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dc.contributor.authorRivera-Juárez, Allan
dc.contributor.authorHernández-Romero, Ismael
dc.contributor.authorPuertas, Carolina
dc.contributor.authorZhang-Wang, Serena
dc.contributor.authorSánchez-Álamo, Beatriz
dc.contributor.authorMartins, Raphael
dc.contributor.authorFiguera, Carlos
dc.contributor.authorGuillem, María S
dc.contributor.authorCliment, Andreu M
dc.contributor.authorFernández-Avilés, Francisco
dc.contributor.authorTejedor, Alberto
dc.contributor.authorJalife, Jose 
dc.contributor.authorAtienza, Felipe
dc.identifier.citationJ Am Heart Assoc. 2019; 8(3):e010115es_ES
dc.description.abstractBackground Several metabolic conditions can cause the Brugada ECG pattern, also called Brugada phenotype (BrPh). We aimed to define the clinical characteristics and outcome of BrPh patients and elucidate the mechanisms underlying BrPh attributed to hyperkalemia. Methods and Results We prospectively identified patients hospitalized with severe hyperkalemia and ECG diagnosis of BrPh and compared their clinical characteristics and outcome with patients with hyperkalemia but no BrPh ECG. Computer simulations investigated the roles of extracellular potassium increase, fibrosis at the right ventricular outflow tract, and epicardial/endocardial gradients in transient outward current. Over a 6-year period, 15 patients presented severe hyperkalemia with BrPh ECG that was transient and disappeared after normalization of their serum potassium. Most patients were admitted because of various severe medical conditions causing hyperkalemia. Six (40%) patients presented malignant arrhythmias and 6 died during admission. Multiple logistic regression analysis revealed that higher serum potassium levels (odds ratio, 15.8; 95% CI, 3.1-79; P=0.001) and male sex (odds ratio, 17; 95% CI, 1.05-286; P=0.045) were risk factors for developing BrPh ECG in patients with severe hyperkalemia. In simulations, hyperkalemia yielded BrPh by promoting delayed and heterogeneous right ventricular outflow tract activation attributed to elevation of resting potential, reduced availability of inward sodium channel conductance, and increased right ventricular outflow tract fibrosis. An elevated transient outward current gradient contributed to, but was not essential for, the BrPh phenotype. Conclusions In patients with severe hyperkalemia, a BrPh ECG is associated with malignant arrhythmias and all-cause mortality secondary to resting potential depolarization, reduced sodium current availability, and fibrosis at the right ventricular outflow tract.es_ES
dc.description.sponsorshipThis work was funded in part by the CIBERCV (Centro de Investigacion Biomedica en Red Enfermedades Cardiovasculares), Instituto de Salud Carlos III (PI14/00857, DTS16/ 0160, PI17/1059, PI01106), Spanish Ministry of Economy (TEC2013-46067-R) and the ERDF (European Regional Development Fund).es_ES
dc.relation.isversionofPublisher's versiones_ES
dc.subjectBrugada syndromees_ES
dc.subjectSudden cardiac deathes_ES
dc.titleClinical Characteristics and Electrophysiological Mechanisms Underlying Brugada ECG in Patients With Severe Hyperkalemiaes_ES
dc.rights.licenseAtribución-NoComercial 4.0 Internacional*
dc.contributor.funderCentro de Investigación Biomedica en Red - CIBERes_ES
dc.contributor.funderInstituto de Salud Carlos III - ISCIIIes_ES
dc.contributor.funderMinisterio de Economía y Competitividad (España)es_ES
dc.contributor.funderEuropean Regional Development Fund (ERDF/FEDER)es_ES
dc.identifier.journalJournal of the American Heart Associationes_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Arritmias Cardíacases_ES

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Atribución-NoComercial 4.0 Internacional
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