ArticleEpilepsia2025
Lamotrigine promotes reentrant ventricular tachycardia in murine hearts.
Article in Epilepsia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Common genetic variants of the cardiac sodium channel alter patient response to class 1b antiarrhythmics.Journal of precision medicine (Amsterdam, Netherlands) · 2026Article
- Selectivity Filter Mutation in NaJACC. Clinical electrophysiology · 2026Article
- Common Genetic Variants of The Cardiac Sodium Channel Alter Patient Response to Class 1b Antiarrhythmics.bioRxiv : the preprint server for biology · 2026Article
- Development and Validation of a Model to Predict Secondary Arrhythmia in Patients With Epilepsy.CNS neuroscience & therapeutics · 2025Article
- Cardiac Electrophysiological Effects of the Sodium Channel-Blocking Antiepileptic Drugs Lamotrigine and Lacosamide.Pharmaceuticals (Basel, Switzerland) · 2025Article
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Authors and funding
6 authors.
Funding
Abstract
objectiveIn 2021, the US Food and Drug Administration issued a safety warning concerning lamotrigine use in patients with underlying cardiac disorders. This warning was based on in vitro data that predicted class Ib antiarrhythmic activity for lamotrigine. Therefore, we investigated the proarrhythmic potential of lamotrigine in the murine heart and compared its effect with flecainide.
methodsMurine hearts were perfused with clinically relevant concentrations of lamotrigine 3.8 μg/mL (15 μmol·L
resultsEx vivo electrocardiography revealed a high prevalence of ventricular tachycardia (VT) in lamotrigine-perfused hearts (7/9 hearts), whereas only two hearts exposed to flecainide evidenced VT. Optical voltage mapping showed that lamotrigine preferentially decreased ventricular conduction velocity (CV) in the longitudinal direction at all pacing frequencies tested (-22% ± 8.6%, -30% ± 15.4%, and -33% ± 13.3% for pacing frequency of 200-ms, 180-ms, and 150-ms cycle length, respectively, p ≤ .05) compared to the transverse direction, which only slowed CV at the fastest pacing frequency (-15% ± 16% for pacing frequency of 150-ms cycle length, p ≤ .01). Notably, the preferential CV slowing in the longitudinal direction altered the anisotropic ratio, giving rise to a functional substrate for reentrant VT. In contrast, flecainide slowed CV uniformly in both longitudinal and transverse directions (-30% ± 8.5% vs. -27% ± 5.3%, -32% ± 9.4% vs. -29% ± 6.9%, and - 29% ± 8.3% vs. -27% ± 10% for pacing frequency of 200-ms, 180-ms, and 150-ms cycle length, respectively, p ≤ .05). SIGNIFICANCE: Our findings provide mechanistic insight into the proarrhythmic impact of lamotrigine.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.