2024-03-29T15:02:28Zhttp://repisalud.isciii.es/oai/requestoai:repisalud.isciii.es:20.500.12105/71242022-10-28T08:19:03Zcom_20.500.12105_2145com_20.500.12105_2051com_20.500.12105_2144col_20.500.12105_2146
Repisalud
author
Rivera-Juárez, Allan
author
Hernández-Romero, Ismael
author
Puertas, Carolina
author
Zhang-Wang, Serena
author
Sánchez-Álamo, Beatriz
author
Martins, Raphael
author
Figuera, Carlos
author
Guillem, María S
author
Climent, Andreu M
author
Fernández-Avilés, Francisco
author
Tejedor, Alberto
author
Jalife, Jose
author
Atienza, Felipe
funder
Centro de Investigación Biomedica en Red - CIBER
funder
Instituto de Salud Carlos III
funder
Ministerio de Economía y Competitividad (España)
funder
Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF)
2019-02-06T08:00:43Z
2019-02-06T08:00:43Z
2019-02-05
J Am Heart Assoc. 2019; 8(3):e010115
2047-9980
http://hdl.handle.net/20.500.12105/7124
30675825
10.1161/JAHA.118.010115
2047-9980
Journal of the American Heart Association
Background 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.
eng
Brugada syndrome
Sudden cardiac death
Hyperkalemia
Clinical Characteristics and Electrophysiological Mechanisms Underlying Brugada ECG in Patients With Severe Hyperkalemia
journal article
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URL
https://repisalud.isciii.es/bitstream/20.500.12105/7124/1/ClinicalCharacteristicsElectrophysiologicalMechanisms_2019.pdf
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https://repisalud.isciii.es/bitstream/20.500.12105/7124/5/ClinicalCharacteristicsElectrophysiologicalMechanisms_2019.pdf.txt
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ClinicalCharacteristicsElectrophysiologicalMechanisms_2019.pdf.txt