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http://dx.doi.org/10.1016/j.hrthm.2016.06.022 | DOI Listing |
Acta Anaesthesiol Scand
February 2025
Department of Anesthesiology and perioperative medicine, University Hospital of Brussels, Free University of Brussels, Brussels, Belgium.
Background: The use of local anesthetics (LA) in individuals with Brugada syndrome (BrS) remains a subject of debate due to the lack of large-scale studies confirming their potential risks. This study primarily aimed to evaluate the incidence of new malignant arrhythmias or defibrillation events in patients diagnosed with BrS during the perioperative period, following the administration of local anesthetics, and within 30 days postoperatively. The secondary objective was to analyze the occurrence of adverse effects during hospitalization, as well as 30-day readmission and mortality rates.
View Article and Find Full Text PDFHeart Rhythm
January 2025
Dante Pazzanese Institute of Cardiology, Department of Electrophysiology, São Paulo, Brazil.
Background: Brugada syndrome (BrS) is a genetic heart disease that predisposes individuals to ventricular arrhythmias and sudden cardiac death. Although implantable cardioverter-defibrillators (ICDs) and quinidine are primary treatments, recurrent BrS-triggered ventricular arrhythmias can persist. In this setting, epicardial substrate ablation has emerged as a promising alternative for symptomatic patients.
View Article and Find Full Text PDFTrends Genet
January 2025
Department of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Hessen, 61231, Germany; German Centre for Cardiovascular Research (DZHK), Partner Site Rhine-Main, Bad Nauheim, Hessen, 61231, Germany; Excellence Cluster Cardio-Pulmonary Institute (CPI), Bad Nauheim, Frankfurt, Giessen, Germany. Electronic address:
The onset and progression of dominant diseases are thought to result from haploinsufficiency or dominant negative effects. Here, we propose transcriptional adaptation (TA), a newly identified response to mRNA decay, as an additional cause of some dominant diseases. TA modulates the expression of so-called adapting genes, likely via mRNA decay products, resulting in genetic compensation or a worsening of the phenotype.
View Article and Find Full Text PDFEur Heart J
December 2024
Department of Cardiology, Beijing Tsinghua Changgung Hospital, School of Clinical Medicine, Tsinghua University, No. 168 of Litang Road, Beijing 102218, China.
J Korean Med Sci
January 2025
Division of Cardiology, Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea.
Background: The ionic mechanism underlying Brugada syndrome (BrS) arises from an imbalance in transient outward current flow between the epicardium and endocardium. Previous studies report that artemisinin, originally derived from a Chinese herb for antimalarial use, inhibits the Ito current in canines. In a prior study, we showed the antiarrhythmic effects of artemisinin in BrS wedge preparation models.
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