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== History == Brugada syndrome is named after the Spanish cardiologists Josep and Pedro Brugada who described the condition in 1992,<ref name=Brug1992/> although the association between the characteristic ECG pattern and sudden cardiac death had been reported in 1989.<ref name=Nava1989>{{cite journal | vauthors = Martini B, Nava A, Thiene G, Buja GF, Canciani B, Scognamiglio R, Daliento L, Dalla Volta S | title = Ventricular fibrillation without apparent heart disease: description of six cases | journal = American Heart Journal | volume = 118 | issue = 6 | pages = 1203β9 | date = December 1989 | pmid = 2589161 | doi = 10.1016/0002-8703(89)90011-2 | s2cid = 24418607 }}</ref> Brugada syndrome was described as a cause for the sudden unexplained cardiac death syndrome seen in Thai men in 1997.<ref name=":0">{{cite journal | vauthors = Nademanee K, Veerakul G, Nimmannit S, Chaowakul V, Bhuripanyo K, Likittanasombat K, Tunsanga K, Kuasirikul S, Malasit P, Tansupasawadikul S, Tatsanavivat P | title = Arrhythmogenic marker for the sudden unexplained death syndrome in Thai men | journal = Circulation | volume = 96 | issue = 8 | pages = 2595β600 | date = October 1997 | pmid = 9355899 | doi = 10.1161/01.CIR.96.8.2595 }}</ref> The first genetic mutations affecting the SCN5A gene associated with the syndrome were identified by their brother Ramon Brugada in 1998,<ref name=Chen2018>{{cite journal | vauthors = Chen Q, Kirsch GE, Zhang D, Brugada R, Brugada J, Brugada P, Potenza D, Moya A, Borggrefe M, Breithardt G, Ortiz-Lopez R, Wang Z, Antzelevitch C, O'Brien RE, Schulze-Bahr E, Keating MT, Towbin JA, Wang Q | s2cid = 4315426 | title = Genetic basis and molecular mechanism for idiopathic ventricular fibrillation | journal = Nature | volume = 392 | issue = 6673 | pages = 293β6 | date = March 1998 | pmid = 9521325 | doi = 10.1038/32675 | bibcode = 1998Natur.392..293C }}</ref> with many more mutations affecting at least 19 genes subsequently identified by others.<ref name="Kapplinger_2010">{{cite journal | vauthors = Kapplinger JD, Tester DJ, Alders M, Benito B, Berthet M, Brugada J, Brugada P, Fressart V, Guerchicoff A, Harris-Kerr C, Kamakura S, Kyndt F, Koopmann TT, Miyamoto Y, Pfeiffer R, Pollevick GD, Probst V, Zumhagen S, Vatta M, Towbin JA, Shimizu W, Schulze-Bahr E, Antzelevitch C, Salisbury BA, Guicheney P, Wilde AA, Brugada R, Schott JJ, Ackerman MJ | display-authors = 6 | title = An international compendium of mutations in the SCN5A-encoded cardiac sodium channel in patients referred for Brugada syndrome genetic testing | journal = Heart Rhythm | volume = 7 | issue = 1 | pages = 33β46 | date = January 2010 | pmid = 20129283 | pmc = 2822446 | doi = 10.1016/j.hrthm.2009.09.069 }}</ref> Studies in the 2000s led to competing theories surrounding the mechanisms by which abnormal heart rhythms were generated.<ref name=Brug2016>{{cite journal | vauthors = Brugada P | title = Brugada syndrome: More than 20 years of scientific excitement | journal = Journal of Cardiology | volume = 67 | issue = 3 | pages = 215β20 | date = March 2016 | pmid = 26627541 | doi = 10.1016/j.jjcc.2015.08.009 | doi-access = free }}</ref> Research into Brugada syndrome is ongoing, identifying new genetic variants, exploring mechanisms of arrhythmias, and searching for better treatments.<ref name=Brug2016 />
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