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==Pathophysiology==
==Pathophysiology==
Approximately 20% of the cases of Brugada syndrome have been shown to be associated with mutation(s) in the [[gene]] that encodes for the [[sodium]] [[ion channel]] in the [[cell (biology)|cell]] [[cell membrane|membrane]]s of the muscle cells of the heart (the [[myocyte]]s). The gene, named [[SCN5A]], is located on the short arm of the third [[chromosome]] (3p21). Loss-of-function mutations in this gene lead to a loss of the action potential dome of some epicardial areas of the right ventricle. This results in transmural and epicardial dispersion of repolarization.  Over 160 mutations in the SCN5A gene have been discovered to date, each having varying mechanisms and effects on function, thereby explaining the varying degrees of penetration and expression of this disorder. <ref name="pmid16972995">{{cite journal |author=Napolitano C, Priori SG |title=Brugada syndrome |journal=Orphanet journal of rare diseases |volume=1 |issue= |pages=35 |year=2006 |pmid=16972995 |doi=10.1186/1750-1172-1-35}}</ref>
Approximately 20% of the cases of Brugada syndrome have been shown to be associated with mutation(s) in the [[gene]] that encodes for the [[sodium]] [[ion channel]] in the [[cell (biology)|cell]] [[cell membrane|membrane]]s of the muscle cells of the heart (the [[myocyte]]s). The gene, named [[SCN5A]], is located on the short arm of the third [[chromosome]] (3p21). Loss-of-function mutations in this gene lead to a loss of the action potential dome of some epicardial areas of the right ventricle. This results in transmural and epicardial dispersion of repolarization.  Over 160 mutations in the SCN5A gene have been discovered to date, each having varying mechanisms and effects on function, thereby explaining the varying degrees of penetration and expression of this disorder. <ref name="pmid16972995">{{cite journal |author=Napolitano C, Priori SG |title=Brugada syndrome |journal=Orphanet journal of rare diseases |volume=1 |issue= |pages=35 |year=2006 |pmid=16972995 |doi=10.1186/1750-1172-1-35}}</ref>
==Differentiating Brugada Syndrome from other Diseases==
Abnormalities that can lead to ST-segment elevation in the right precordial leads include the following:<ref name="pmid14687250">{{cite journal |author=Takehara N, Makita N, Kawabe J, Sato N, Kawamura Y, Kitabatake A, Kikuchi K |title=A cardiac sodium channel mutation identified in Brugada syndrome associated with atrial standstill |journal=[[Journal of Internal Medicine]] |volume=255 |issue=1 |pages=137–42 |year=2004 |month=January |pmid=14687250 |doi= |url=http://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0954-6820&date=2004&volume=255&issue=1&spage=137 |issn= |accessdate=2012-10-13}}</ref>
* [[myocardial ischemia|Acute myocardial ischemia]] or [[Acute myocardial infarction|infarction]]
* [[Acute myocarditis]]
* [[Acute pericarditis]]
* [[Acute pulmonary thromboemboli]]
* [[Arrhythmogenic right ventricular dysplasia]] / [[Arrhythmogenic right ventricular dysplasia|cardiomyopathy]] ([[Arrhythmogenic right ventricular dysplasia|ARVD/C]])<ref>Corrado  D,  Nava  A,  Buja  G,  Martini  B,  Fasoli  G,  Oselladore  L,  Turrini  P,  Thiene  G.  Familial cardiomyopathy  underlies syndrome of right bundle branch block, ST segment elevation and sudden death. J Am Coll Cardiol.  1996;  27:  443–448.</ref><ref> Corrado  D,  Basso  C,  Buja  G,  Nava  A,  Rossi  L,  Thiene  G.  Right bundle branch block, right precordial ST-segment elevation, and sudden death in young people. Circulation.  2001;  103:  710–717.</ref>
* [[Cardioversion]]. Brugada-like ECG changes can be observed briefly after direct-current cardioversion.  It is currently unclear if this is a sign that the patient is a gene carrier for Brugada syndrome.<ref name="pmid10758932">{{cite journal |author=Kok LC, Mitchell MA, Haines DE, Mounsey JP, DiMarco JP |title=Transient ST elevation after transthoracic cardioversion in patients with hemodynamically unstable ventricular tachyarrhythmia |journal=[[The American Journal of Cardiology]] |volume=85 |issue=7 |pages=878–81, A9 |year=2000 |month=April |pmid=10758932 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002914999008863 |issn= |accessdate=2012-10-14}}</ref><ref name="pmid12929296">{{cite journal |author=Gurevitz O, Glikson M |title=Cardiac resynchronization therapy: a new frontier in the management of heart failure |journal=[[The Israel Medical Association Journal : IMAJ]] |volume=5 |issue=8 |pages=571–5 |year=2003 |month=August |pmid=12929296 |doi= |url= |issn= |accessdate=2012-10-14}}</ref><ref name="pmid12418739">{{cite journal |author=Gurevitz O, Lipchenca I, Yaacoby E, Segal E, Perel A, Eldar M, Glikson M |title=ST-segment deviation following implantable cardioverter defibrillator shocks: incidence, timing, and clinical significance |journal=[[Pacing and Clinical Electrophysiology : PACE]] |volume=25 |issue=10 |pages=1429–32 |year=2002 |month=October |pmid=12418739 |doi= |url= |issn= |accessdate=2012-10-14}}</ref>
* [[Cocaine intoxication]]
* [[Coronary spasm]]
* [[Dissecting aortic aneurysm]]<ref>
Myers  GB.  Other QRS-T patterns that may be mistaken for myocardial infarction; IV. Alterations in blood potassium; myocardial ischemia; subepicardial myocarditis; distortion associated with arrhythmias. Circulation.  1950;  2:  75–93.</ref>
* [[Duchenne muscular dystrophy]]<ref>''Perloff JK, Henze E, Schelbert HR. Alterations in regional myocardial metabolism, perfusion, and wall motion in Duchenne muscular dystrophy studied by radionuclide imaging. Circulation''. '' 1984; 69: 33–42.''</ref>
* [[Early repolarization]]
* [[Friedreich ataxia]]
* [[Heterocyclic antidepressant overdose]]
* [[Hypercalcemia]]<ref name="pmid6475795">{{cite journal |author=Douglas PS, Carmichael KA, Palevsky PM |title=Extreme hypercalcemia and electrocardiographic changes |journal=[[The American Journal of Cardiology]] |volume=54 |issue=6 |pages=674–5 |year=1984 |month=September |pmid=6475795 |doi= |url= |issn= |accessdate=2012-10-13}}</ref><ref name="pmid6475794">{{cite journal |author=Sridharan MR, Horan LG |title=Electrocardiographic J wave of hypercalcemia |journal=[[The American Journal of Cardiology]] |volume=54 |issue=6 |pages=672–3 |year=1984 |month=September |pmid=6475794 |doi= |url= |issn= |accessdate=2012-10-13}}</ref>
* [[Hyperkalemia]]<ref>Myers  GB.  Other QRS-T patterns that may be mistaken for myocardial infarction; IV. Alterations in blood potassium; myocardial ischemia; subepicardial myocarditis; distortion associated with arrhythmias. Circulation. 1950;  2:  75–93.</ref><ref>Merrill  JP,  Levine  HD, Somerville  W,  Smith  S.  Clinical recognition and treatment of acute potassium intoxication.        Ann Intern Med.  1950;  33:  797–830.</ref><ref name="pmid12413761">{{cite journal |author=Ortega-Carnicer J, Benezet J, Ruiz-Lorenzo F, Alcázar R |title=Transient Brugada-type electrocardiographic abnormalities in renal failure reversed by dialysis |journal=[[Resuscitation]] |volume=55 |issue=2 |pages=215–9 |year=2002 |month=November |pmid=12413761 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0300957202002101 |issn= |accessdate=2012-10-13}}</ref>
* [[Hypothermia]], can cause an [[Osborn wave]] on the ECG which can sometimes resemble Brugada syndrome<ref> <div>'' Osborn JJ. Experimental hypothermia; respiratory and blood pH changes in relation to cardiac function. Am J Physiol''. '' 1953; 175: 389–398.''</div> </ref><ref name="pmid12693512">{{cite journal |author=Noda T, Shimizu W, Tanaka K, Chayama K |title=Prominent J wave and ST segment elevation: serial electrocardiographic changes in accidental hypothermia |journal=[[Journal of Cardiovascular Electrophysiology]] |volume=14 |issue=2 |pages=223 |year=2003 |month=February |pmid=12693512 |doi= |url=http://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=1045-3873&date=2003&volume=14&issue=2&spage=223 |issn= |accessdate=2012-10-13}}</ref>
* [[Left ventricular hypertrophy]]
* [[Pectus excavatum]]<ref> <div>'' Kataoka H. Electrocardiographic patterns of the Brugada syndrome in right ventricular infarction/ischemia. Am J Cardiol''. '' 2000; 86: 1056.''</div></ref>
* [[Prinzmetal's angina]]<ref name="pmid14645641">{{cite journal |author=Wang K, Asinger RW, Marriott HJ |title=ST-segment elevation in conditions other than acute myocardial infarction |journal=[[The New England Journal of Medicine]] |volume=349 |issue=22 |pages=2128–35 |year=2003 |month=November |pmid=14645641 |doi=10.1056/NEJMra022580 |url=http://www.nejm.org/doi/abs/10.1056/NEJMra022580?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed |issn= |accessdate=2012-10-13}}</ref>
* [[Right ventricular outflow tract obstruction|Mediastinal tumor compressing the right ventricular outflow tract]] ([[RVOT]])
* [[RBBB|Right]] or [[left bundle-branch block]] (atypical)
* [[Right ventricular infarction]]
* [[Right ventricular ischemia]]
* [[Right ventricular outflow tract]] compression due to a [[mediastinal tumor]]<ref name="pmid10461308">{{cite journal |author=Tarín N, Farré J, Rubio JM, Tuñón J, Castro-Dorticós J |title=Brugada-like electrocardiographic pattern in a patient with a mediastinal tumor |journal=[[Pacing and Clinical Electrophysiology : PACE]] |volume=22 |issue=8 |pages=1264–6 |year=1999 |month=August |pmid=10461308 |doi= |url= |issn= |accessdate=2012-10-13}}</ref>or [[hemopericardium]]<ref>''Tomcsanyi J, Simor T, Papp L. Images in cardiology. Haemopericardium and Brugada-like ECG pattern in rheumatoid arthritis. Heart''. '' 2002; 87: 234.''</ref>
* [[Thiamine deficiency]]<ref name="pmid7197132">{{cite journal |author=Read DH, Harrington DD |title=Experimentally induced thiamine deficiency in beagle dogs: clinical observations |journal=[[American Journal of Veterinary Research]] |volume=42 |issue=6 |pages=984–91 |year=1981 |month=June |pmid=7197132 |doi= |url= |issn= |accessdate=2012-10-13}}</ref>
* Various central and autonomic nervous system abnormalities
* [[Other conditions that can lead to ST-segment elevation in the right precordial leads]]
* [[Early repolarization syndrome]]
* Other normal variants (particularly in males)
==Differentiating Brugada Syndrome from Arrhythmogenic Right Ventricular Dysplasia==
Although both Brugada syndrome and [[Arrhythmogenic Right Ventricular Dysplasia]] are associated with [[sudden cardiac death]] in young patients, the two syndromes are fairly easy to distinguish electrocardiographically and clinically.
===Genetics===
There is only one gene associated with Brugada syndrome, namely the SCN5A gene, and there is no overlap of the genetic abnormalities associated with [[Arrhythmogenic Right Ventricular Dysplasia]].
=== Structural Abnormalities of the right Ventricle===
While Brugada syndrome is not associated with structural abnormalities in the right ventricle, [[arrhythmogenic right ventricular dysplasia]] is associated with fibrofatty infiltration.
=== Precipitant of Ventricular Arrhythmias===
[[Arrhythmogenic right ventricular dysplasia]] is associated with [[monomorphic ventricular tachycardia]] with a left bundle branch morphology and is precipitated by catecholamines or exercise. In contrast, Brugada syndrome is associated with [[polymorphic ventricular tachycardia]] and occurs predominantly during sleep or rest.
=== Response to Pharmacologic Agents===
The EKG abnormalities of Brugada syndrome are enhanced by [[vagotonic]] agents, beta-adrenergic blockers, and sodium channel blockers whereas the EKG changes of [[arrhythmogenic right ventricular dysplasia]] are constant and do not very with vagotonic agents, beta-adrenergic blockers, or sodium channel blockers.


==Epidemiology and Demographics==
==Epidemiology and Demographics==

Revision as of 23:39, 14 October 2012

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

The Brugada syndrome is a genetic disease that is characterized by abnormal electrocardiogram (ECG) findings and an increased risk of sudden cardiac death in young adults, and occasionally in children and infants.

Historical Perspective

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 ventricular myocardial infarction. In 1953 a publication by Oscher mentioned that despite being mistaken for right ventricular myocardial infarction, the ECG findings were not associated with myocardial ischemia.[1]

Although the ECG findings of Brugada syndrome were first reported[2] among survivors of cardiac arrest in 1989, it was only in 1992 that the Brugada brothers[3] recognized it as a distinct clinical entity, causing sudden death by causing ventricular fibrillation.

Pathophysiology

Approximately 20% of the cases of Brugada syndrome have been shown to be associated with mutation(s) in the gene that encodes for the sodium ion channel in the cell membranes of the muscle cells of the heart (the myocytes). The gene, named SCN5A, is located on the short arm of the third chromosome (3p21). Loss-of-function mutations in this gene lead to a loss of the action potential dome of some epicardial areas of the right ventricle. This results in transmural and epicardial dispersion of repolarization. Over 160 mutations in the SCN5A gene have been discovered to date, each having varying mechanisms and effects on function, thereby explaining the varying degrees of penetration and expression of this disorder. [4]

Differentiating Brugada Syndrome from other Diseases

Abnormalities that can lead to ST-segment elevation in the right precordial leads include the following:[5]

Differentiating Brugada Syndrome from Arrhythmogenic Right Ventricular Dysplasia

Although both Brugada syndrome and Arrhythmogenic Right Ventricular Dysplasia are associated with sudden cardiac death in young patients, the two syndromes are fairly easy to distinguish electrocardiographically and clinically.

Genetics

There is only one gene associated with Brugada syndrome, namely the SCN5A gene, and there is no overlap of the genetic abnormalities associated with Arrhythmogenic Right Ventricular Dysplasia.

Structural Abnormalities of the right Ventricle

While Brugada syndrome is not associated with structural abnormalities in the right ventricle, arrhythmogenic right ventricular dysplasia is associated with fibrofatty infiltration.

Precipitant of Ventricular Arrhythmias

Arrhythmogenic right ventricular dysplasia is associated with monomorphic ventricular tachycardia with a left bundle branch morphology and is precipitated by catecholamines or exercise. In contrast, Brugada syndrome is associated with polymorphic ventricular tachycardia and occurs predominantly during sleep or rest.

Response to Pharmacologic Agents

The EKG abnormalities of Brugada syndrome are enhanced by vagotonic agents, beta-adrenergic blockers, and sodium channel blockers whereas the EKG changes of arrhythmogenic right ventricular dysplasia are constant and do not very with vagotonic agents, beta-adrenergic blockers, or sodium channel blockers.

Epidemiology and Demographics

Insofar as Brugada syndrome is a relatively newly recognized syndrome, its incidence and prevalence continues to increase. Brugada syndrome is quite common in Southeast Asia where it is endemic, and affects 50 out of every 10,000 individuals. [25] It is the second leading cause of death after car accidents among young people in these countries. It has been estimated that Brugada syndrome accounts for 4% of all sudden cardiac deaths and 20% of sudden cardiac deaths among patients with structurally normal hearts. [25] It is 8-10 times more common in men.

Risk Factors: Agents and Scenarios that Provoke the Brugada Syndrome Pattern

The electrocardiographic findings of Brugada syndrome are often concealed, but can be unmasked or modulated by a number of drugs and pathophysiological states including (in alphabetical order)[25]:

EKG Characteristics

As shown by the racing below, The EKG characteristics of Bugada syndrome include:

References

  1. ↑ OSHER HL, WOLFF L (1953). "Electrocardiographic pattern simulating acute myocardial injury". The American Journal of the Medical Sciences. 226 (5): 541–5. PMID 13104407. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  2. ↑ Martini B, Nava A, Thiene G, Buja GF, Canciani B, Scognamiglio R, Daliento L, Dalla Volta S. Ventricular fibrillation without apparent heart disease: description of six cases. Am Heart J 1989 Dec;118(6):1203-9 PMID 2589161
  3. ↑ Brugada P, Brugada J. Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome. A multicenter report. J Am Coll Cardiol. 1992 Nov 15;20(6):1391-6. PMID 1309182
  4. ↑ Napolitano C, Priori SG (2006). "Brugada syndrome". Orphanet journal of rare diseases. 1: 35. doi:10.1186/1750-1172-1-35. PMID 16972995.
  5. ↑ Takehara N, Makita N, Kawabe J, Sato N, Kawamura Y, Kitabatake A, Kikuchi K (2004). "A cardiac sodium channel mutation identified in Brugada syndrome associated with atrial standstill". Journal of Internal Medicine. 255 (1): 137–42. PMID 14687250. Retrieved 2012-10-13. Unknown parameter |month= ignored (help)
  6. ↑ Corrado D, Nava A, Buja G, Martini B, Fasoli G, Oselladore L, Turrini P, Thiene G. Familial cardiomyopathy underlies syndrome of right bundle branch block, ST segment elevation and sudden death. J Am Coll Cardiol. 1996; 27: 443–448.
  7. ↑ Corrado D, Basso C, Buja G, Nava A, Rossi L, Thiene G. Right bundle branch block, right precordial ST-segment elevation, and sudden death in young people. Circulation. 2001; 103: 710–717.
  8. ↑ Kok LC, Mitchell MA, Haines DE, Mounsey JP, DiMarco JP (2000). "Transient ST elevation after transthoracic cardioversion in patients with hemodynamically unstable ventricular tachyarrhythmia". The American Journal of Cardiology. 85 (7): 878–81, A9. PMID 10758932. Retrieved 2012-10-14. Unknown parameter |month= ignored (help)
  9. ↑ Gurevitz O, Glikson M (2003). "Cardiac resynchronization therapy: a new frontier in the management of heart failure". The Israel Medical Association Journal : IMAJ. 5 (8): 571–5. PMID 12929296. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  10. ↑ Gurevitz O, Lipchenca I, Yaacoby E, Segal E, Perel A, Eldar M, Glikson M (2002). "ST-segment deviation following implantable cardioverter defibrillator shocks: incidence, timing, and clinical significance". Pacing and Clinical Electrophysiology : PACE. 25 (10): 1429–32. PMID 12418739. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  11. ↑ Myers GB. Other QRS-T patterns that may be mistaken for myocardial infarction; IV. Alterations in blood potassium; myocardial ischemia; subepicardial myocarditis; distortion associated with arrhythmias. Circulation. 1950; 2: 75–93.
  12. ↑ Perloff JK, Henze E, Schelbert HR. Alterations in regional myocardial metabolism, perfusion, and wall motion in Duchenne muscular dystrophy studied by radionuclide imaging. Circulation. 1984; 69: 33–42.
  13. ↑ Douglas PS, Carmichael KA, Palevsky PM (1984). "Extreme hypercalcemia and electrocardiographic changes". The American Journal of Cardiology. 54 (6): 674–5. PMID 6475795. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  14. ↑ Sridharan MR, Horan LG (1984). "Electrocardiographic J wave of hypercalcemia". The American Journal of Cardiology. 54 (6): 672–3. PMID 6475794. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  15. ↑ Myers GB. Other QRS-T patterns that may be mistaken for myocardial infarction; IV. Alterations in blood potassium; myocardial ischemia; subepicardial myocarditis; distortion associated with arrhythmias. Circulation. 1950; 2: 75–93.
  16. ↑ Merrill JP, Levine HD, Somerville W, Smith S. Clinical recognition and treatment of acute potassium intoxication. Ann Intern Med. 1950; 33: 797–830.
  17. ↑ Ortega-Carnicer J, Benezet J, Ruiz-Lorenzo F, Alcázar R (2002). "Transient Brugada-type electrocardiographic abnormalities in renal failure reversed by dialysis". Resuscitation. 55 (2): 215–9. PMID 12413761. Retrieved 2012-10-13. Unknown parameter |month= ignored (help)
  18. ↑
    Osborn JJ. Experimental hypothermia; respiratory and blood pH changes in relation to cardiac function. Am J Physiol. 1953; 175: 389–398.
  19. ↑ Noda T, Shimizu W, Tanaka K, Chayama K (2003). "Prominent J wave and ST segment elevation: serial electrocardiographic changes in accidental hypothermia". Journal of Cardiovascular Electrophysiology. 14 (2): 223. PMID 12693512. Retrieved 2012-10-13. Unknown parameter |month= ignored (help)
  20. ↑
    Kataoka H. Electrocardiographic patterns of the Brugada syndrome in right ventricular infarction/ischemia. Am J Cardiol. 2000; 86: 1056.
  21. ↑ Wang K, Asinger RW, Marriott HJ (2003). "ST-segment elevation in conditions other than acute myocardial infarction". The New England Journal of Medicine. 349 (22): 2128–35. doi:10.1056/NEJMra022580. PMID 14645641. Retrieved 2012-10-13. Unknown parameter |month= ignored (help)
  22. ↑ Tarín N, Farré J, Rubio JM, Tuñón J, Castro-Dorticós J (1999). "Brugada-like electrocardiographic pattern in a patient with a mediastinal tumor". Pacing and Clinical Electrophysiology : PACE. 22 (8): 1264–6. PMID 10461308. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  23. ↑ Tomcsanyi J, Simor T, Papp L. Images in cardiology. Haemopericardium and Brugada-like ECG pattern in rheumatoid arthritis. Heart. 2002; 87: 234.
  24. ↑ Read DH, Harrington DD (1981). "Experimentally induced thiamine deficiency in beagle dogs: clinical observations". American Journal of Veterinary Research. 42 (6): 984–91. PMID 7197132. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  25. ↑ 25.0 25.1 25.2 Antzelevitch C, Brugada P, Borggrefe M, Brugada J, Brugada R, Corrado D, Gussak I, LeMarec H, Nademanee K, Perez Riera AR, Shimizu W, Schulze-Bahr E, Tan H, Wilde A (2005). "Brugada syndrome: report of the second consensus conference". Heart Rhythm : the Official Journal of the Heart Rhythm Society. 2 (4): 429–40. PMID 15898165. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)

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