Background: Lacosamide is frequently used as a mono- or adjunctive therapy for the treatment of adults with epilepsy. Although lacosamide is known to act on both neuronal and cardiac sodium channels, potentially leading to cardiac arrhythmias, including Brugada syndrome (BrS), its adverse effects in individuals with genetic susceptibility are less understood.
Case: We report a 33-year-old female with underlying epilepsy who presented to the emergency department with a four-day history of seizure clusters, and was initially treated with lacosamide therapy. During the intravenous lacosamide infusion, the patient developed sudden cardiac arrest caused by ventricular arrhythmias necessitating resuscitation. Of note, the patient had a family history of sudden cardiac death. Workup including routine laboratory results, 12-lead electrocardiogram (ECG), echocardiogram, and coronary angiogram was non-specific. However, a characteristic type 1 Brugada ECG pattern was identified by ajmaline provocation testing; thus, confirming the diagnosis of BrS. Subsequently, the genotypic diagnosis was confirmed by Sanger sequencing, which revealed a heterozygous mutation (c.2893C>T, p.Arg965Cys) in the gene. Eventually, the patient underwent implantable cardioverter-defibrillator implantation and was discharged with full neurological recovery.
Conclusion: This case highlights a rare but lethal adverse event associated with lacosamide treatment in patients with genetic susceptibility. Further research is warranted to investigate the interactions between lacosamide and variants.
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http://dx.doi.org/10.3389/fcvm.2024.1406614 | DOI Listing |
Trends 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.
View Article and Find Full Text PDFJ Mol Cell Cardiol
January 2025
Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, UK. Electronic address:
Introduction: Brugada Syndrome (BrS) is an inherited arrhythmia syndrome characterised by ST-segment elevation in the right precordial ECG leads and is associated with an increased risk of sudden cardiac death. We identify and characterise a novel SCN3B variant encoding the regulatory β3-subunit of the cardiac voltage-gated sodium channel, Na1.5.
View Article and Find Full Text PDFA A Pract
January 2025
Division of Anaesthesiology and Perioperative Medicine, Department of Pain Medicine, Singapore General Hospital, Singapore.
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