image:Brugada_syndrome_type1_example1.png<br />
Image:Brugada_syndrome_type1_example2.png<br />
Image:Brugada_syndrome_type1_example3.png<br />
Image:Brugada_syndrome_type1_example4.png<br />
Image:Brugada_syndrome_type1_example5.png<br />
</gallery><br />
<gallery><br />
Image:Brugada_syndrome_type2_example1.png<br />
</gallery><br />
<br />
==External links==<br />
*Cardiogenetics website of the AMC [http://www.cardiogenetica.nl cardiogentica.nl]<br />
*[http://www.brugada.org Brugada.org ]<br />
*[http://www.genereviews.org/servlet/access?id=8888891&key=ghdBRjkdNXE6y&gry=INSERTGRY&fcn=y&fw=E0gK&filename=/profiles/brugada/index.html Genereview Brugada]<br />
<br />
==Referenties==<br />
<biblio><br />
#Wilde pmid=15898165<br />
#Brugada pmid=1309182<br />
#osher pmid=13104407<br />
#brug2 pmid=11772879 <br />
#brug3 pmid=12776858<br />
#priori pmid=11901046<br />
#eckhardt pmid=15642768<br />
#Wilde2 pmid=12417552<br />
</biblio></div>145.117.40.234https://en.ecgpedia.org/index.php?title=Brugada_Syndrome&diff=5484Brugada Syndrome2007-11-29T16:41:48Z<p>145.117.40.234: /* Electrocardiographic criteria */</p>
<hr />
<div>{{authors|<br />
|mainauthor= [[user:Pgpostema|P.G. Postema, MD]]<br />
|advisor=<br />
|coauthor= [[user:Drj|J.S.S.G. de Jong, MD]]<br />
|moderator= [[user:Pgpostema|P.G. Postema, MD]]<br />
|editor= <br />
}}<br />
[[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 four members of the Brugada family conduct research after the syndrome that has been named after them.]]<br />
[[Image:Brugada.png|thumb|Typical ECG abnormalities in Brugada syndrome: ST elevation in V1-V3, without ischemia.]]<br />
[[Image:scn5a.jpg|thumb| The SCN5a gen is located on the short arm (p) of chromosome 3]]<br />
<br />
<br />
The '''Brugada syndrome is an hereditary disease that is associated with higher risk of sudden cardiac death'''. It is characterized by typical ECG abnormalities: '''ST segment elevation in the precordial leads (V1 - V3)'''.<br />
<br />
==Characteristics of the Brugada syndrome:==<br />
*[[w:Autosomal_dominant|autosomal dominant]] inheritance. If one of both parents are affected, their children have a 50% chance of inheriting the disease.<br />
*Man are more often symptomatic than women, probably by the influence of sex hormones on cardiac arrhythmias. <br />
*The arrhythmias usually occur between 30 and 40 years of age. (range 1-77 yrs) and often during rest or while sleeping.<br />
*Only in about 30% of patients, genetic defects can be detected in the ([http://ghr.nlm.nih.gov/gene=scn5a SCN5A]) gen. In the other patients the disease is probably multi-genetic or caused by yet unknown genetic defects.<br />
*The right ventricular outflow tract (right before the pulmonary valve) is most affected in the Brugada syndrome. <br />
*The prevalence varies between 5-50:10.000, largely depending on geographic location. In some south-east Asian countries the disease is endemic and sometimes considered the second cause of death amongst young men (after car accidents). There it is called 'Sudden Unexpected Death Syndrome' (SUDS). In different Asian countries, different names have been given to the syndrome: in the Phillipines it is called ''bangungut'' (to rise and moan in sleep) and in Thailand ''lai tai'' (death during sleep)<br />
<br />
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><br />
<br />
==Diagnosis and treatment==<br />
*Patients who are symptomatic (syncope, ventricular tachycardias or survivors of sudden cardiac death) have a mortality risk of up to 10% per year. In these patients an [[:w:nl:Internal_Cardiac_Defibrillator|ICD]] should be implanted. <br />
*Some groups advice an electrofysiologic investigation for risk assessment in Brugada patients,<cite>brug2</cite><cite>brug3</cite> but others could not reproduce the predicive value of these tests,<cite>priori</cite><cite>eckhardt</cite> so this is still controversial.<br />
*In large studies familiar sudden death is not a risk factor for sudden death in siblings.<br />
*In asymptomatic patients in whom the Brugada ECG characteristics are present either spontaneously or provoked by fever or sodium channel blockers (ajmaline, flecainide) life style advices are given, which include:<br />
**A number of medications should not be taken (amongst others beta-blockers, and sodium channel blockers such as certain anti-depressants and anti-arrhythmics)<br />
**Rigorous treatment of fever with paracetamol / Tylenol<br />
<br />
For a full list of the diagnostic criteria, see <cite>Wilde</cite><br />
<br />
==Electrocardiographic criteria==<br />
Three ECG repolarization patterns in the right precordial leads are recognized in the diagnosis of Brugada syndrome.<br />
<br />
'''Type I''' is the only ECG criterium that is diagnostic of Brugada syndrome. Type I repolarization is characterized by a coved ST-segment elevation >=2 mm (0.2 mV) followed by a negative T wave (see figure). Brugada syndrome is definitively diagnosed when a type 1 ST-segment elevation 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, or nocturnal agonal respiration.<br />
<br />
{| class="wikitable" font-size="90%"<br />
|- style="text-align:center;background-color:#6EB4EB;"<br />
|+'''ST segment abnormalities in the different types of Brugada syndrome'''<cite>Wilde2</cite><br />
|-<br />
!<br />
!Type I<br />
!Type II<br />
!Type III<br />
|- <br />
!J wave amplitude<br />
|>= 2mm<br />
|>= 2mm<br />
|>= 2mm<br />
|-<br />
!T wave<br />
|negative<br />
|positive or biphasis<br />
|positive<br />
|-<br />
!ST-T configuration<br />
|coved type<br />
|saddleback<br />
|saddleback<br />
|-<br />
!ST segment (terminal portion)<br />
|gradually descending<br />
|elevated >= 1mm<br />
|elevated < 1mm<br />
|-<br />
|}<br />
<br />
<br />
<gallery><br />
Image:Brugada_syndrome_type1_example1.png<br />
Image:Brugada_syndrome_type1_example2.png<br />
Image:Brugada_syndrome_type1_example3.png<br />
Image:Brugada_syndrome_type1_example4.png<br />
Image:Brugada_syndrome_type1_example5.png<br />
</gallery><br />
<gallery><br />
Image:Brugada_syndrome_type2_example1.png<br />
</gallery><br />
<br />
==External links==<br />
*Cardiogenetics website of the AMC [http://www.cardiogenetica.nl cardiogentica.nl]<br />
*[http://www.brugada.org Brugada.org ]<br />
*[http://www.genereviews.org/servlet/access?id=8888891&key=ghdBRjkdNXE6y&gry=INSERTGRY&fcn=y&fw=E0gK&filename=/profiles/brugada/index.html Genereview Brugada]<br />
<br />
==Referenties==<br />
<biblio><br />
#Wilde pmid=15898165<br />
#Brugada pmid=1309182<br />
#osher pmid=13104407<br />
#brug2 pmid=11772879 <br />
#brug3 pmid=12776858<br />
#priori pmid=11901046<br />
#eckhardt pmid=15642768<br />
</biblio></div>145.117.40.234https://en.ecgpedia.org/index.php?title=Brugada_Syndrome&diff=5483Brugada Syndrome2007-11-29T16:41:14Z<p>145.117.40.234: /* Electrocardiographic criteria */</p>
<hr />
<div>{{authors|<br />
|mainauthor= [[user:Pgpostema|P.G. Postema, MD]]<br />
|advisor=<br />
|coauthor= [[user:Drj|J.S.S.G. de Jong, MD]]<br />
|moderator= [[user:Pgpostema|P.G. Postema, MD]]<br />
|editor= <br />
}}<br />
[[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 four members of the Brugada family conduct research after the syndrome that has been named after them.]]<br />
[[Image:Brugada.png|thumb|Typical ECG abnormalities in Brugada syndrome: ST elevation in V1-V3, without ischemia.]]<br />
[[Image:scn5a.jpg|thumb| The SCN5a gen is located on the short arm (p) of chromosome 3]]<br />
<br />
<br />
The '''Brugada syndrome is an hereditary disease that is associated with higher risk of sudden cardiac death'''. It is characterized by typical ECG abnormalities: '''ST segment elevation in the precordial leads (V1 - V3)'''.<br />
<br />
==Characteristics of the Brugada syndrome:==<br />
*[[w:Autosomal_dominant|autosomal dominant]] inheritance. If one of both parents are affected, their children have a 50% chance of inheriting the disease.<br />
*Man are more often symptomatic than women, probably by the influence of sex hormones on cardiac arrhythmias. <br />
*The arrhythmias usually occur between 30 and 40 years of age. (range 1-77 yrs) and often during rest or while sleeping.<br />
*Only in about 30% of patients, genetic defects can be detected in the ([http://ghr.nlm.nih.gov/gene=scn5a SCN5A]) gen. In the other patients the disease is probably multi-genetic or caused by yet unknown genetic defects.<br />
*The right ventricular outflow tract (right before the pulmonary valve) is most affected in the Brugada syndrome. <br />
*The prevalence varies between 5-50:10.000, largely depending on geographic location. In some south-east Asian countries the disease is endemic and sometimes considered the second cause of death amongst young men (after car accidents). There it is called 'Sudden Unexpected Death Syndrome' (SUDS). In different Asian countries, different names have been given to the syndrome: in the Phillipines it is called ''bangungut'' (to rise and moan in sleep) and in Thailand ''lai tai'' (death during sleep)<br />
<br />
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><br />
<br />
==Diagnosis and treatment==<br />
*Patients who are symptomatic (syncope, ventricular tachycardias or survivors of sudden cardiac death) have a mortality risk of up to 10% per year. In these patients an [[:w:nl:Internal_Cardiac_Defibrillator|ICD]] should be implanted. <br />
*Some groups advice an electrofysiologic investigation for risk assessment in Brugada patients,<cite>brug2</cite><cite>brug3</cite> but others could not reproduce the predicive value of these tests,<cite>priori</cite><cite>eckhardt</cite> so this is still controversial.<br />
*In large studies familiar sudden death is not a risk factor for sudden death in siblings.<br />
*In asymptomatic patients in whom the Brugada ECG characteristics are present either spontaneously or provoked by fever or sodium channel blockers (ajmaline, flecainide) life style advices are given, which include:<br />
**A number of medications should not be taken (amongst others beta-blockers, and sodium channel blockers such as certain anti-depressants and anti-arrhythmics)<br />
**Rigorous treatment of fever with paracetamol / Tylenol<br />
<br />
For a full list of the diagnostic criteria, see <cite>Wilde</cite><br />
<br />
==Electrocardiographic criteria==<br />
Three ECG repolarization patterns in the right precordial leads are recognized in the diagnosis of Brugada syndrome.<br />
'''Type I''' is the only ECG criterium that is diagnostic of Brugada syndrome. Type I repolarization is characterized by a coved ST-segment elevation >=2 mm (0.2 mV) followed by a negative T wave (see figure). Brugada syndrome is definitively diagnosed when a type 1 ST-segment elevation 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, or nocturnal agonal respiration.<br />
<br />
{| class="wikitable" font-size="90%"<br />
|- style="text-align:center;background-color:#6EB4EB;"<br />
|+'''ST segment abnormalities in the different types of Brugada syndrome'''<br />
|-<br />
!<br />
!Type I<br />
!Type II<br />
!Type III<br />
|- <br />
!J wave amplitude<br />
|>= 2mm<br />
|>= 2mm<br />
|>= 2mm<br />
|-<br />
!T wave<br />
|negative<br />
|positive or biphasis<br />
|positive<br />
|-<br />
!ST-T configuration<br />
|coved type<br />
|saddleback<br />
|saddleback<br />
|-<br />
!ST segment (terminal portion)<br />
|gradually descending<br />
|elevated >= 1mm<br />
|elevated < 1mm<br />
|-<br />
|}<br />
<br />
<br />
<gallery><br />
Image:Brugada_syndrome_type1_example1.png<br />
Image:Brugada_syndrome_type1_example2.png<br />
Image:Brugada_syndrome_type1_example3.png<br />
Image:Brugada_syndrome_type1_example4.png<br />
Image:Brugada_syndrome_type1_example5.png<br />
</gallery><br />
<gallery><br />
Image:Brugada_syndrome_type2_example1.png<br />
</gallery><br />
<br />
==External links==<br />
*Cardiogenetics website of the AMC [http://www.cardiogenetica.nl cardiogentica.nl]<br />
*[http://www.brugada.org Brugada.org ]<br />
*[http://www.genereviews.org/servlet/access?id=8888891&key=ghdBRjkdNXE6y&gry=INSERTGRY&fcn=y&fw=E0gK&filename=/profiles/brugada/index.html Genereview Brugada]<br />
<br />
==Referenties==<br />
<biblio><br />
#Wilde pmid=15898165<br />
#Brugada pmid=1309182<br />
#osher pmid=13104407<br />
#brug2 pmid=11772879 <br />
#brug3 pmid=12776858<br />
#priori pmid=11901046<br />
#eckhardt pmid=15642768<br />
</biblio></div>145.117.40.234https://en.ecgpedia.org/index.php?title=Brugada_Syndrome&diff=5482Brugada Syndrome2007-11-29T16:30:54Z<p>145.117.40.234: /* Electrocardiographic criteria */</p>
<hr />
<div>{{authors|<br />
|mainauthor= [[user:Pgpostema|P.G. Postema, MD]]<br />
|advisor=<br />
|coauthor= [[user:Drj|J.S.S.G. de Jong, MD]]<br />
|moderator= [[user:Pgpostema|P.G. Postema, MD]]<br />
|editor= <br />
}}<br />
[[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 four members of the Brugada family conduct research after the syndrome that has been named after them.]]<br />
[[Image:Brugada.png|thumb|Typical ECG abnormalities in Brugada syndrome: ST elevation in V1-V3, without ischemia.]]<br />
[[Image:scn5a.jpg|thumb| The SCN5a gen is located on the short arm (p) of chromosome 3]]<br />
<br />
<br />
The '''Brugada syndrome is an hereditary disease that is associated with higher risk of sudden cardiac death'''. It is characterized by typical ECG abnormalities: '''ST segment elevation in the precordial leads (V1 - V3)'''.<br />
<br />
==Characteristics of the Brugada syndrome:==<br />
*[[w:Autosomal_dominant|autosomal dominant]] inheritance. If one of both parents are affected, their children have a 50% chance of inheriting the disease.<br />
*Man are more often symptomatic than women, probably by the influence of sex hormones on cardiac arrhythmias. <br />
*The arrhythmias usually occur between 30 and 40 years of age. (range 1-77 yrs) and often during rest or while sleeping.<br />
*Only in about 30% of patients, genetic defects can be detected in the ([http://ghr.nlm.nih.gov/gene=scn5a SCN5A]) gen. In the other patients the disease is probably multi-genetic or caused by yet unknown genetic defects.<br />
*The right ventricular outflow tract (right before the pulmonary valve) is most affected in the Brugada syndrome. <br />
*The prevalence varies between 5-50:10.000, largely depending on geographic location. In some south-east Asian countries the disease is endemic and sometimes considered the second cause of death amongst young men (after car accidents). There it is called 'Sudden Unexpected Death Syndrome' (SUDS). In different Asian countries, different names have been given to the syndrome: in the Phillipines it is called ''bangungut'' (to rise and moan in sleep) and in Thailand ''lai tai'' (death during sleep)<br />
<br />
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><br />
<br />
==Diagnosis and treatment==<br />
*Patients who are symptomatic (syncope, ventricular tachycardias or survivors of sudden cardiac death) have a mortality risk of up to 10% per year. In these patients an [[:w:nl:Internal_Cardiac_Defibrillator|ICD]] should be implanted. <br />
*Some groups advice an electrofysiologic investigation for risk assessment in Brugada patients,<cite>brug2</cite><cite>brug3</cite> but others could not reproduce the predicive value of these tests,<cite>priori</cite><cite>eckhardt</cite> so this is still controversial.<br />
*In large studies familiar sudden death is not a risk factor for sudden death in siblings.<br />
*In asymptomatic patients in whom the Brugada ECG characteristics are present either spontaneously or provoked by fever or sodium channel blockers (ajmaline, flecainide) life style advices are given, which include:<br />
**A number of medications should not be taken (amongst others beta-blockers, and sodium channel blockers such as certain anti-depressants and anti-arrhythmics)<br />
**Rigorous treatment of fever with paracetamol / Tylenol<br />
<br />
For a full list of the diagnostic criteria, see <cite>Wilde</cite><br />
<br />
==Electrocardiographic criteria==<br />
Three ECG repolarization patterns in the right precordial leads are recognized in the diagnosis of Brugada syndrome.<br />
'''Type I''' is the only ECG criterium that is diagnostic of Brugada syndrome. Type I repolarization is characterized by a coved ST-segment elevation >=2 mm (0.2 mV) followed by a negative T wave (see figure). Brugada syndrome is definitively diagnosed when a type 1 ST-segment elevation 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, or nocturnal agonal respiration.<br />
<br />
<br />
<br />
<gallery><br />
Image:Brugada_syndrome_type1_example1.png<br />
Image:Brugada_syndrome_type1_example2.png<br />
Image:Brugada_syndrome_type1_example3.png<br />
Image:Brugada_syndrome_type1_example4.png<br />
Image:Brugada_syndrome_type1_example5.png<br />
</gallery><br />
<gallery><br />
Image:Brugada_syndrome_type2_example1.png<br />
</gallery><br />
<br />
==External links==<br />
*Cardiogenetics website of the AMC [http://www.cardiogenetica.nl cardiogentica.nl]<br />
*[http://www.brugada.org Brugada.org ]<br />
*[http://www.genereviews.org/servlet/access?id=8888891&key=ghdBRjkdNXE6y&gry=INSERTGRY&fcn=y&fw=E0gK&filename=/profiles/brugada/index.html Genereview Brugada]<br />
<br />
==Referenties==<br />
<biblio><br />
#Wilde pmid=15898165<br />
#Brugada pmid=1309182<br />
#osher pmid=13104407<br />
#brug2 pmid=11772879 <br />
#brug3 pmid=12776858<br />
#priori pmid=11901046<br />
#eckhardt pmid=15642768<br />
</biblio></div>145.117.40.234https://en.ecgpedia.org/index.php?title=Brugada_Syndrome&diff=5481Brugada Syndrome2007-11-29T16:22:29Z<p>145.117.40.234: /* Referenties */</p>
<hr />
<div>{{authors|<br />
|mainauthor= [[user:Pgpostema|P.G. Postema, MD]]<br />
|advisor=<br />
|coauthor= [[user:Drj|J.S.S.G. de Jong, MD]]<br />
|moderator= [[user:Pgpostema|P.G. Postema, MD]]<br />
|editor= <br />
}}<br />
[[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 four members of the Brugada family conduct research after the syndrome that has been named after them.]]<br />
[[Image:Brugada.png|thumb|Typical ECG abnormalities in Brugada syndrome: ST elevation in V1-V3, without ischemia.]]<br />
[[Image:scn5a.jpg|thumb| The SCN5a gen is located on the short arm (p) of chromosome 3]]<br />
<br />
<br />
The '''Brugada syndrome is an hereditary disease that is associated with higher risk of sudden cardiac death'''. It is characterized by typical ECG abnormalities: '''ST segment elevation in the precordial leads (V1 - V3)'''.<br />
<br />
==Characteristics of the Brugada syndrome:==<br />
*[[w:Autosomal_dominant|autosomal dominant]] inheritance. If one of both parents are affected, their children have a 50% chance of inheriting the disease.<br />
*Man are more often symptomatic than women, probably by the influence of sex hormones on cardiac arrhythmias. <br />
*The arrhythmias usually occur between 30 and 40 years of age. (range 1-77 yrs) and often during rest or while sleeping.<br />
*Only in about 30% of patients, genetic defects can be detected in the ([http://ghr.nlm.nih.gov/gene=scn5a SCN5A]) gen. In the other patients the disease is probably multi-genetic or caused by yet unknown genetic defects.<br />
*The right ventricular outflow tract (right before the pulmonary valve) is most affected in the Brugada syndrome. <br />
*The prevalence varies between 5-50:10.000, largely depending on geographic location. In some south-east Asian countries the disease is endemic and sometimes considered the second cause of death amongst young men (after car accidents). There it is called 'Sudden Unexpected Death Syndrome' (SUDS). In different Asian countries, different names have been given to the syndrome: in the Phillipines it is called ''bangungut'' (to rise and moan in sleep) and in Thailand ''lai tai'' (death during sleep)<br />
<br />
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><br />
<br />
==Diagnosis and treatment==<br />
*Patients who are symptomatic (syncope, ventricular tachycardias or survivors of sudden cardiac death) have a mortality risk of up to 10% per year. In these patients an [[:w:nl:Internal_Cardiac_Defibrillator|ICD]] should be implanted. <br />
*Some groups advice an electrofysiologic investigation for risk assessment in Brugada patients,<cite>brug2</cite><cite>brug3</cite> but others could not reproduce the predicive value of these tests,<cite>priori</cite><cite>eckhardt</cite> so this is still controversial.<br />
*In large studies familiar sudden death is not a risk factor for sudden death in siblings.<br />
*In asymptomatic patients in whom the Brugada ECG characteristics are present either spontaneously or provoked by fever or sodium channel blockers (ajmaline, flecainide) life style advices are given, which include:<br />
**A number of medications should not be taken (amongst others beta-blockers, and sodium channel blockers such as certain anti-depressants and anti-arrhythmics)<br />
**Rigorous treatment of fever with paracetamol / Tylenol<br />
<br />
For a full list of the diagnostic criteria, see <cite>Wilde</cite><br />
<br />
==Electrocardiographic criteria==<br />
*type 1<br />
*type 2<br />
<gallery><br />
Image:Brugada_syndrome_type1_example1.png<br />
Image:Brugada_syndrome_type1_example2.png<br />
Image:Brugada_syndrome_type1_example3.png<br />
Image:Brugada_syndrome_type1_example4.png<br />
Image:Brugada_syndrome_type1_example5.png<br />
</gallery><br />
<gallery><br />
Image:Brugada_syndrome_type2_example1.png<br />
</gallery><br />
<br />
==External links==<br />
*Cardiogenetics website of the AMC [http://www.cardiogenetica.nl cardiogentica.nl]<br />
*[http://www.brugada.org Brugada.org ]<br />
*[http://www.genereviews.org/servlet/access?id=8888891&key=ghdBRjkdNXE6y&gry=INSERTGRY&fcn=y&fw=E0gK&filename=/profiles/brugada/index.html Genereview Brugada]<br />
<br />
==Referenties==<br />
<biblio><br />
#Wilde pmid=15898165<br />
#Brugada pmid=1309182<br />
#osher pmid=13104407<br />
#brug2 pmid=11772879 <br />
#brug3 pmid=12776858<br />
#priori pmid=11901046<br />
#eckhardt pmid=15642768<br />
</biblio></div>145.117.40.234https://en.ecgpedia.org/index.php?title=Brugada_Syndrome&diff=5480Brugada Syndrome2007-11-29T16:20:34Z<p>145.117.40.234: /* Electrocardiographic criteria */</p>
<hr />
<div>{{authors|<br />
|mainauthor= [[user:Pgpostema|P.G. Postema, MD]]<br />
|advisor=<br />
|coauthor= [[user:Drj|J.S.S.G. de Jong, MD]]<br />
|moderator= [[user:Pgpostema|P.G. Postema, MD]]<br />
|editor= <br />
}}<br />
[[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 four members of the Brugada family conduct research after the syndrome that has been named after them.]]<br />
[[Image:Brugada.png|thumb|Typical ECG abnormalities in Brugada syndrome: ST elevation in V1-V3, without ischemia.]]<br />
[[Image:scn5a.jpg|thumb| The SCN5a gen is located on the short arm (p) of chromosome 3]]<br />
<br />
<br />
The '''Brugada syndrome is an hereditary disease that is associated with higher risk of sudden cardiac death'''. It is characterized by typical ECG abnormalities: '''ST segment elevation in the precordial leads (V1 - V3)'''.<br />
<br />
==Characteristics of the Brugada syndrome:==<br />
*[[w:Autosomal_dominant|autosomal dominant]] inheritance. If one of both parents are affected, their children have a 50% chance of inheriting the disease.<br />
*Man are more often symptomatic than women, probably by the influence of sex hormones on cardiac arrhythmias. <br />
*The arrhythmias usually occur between 30 and 40 years of age. (range 1-77 yrs) and often during rest or while sleeping.<br />
*Only in about 30% of patients, genetic defects can be detected in the ([http://ghr.nlm.nih.gov/gene=scn5a SCN5A]) gen. In the other patients the disease is probably multi-genetic or caused by yet unknown genetic defects.<br />
*The right ventricular outflow tract (right before the pulmonary valve) is most affected in the Brugada syndrome. <br />
*The prevalence varies between 5-50:10.000, largely depending on geographic location. In some south-east Asian countries the disease is endemic and sometimes considered the second cause of death amongst young men (after car accidents). There it is called 'Sudden Unexpected Death Syndrome' (SUDS). In different Asian countries, different names have been given to the syndrome: in the Phillipines it is called ''bangungut'' (to rise and moan in sleep) and in Thailand ''lai tai'' (death during sleep)<br />
<br />
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><br />
<br />
==Diagnosis and treatment==<br />
*Patients who are symptomatic (syncope, ventricular tachycardias or survivors of sudden cardiac death) have a mortality risk of up to 10% per year. In these patients an [[:w:nl:Internal_Cardiac_Defibrillator|ICD]] should be implanted. <br />
*Some groups advice an electrofysiologic investigation for risk assessment in Brugada patients,<cite>brug2</cite><cite>brug3</cite> but others could not reproduce the predicive value of these tests,<cite>priori</cite><cite>eckhardt</cite> so this is still controversial.<br />
*In large studies familiar sudden death is not a risk factor for sudden death in siblings.<br />
*In asymptomatic patients in whom the Brugada ECG characteristics are present either spontaneously or provoked by fever or sodium channel blockers (ajmaline, flecainide) life style advices are given, which include:<br />
**A number of medications should not be taken (amongst others beta-blockers, and sodium channel blockers such as certain anti-depressants and anti-arrhythmics)<br />
**Rigorous treatment of fever with paracetamol / Tylenol<br />
<br />
For a full list of the diagnostic criteria, see <cite>Wilde</cite><br />
<br />
==Electrocardiographic criteria==<br />
*type 1<br />
*type 2<br />
<gallery><br />
Image:Brugada_syndrome_type1_example1.png<br />
Image:Brugada_syndrome_type1_example2.png<br />
Image:Brugada_syndrome_type1_example3.png<br />
Image:Brugada_syndrome_type1_example4.png<br />
Image:Brugada_syndrome_type1_example5.png<br />
</gallery><br />
<gallery><br />
Image:Brugada_syndrome_type2_example1.png<br />
</gallery><br />
<br />
==External links==<br />
*Cardiogenetics website of the AMC [http://www.cardiogenetica.nl cardiogentica.nl]<br />
*[http://www.brugada.org Brugada.org ]<br />
*[http://www.genereviews.org/servlet/access?id=8888891&key=ghdBRjkdNXE6y&gry=INSERTGRY&fcn=y&fw=E0gK&filename=/profiles/brugada/index.html Genereview Brugada]<br />
<br />
==Referenties==<br />
<biblio><br />
#Wilde pmid=15898165<br />
#Brugada pmid=1309182<br />
#osher pmid=13104407<br />
#brug2 pmid=11772879 <br />
#brug3 pmid=12776858<br />
#priori pmid=11901046<br />
#eckhardt pmid=15642768<br />
<br />
</biblio><br />
<br />
<analytics uacct="UA-807577-6"></analytics></div>145.117.40.234https://en.ecgpedia.org/index.php?title=Brugada_Syndrome&diff=5479Brugada Syndrome2007-11-29T15:29:42Z<p>145.117.40.234: /* Electrocardiographic criteria */</p>
<hr />
<div>{{authors|<br />
|mainauthor= [[user:Pgpostema|P.G. Postema, MD]]<br />
|advisor=<br />
|coauthor= [[user:Drj|J.S.S.G. de Jong, MD]]<br />
|moderator= [[user:Pgpostema|P.G. Postema, MD]]<br />
|editor= <br />
}}<br />
[[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 four members of the Brugada family conduct research after the syndrome that has been named after them.]]<br />
[[Image:Brugada.png|thumb|Typical ECG abnormalities in Brugada syndrome: ST elevation in V1-V3, without ischemia.]]<br />
[[Image:scn5a.jpg|thumb| The SCN5a gen is located on the short arm (p) of chromosome 3]]<br />
<br />
<br />
The '''Brugada syndrome is an hereditary disease that is associated with higher risk of sudden cardiac death'''. It is characterized by typical ECG abnormalities: '''ST segment elevation in the precordial leads (V1 - V3)'''.<br />
<br />
==Characteristics of the Brugada syndrome:==<br />
*[[w:Autosomal_dominant|autosomal dominant]] inheritance. If one of both parents are affected, their children have a 50% chance of inheriting the disease.<br />
*Man are more often symptomatic than women, probably by the influence of sex hormones on cardiac arrhythmias. <br />
*The arrhythmias usually occur between 30 and 40 years of age. (range 1-77 yrs) and often during rest or while sleeping.<br />
*Only in about 30% of patients, genetic defects can be detected in the ([http://ghr.nlm.nih.gov/gene=scn5a SCN5A]) gen. In the other patients the disease is probably multi-genetic or caused by yet unknown genetic defects.<br />
*The right ventricular outflow tract (right before the pulmonary valve) is most affected in the Brugada syndrome. <br />
*The prevalence varies between 5-50:10.000, largely depending on geographic location. In some south-east Asian countries the disease is endemic and sometimes considered the second cause of death amongst young men (after car accidents). There it is called 'Sudden Unexpected Death Syndrome' (SUDS). In different Asian countries, different names have been given to the syndrome: in the Phillipines it is called ''bangungut'' (to rise and moan in sleep) and in Thailand ''lai tai'' (death during sleep)<br />
<br />
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><br />
<br />
==Diagnosis and treatment==<br />
*Patients who are symptomatic (syncope, ventricular tachycardias or survivors of sudden cardiac death) have a mortality risk of up to 10% per year. In these patients an [[:w:nl:Internal_Cardiac_Defibrillator|ICD]] should be implanted. <br />
*Some groups advice an electrofysiologic investigation for risk assessment in Brugada patients,<cite>brug2</cite><cite>brug3</cite> but others could not reproduce the predicive value of these tests,<cite>priori</cite><cite>eckhardt</cite> so this is still controversial.<br />
*In large studies familiar sudden death is not a risk factor for sudden death in siblings.<br />
*In asymptomatic patients in whom the Brugada ECG characteristics are present either spontaneously or provoked by fever or sodium channel blockers (ajmaline, flecainide) life style advices are given, which include:<br />
**A number of medications should not be taken (amongst others beta-blockers, and sodium channel blockers such as certain anti-depressants and anti-arrhythmics)<br />
**Rigorous treatment of fever with paracetamol / Tylenol<br />
<br />
For a full list of the diagnostic criteria, see <cite>Wilde</cite><br />
<br />
==Electrocardiographic criteria==<br />
*type 1<br />
*type 2<br />
<gallery examples of type I Brugada syndrome><br />
Image:Brugada_syndrome_type1_example1.png<br />
Image:Brugada_syndrome_type1_example2.png<br />
Image:Brugada_syndrome_type1_example3.png<br />
Image:Brugada_syndrome_type1_example4.png<br />
Image:Brugada_syndrome_type1_example5.png<br />
</gallery><br />
<gallery examples of type II Brugada syndrome><br />
Image:Brugada_syndrome_type2_example1.png<br />
</gallery><br />
<br />
==External links==<br />
*Cardiogenetics website of the AMC [http://www.cardiogenetica.nl cardiogentica.nl]<br />
*[http://www.brugada.org Brugada.org ]<br />
*[http://www.genereviews.org/servlet/access?id=8888891&key=ghdBRjkdNXE6y&gry=INSERTGRY&fcn=y&fw=E0gK&filename=/profiles/brugada/index.html Genereview Brugada]<br />
<br />
==Referenties==<br />
<biblio><br />
#Wilde pmid=15898165<br />
#Brugada pmid=1309182<br />
#osher pmid=13104407<br />
#brug2 pmid=11772879 <br />
#brug3 pmid=12776858<br />
#priori pmid=11901046<br />
#eckhardt pmid=15642768<br />
<br />
</biblio><br />
<br />
<analytics uacct="UA-807577-6"></analytics></div>145.117.40.234https://en.ecgpedia.org/index.php?title=Brugada_Syndrome&diff=5478Brugada Syndrome2007-11-29T15:26:43Z<p>145.117.40.234: /* Electrocardiographic criteria */</p>
<hr />
<div>{{authors|<br />
|mainauthor= [[user:Pgpostema|P.G. Postema, MD]]<br />
|advisor=<br />
|coauthor= [[user:Drj|J.S.S.G. de Jong, MD]]<br />
|moderator= [[user:Pgpostema|P.G. Postema, MD]]<br />
|editor= <br />
}}<br />
[[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 four members of the Brugada family conduct research after the syndrome that has been named after them.]]<br />
[[Image:Brugada.png|thumb|Typical ECG abnormalities in Brugada syndrome: ST elevation in V1-V3, without ischemia.]]<br />
[[Image:scn5a.jpg|thumb| The SCN5a gen is located on the short arm (p) of chromosome 3]]<br />
<br />
<br />
The '''Brugada syndrome is an hereditary disease that is associated with higher risk of sudden cardiac death'''. It is characterized by typical ECG abnormalities: '''ST segment elevation in the precordial leads (V1 - V3)'''.<br />
<br />
==Characteristics of the Brugada syndrome:==<br />
*[[w:Autosomal_dominant|autosomal dominant]] inheritance. If one of both parents are affected, their children have a 50% chance of inheriting the disease.<br />
*Man are more often symptomatic than women, probably by the influence of sex hormones on cardiac arrhythmias. <br />
*The arrhythmias usually occur between 30 and 40 years of age. (range 1-77 yrs) and often during rest or while sleeping.<br />
*Only in about 30% of patients, genetic defects can be detected in the ([http://ghr.nlm.nih.gov/gene=scn5a SCN5A]) gen. In the other patients the disease is probably multi-genetic or caused by yet unknown genetic defects.<br />
*The right ventricular outflow tract (right before the pulmonary valve) is most affected in the Brugada syndrome. <br />
*The prevalence varies between 5-50:10.000, largely depending on geographic location. In some south-east Asian countries the disease is endemic and sometimes considered the second cause of death amongst young men (after car accidents). There it is called 'Sudden Unexpected Death Syndrome' (SUDS). In different Asian countries, different names have been given to the syndrome: in the Phillipines it is called ''bangungut'' (to rise and moan in sleep) and in Thailand ''lai tai'' (death during sleep)<br />
<br />
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><br />
<br />
==Diagnosis and treatment==<br />
*Patients who are symptomatic (syncope, ventricular tachycardias or survivors of sudden cardiac death) have a mortality risk of up to 10% per year. In these patients an [[:w:nl:Internal_Cardiac_Defibrillator|ICD]] should be implanted. <br />
*Some groups advice an electrofysiologic investigation for risk assessment in Brugada patients,<cite>brug2</cite><cite>brug3</cite> but others could not reproduce the predicive value of these tests,<cite>priori</cite><cite>eckhardt</cite> so this is still controversial.<br />
*In large studies familiar sudden death is not a risk factor for sudden death in siblings.<br />
*In asymptomatic patients in whom the Brugada ECG characteristics are present either spontaneously or provoked by fever or sodium channel blockers (ajmaline, flecainide) life style advices are given, which include:<br />
**A number of medications should not be taken (amongst others beta-blockers, and sodium channel blockers such as certain anti-depressants and anti-arrhythmics)<br />
**Rigorous treatment of fever with paracetamol / Tylenol<br />
<br />
For a full list of the diagnostic criteria, see <cite>Wilde</cite><br />
<br />
==Electrocardiographic criteria==<br />
*type 1<br />
*type 2<br />
<gallery examples of type I Brugada syndrome><br />
Image:Brugada_syndrome_type1_example1.png<br />
Image:Brugada_syndrome_type1_example2.png<br />
Image:Brugada_syndrome_type1_example3.png<br />
</gallery><br />
<gallery examples of type II Brugada syndrome><br />
Image:Brugada_syndrome_type2_example1.png<br />
Image:Brugada_syndrome_type2_example2.png<br />
Image:Brugada_syndrome_type2_example3.png<br />
</gallery><br />
<br />
==External links==<br />
*Cardiogenetics website of the AMC [http://www.cardiogenetica.nl cardiogentica.nl]<br />
*[http://www.brugada.org Brugada.org ]<br />
*[http://www.genereviews.org/servlet/access?id=8888891&key=ghdBRjkdNXE6y&gry=INSERTGRY&fcn=y&fw=E0gK&filename=/profiles/brugada/index.html Genereview Brugada]<br />
<br />
==Referenties==<br />
<biblio><br />
#Wilde pmid=15898165<br />
#Brugada pmid=1309182<br />
#osher pmid=13104407<br />
#brug2 pmid=11772879 <br />
#brug3 pmid=12776858<br />
#priori pmid=11901046<br />
#eckhardt pmid=15642768<br />
<br />
</biblio><br />
<br />
<analytics uacct="UA-807577-6"></analytics></div>145.117.40.234https://en.ecgpedia.org/index.php?title=Brugada_Syndrome&diff=5477Brugada Syndrome2007-11-29T15:24:23Z<p>145.117.40.234: </p>
<hr />
<div>{{authors|<br />
|mainauthor= [[user:Pgpostema|P.G. Postema, MD]]<br />
|advisor=<br />
|coauthor= [[user:Drj|J.S.S.G. de Jong, MD]]<br />
|moderator= [[user:Pgpostema|P.G. Postema, MD]]<br />
|editor= <br />
}}<br />
[[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 four members of the Brugada family conduct research after the syndrome that has been named after them.]]<br />
[[Image:Brugada.png|thumb|Typical ECG abnormalities in Brugada syndrome: ST elevation in V1-V3, without ischemia.]]<br />
[[Image:scn5a.jpg|thumb| The SCN5a gen is located on the short arm (p) of chromosome 3]]<br />
<br />
<br />
The '''Brugada syndrome is an hereditary disease that is associated with higher risk of sudden cardiac death'''. It is characterized by typical ECG abnormalities: '''ST segment elevation in the precordial leads (V1 - V3)'''.<br />
<br />
==Characteristics of the Brugada syndrome:==<br />
*[[w:Autosomal_dominant|autosomal dominant]] inheritance. If one of both parents are affected, their children have a 50% chance of inheriting the disease.<br />
*Man are more often symptomatic than women, probably by the influence of sex hormones on cardiac arrhythmias. <br />
*The arrhythmias usually occur between 30 and 40 years of age. (range 1-77 yrs) and often during rest or while sleeping.<br />
*Only in about 30% of patients, genetic defects can be detected in the ([http://ghr.nlm.nih.gov/gene=scn5a SCN5A]) gen. In the other patients the disease is probably multi-genetic or caused by yet unknown genetic defects.<br />
*The right ventricular outflow tract (right before the pulmonary valve) is most affected in the Brugada syndrome. <br />
*The prevalence varies between 5-50:10.000, largely depending on geographic location. In some south-east Asian countries the disease is endemic and sometimes considered the second cause of death amongst young men (after car accidents). There it is called 'Sudden Unexpected Death Syndrome' (SUDS). In different Asian countries, different names have been given to the syndrome: in the Phillipines it is called ''bangungut'' (to rise and moan in sleep) and in Thailand ''lai tai'' (death during sleep)<br />
<br />
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><br />
<br />
==Diagnosis and treatment==<br />
*Patients who are symptomatic (syncope, ventricular tachycardias or survivors of sudden cardiac death) have a mortality risk of up to 10% per year. In these patients an [[:w:nl:Internal_Cardiac_Defibrillator|ICD]] should be implanted. <br />
*Some groups advice an electrofysiologic investigation for risk assessment in Brugada patients,<cite>brug2</cite><cite>brug3</cite> but others could not reproduce the predicive value of these tests,<cite>priori</cite><cite>eckhardt</cite> so this is still controversial.<br />
*In large studies familiar sudden death is not a risk factor for sudden death in siblings.<br />
*In asymptomatic patients in whom the Brugada ECG characteristics are present either spontaneously or provoked by fever or sodium channel blockers (ajmaline, flecainide) life style advices are given, which include:<br />
**A number of medications should not be taken (amongst others beta-blockers, and sodium channel blockers such as certain anti-depressants and anti-arrhythmics)<br />
**Rigorous treatment of fever with paracetamol / Tylenol<br />
<br />
For a full list of the diagnostic criteria, see <cite>Wilde</cite><br />
<br />
==Electrocardiographic criteria==<br />
*type 1<br />
*type 2<br />
<gallery examples of type I><br />
<br />
</gallery><br />
<br />
==External links==<br />
*Cardiogenetics website of the AMC [http://www.cardiogenetica.nl cardiogentica.nl]<br />
*[http://www.brugada.org Brugada.org ]<br />
*[http://www.genereviews.org/servlet/access?id=8888891&key=ghdBRjkdNXE6y&gry=INSERTGRY&fcn=y&fw=E0gK&filename=/profiles/brugada/index.html Genereview Brugada]<br />
<br />
==Referenties==<br />
<biblio><br />
#Wilde pmid=15898165<br />
#Brugada pmid=1309182<br />
#osher pmid=13104407<br />
#brug2 pmid=11772879 <br />
#brug3 pmid=12776858<br />
#priori pmid=11901046<br />
#eckhardt pmid=15642768<br />
<br />
</biblio><br />
<br />
<analytics uacct="UA-807577-6"></analytics></div>145.117.40.234https://en.ecgpedia.org/index.php?title=Example_14&diff=5471Example 142007-11-28T20:37:21Z<p>145.117.40.234: New page: The ECG * Following the 7+2 steps: **Rhythm ***'''The ECG shows an irregular rhythm. There are no P waves. Atrial fibrillation.''' **Heart rate ***'''150 bpm...</p>
<hr />
<div>[[Image:KJcasus14.jpg|thumb| The ECG]]<br />
* Following the 7+2 steps:<br />
**Rhythm<br />
***'''The ECG shows an irregular rhythm. There are no P waves. Atrial fibrillation.'''<br />
**Heart rate<br />
***'''150 bpm'''<br />
**Conduction (PQ,QRS,QT) <br />
***'''PQ: not appropiate QRS: 110ms QT: 360ms QTc: 560ms (prolonged)<br />
**Heartaxis<br />
***'''QRS positive in I and iso-electric in AVF: horizontal heart axis'''<br />
**P wave morphology<br />
***'''No P waves present'''<br />
**QRS morphology<br />
***'''Incompleter right bundle branch block. QS V4-V6. Q in III and AVF.'''<br />
**ST morphology<br />
***'''ST elevation in III,AVF and V6. ST depression in I, AVL, V2.'''<br />
**Compare with the old ECG (not available, so skip this step)<br />
**Conclusion?<br />
<br />
<br />
'''Atrial fibrillation with inferior-posterior-lateral myocardial infarction and incomplete right bundle branch block. Lead I shows ST depression, suggestive of right coronary artery involvement.'''<br />
<br />
{{clr}}</div>145.117.40.234https://en.ecgpedia.org/index.php?title=Answer_MI_22&diff=5470Answer MI 222007-11-28T20:29:55Z<p>145.117.40.234: New page: The ECG * Following the 7+2 steps: **Rhythm ***'''The ECG shows a regular rhythm with normal P waves (positive in I, III and AVF, negative in AVR), followed ...</p>
<hr />
<div>[[Image:KJcasus13.jpg|thumb| The ECG]]<br />
* Following the 7+2 steps:<br />
**Rhythm<br />
***'''The ECG shows a regular rhythm with normal P waves (positive in I, III and AVF, negative in AVR), followed by QRS complexes. Sinusrhythm'''<br />
**Heart rate<br />
***'''60 bpm'''<br />
**Conduction (PQ,QRS,QT) <br />
***'''PQ: 260ms QRS: 100ms QT: 420ms QTc: 420ms <br />
**Heartaxis<br />
***'''QRS positive in I and AVF: normal heart axis'''<br />
**P wave morphology<br />
***'''The P waves have normal morphology.'''<br />
**QRS morphology<br />
***'''Narrow QRS. No left ventricular hypertrophy. Narrow Q waves in lead II,III, AVF, V5 and V6.'''<br />
**ST morphology<br />
***'''Pronounced ST elevation in II, III and AVF and V5 and V6. Also ST elevation in V3 which is located at the V4R position. Pronounced ST depression in I, AVL, V1-V2'''<br />
**Compare with the old ECG (not available, so skip this step)<br />
**Conclusion?<br />
<br />
<br />
'''Sinusbradycardia with first degree AV block and inferior-posterior-lateral myocardial infarction. Lead V4R is clearly elevated, which strongly suggests occlusion of the right coronary artery (RCA).'''<br />
<br />
{{clr}}</div>145.117.40.234https://en.ecgpedia.org/index.php?title=Answer_MI_21&diff=5469Answer MI 212007-11-28T20:25:02Z<p>145.117.40.234: New page: The ECG * Following the 7+2 steps: **Rhythm ***'''The ECG shows a regular rhythm with normal P waves (positive in I, III and AVF, negative in AVR), followed ...</p>
<hr />
<div>[[Image:KJcasus12.jpg|thumb| The ECG]]<br />
* Following the 7+2 steps:<br />
**Rhythm<br />
***'''The ECG shows a regular rhythm with normal P waves (positive in I, III and AVF, negative in AVR), followed by QRS complexes. Sinusrhythm'''<br />
**Heart rate<br />
***'''90 bpm'''<br />
**Conduction (PQ,QRS,QT) <br />
***'''PQ: 160ms QRS: 80 ms QT: 340ms QTc: 416ms <br />
**Heartaxis<br />
***'''QRS positive in I and negative in II and AVF: left heart axis deviation'''<br />
**P wave morphology<br />
***'''P wave positive in II, III and AVF, biphasic in V1. The P waves have normal morphology.'''<br />
**QRS morphology<br />
***'''Narrow QRS. QS in V1-V2. Q in V4. Reduced R wave progression.'''<br />
**ST morphology<br />
***'''ST elevation in I, AVL, V1-V5 (V3=V4R and not elevated). ST depression in III and AVF.'''<br />
**Compare with the old ECG (not available, so skip this step)<br />
**Conclusion?<br />
<br />
<br />
'''Sinusrhythm with anteroseptal infarction. Ischemic vector is pointing upwards (ST depression in AVF), a sign of proximal LAD occlusion.'''<br />
<br />
{{clr}}</div>145.117.40.234https://en.ecgpedia.org/index.php?title=Example_11&diff=5468Example 112007-11-28T20:13:33Z<p>145.117.40.234: New page: The ECG * Following the 7+2 steps: **Rhythm ***'''The ECG shows a regular rhythm with normal P waves (positive in II, III and AVF, negative in AVR), all foll...</p>
<hr />
<div>[[Image:KJcasus11.jpg|thumb| The ECG]]<br />
* Following the 7+2 steps:<br />
**Rhythm<br />
***'''The ECG shows a regular rhythm with normal P waves (positive in II, III and AVF, negative in AVR), all followed by QRS complexes. Sinusrhythm'''<br />
**Heart rate<br />
***'''About 100 bpm'''<br />
**Conduction (PQ,QRS,QT) <br />
***'''PQ: 160ms QRS: 80ms QT: 340ms QTc: 439ms <br />
**Heartaxis<br />
***'''QRS positive in I and AVF: normal heart axis'''<br />
**P wave morphology<br />
***'''Tall P waves in II, but no more than 2.5mm. Otherwise normal P wave morphology.'''<br />
**QRS morphology<br />
***'''Narrow QRS. No pathologic Q waves. Slow R wave progreesion. (However, lead V3 is probably at position V4R) '''<br />
**ST morphology<br />
***'''ST elevation in V2. Some ST elevation in leads I and AVL. Some ST depression in V6. Lead V3 again shows V4R which is not elevated.'''<br />
**Compare with the old ECG (not available, so skip this step)<br />
**Conclusion?<br />
<br />
<br />
'''Sinustachycardia with anteroseptal infarction.'''<br />
<br />
{{clr}}</div>145.117.40.234https://en.ecgpedia.org/index.php?title=MI_10&diff=5446MI 102007-11-27T20:51:59Z<p>145.117.40.234: New page: Culprit lesion: '''RCX''' # sinus rhythm # about 77/min # normal conduction # intermediate axis # normal p wave morphology # No pathologic Q or LVH. Tall R in V2, V3. # ST depression in V...</p>
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<div>Culprit lesion: '''RCX'''<br />
<br />
# sinus rhythm<br />
# about 77/min<br />
# normal conduction<br />
# intermediate axis<br />
# normal p wave morphology<br />
# No pathologic Q or LVH. Tall R in V2, V3.<br />
# ST depression in V1, V4, tall R in V2. ST elevation in V5, V6. Some ST elevation in II, III and AVF.<br />
<br />
* Conclusion: '''Inferior-lateral MI caused by an RCX occlusion.'''</div>145.117.40.234https://en.ecgpedia.org/index.php?title=MI_9&diff=5445MI 92007-11-27T20:50:47Z<p>145.117.40.234: New page: Culprit lesion: '''LAD''' # sinus rhythm # about 75/min # normal conduction # horizontal axis # normal p wave morphology # Microvoltages in the extremity leads. QS in V1, V2. # ST elevati...</p>
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<div>Culprit lesion: '''LAD'''<br />
<br />
# sinus rhythm<br />
# about 75/min<br />
# normal conduction<br />
# horizontal axis<br />
# normal p wave morphology<br />
# Microvoltages in the extremity leads. QS in V1, V2.<br />
# ST elevation in V1-V3<br />
<br />
* Conclusion: '''Anteroseptal MI caused by an LAD occlusion.'''</div>145.117.40.234https://en.ecgpedia.org/index.php?title=MI_8&diff=5444MI 82007-11-27T20:49:27Z<p>145.117.40.234: New page: Culprit lesion: '''LAD''' # sinus rhythm # about 75/min # normal conduction # intermediate axis # normal p wave morphology # No pathologic Q or LVH. # ST elevation in II, III, AVF and V4...</p>
<hr />
<div>Culprit lesion: '''LAD'''<br />
<br />
# sinus rhythm<br />
# about 75/min<br />
# normal conduction<br />
# intermediate axis<br />
# normal p wave morphology<br />
# No pathologic Q or LVH. <br />
# ST elevation in II, III, AVF and V4-V6. ST depression in AVR. The ST vector is pointing downwards.<br />
<br />
* Conclusion: '''Distal LAD occlusion'''.</div>145.117.40.234https://en.ecgpedia.org/index.php?title=MI_7&diff=5443MI 72007-11-27T20:47:46Z<p>145.117.40.234: New page: Culprit lesion: '''RCA''' # sinus rhythm # about 95/min # normal PQ and QRS interval. QT 360 ms, QTc 461ms (prolonged) # intermediate heart axis # tall p wave. possibly right atrial stres...</p>
<hr />
<div>Culprit lesion: '''RCA'''<br />
<br />
# sinus rhythm<br />
# about 95/min<br />
# normal PQ and QRS interval. QT 360 ms, QTc 461ms (prolonged)<br />
# intermediate heart axis<br />
# tall p wave. possibly right atrial stress<br />
# No pathologic Q or LVH (however the inferior leads show small q waves)<br />
# ST elevation in II, III and AVF. ST depression in V2-V5. Lead V6 is missing (the electrode possibly fell off)<br />
<br />
* Conclusion: '''Infero-posterior MI caused by an RCA occlusion.'''</div>145.117.40.234https://en.ecgpedia.org/index.php?title=MI_6&diff=5442MI 62007-11-27T20:44:16Z<p>145.117.40.234: New page: Culprit lesion: '''RCA''' # sinusbradycardia # about 48/min # normal conduction # intermediate axis # normal p wave morphology # No pathologic Q or LVH # ST elevation in II and V5. ST dep...</p>
<hr />
<div>Culprit lesion: '''RCA'''<br />
<br />
# sinusbradycardia<br />
# about 48/min<br />
# normal conduction<br />
# intermediate axis<br />
# normal p wave morphology<br />
# No pathologic Q or LVH<br />
# ST elevation in II and V5. ST depression in AVR, V2, V3. Also depression in III and AVF. Some elevation in I and AVL.<br />
<br />
* Conclusion: '''Infero-lateral MI caused by an RCA occlusion.'''<br />
<br />
Note! Usually RCA occlusions lead to ST elevation in leads III and AVF, which is not the case here. However, there is evident bradycardia which suggests RCA occlusion. V3 and V4 show slight ST elevation, but no more than 2 mm and therefore this elevation should not be considered significant.</div>145.117.40.234