ArticleCardiac electrophysiology clinics2014
Pharmacology and Toxicology of Nav1.5-Class 1 anti-arrhythmic drugs.
Article in Cardiac electrophysiology clinics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 44 citations in OpenAlex.
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- A bifunctional actuator to correct loss-of-function deficits in cardiac voltage-gated sodium channels.Science advances · 2026Article
- Cardiosim-Tox: an interpretable multitask deep learning QSAR platform with multimodal feature fusion for predicting hERG, Cav1.2, and Nav1.5 blockade risk and potency.Archives of toxicology · 2026Article
- Discovery of a novel NaActa pharmacologica Sinica · 2026Article
- Cardiac Electrophysiological Effects of the Sodium Channel-Blocking Antiepileptic Drugs Lamotrigine and Lacosamide.Pharmaceuticals (Basel, Switzerland) · 2025Article
- How could simulations elucidate Nav1.5 channel blockers mechanism?The Journal of general physiology · 2025Article
- Association of dysautonomia with refractory ventricular tachyarrhythmia in patients requiring thoracoscopic surgical cardiac sympathetic denervation.JTCVS open · 2025Article
- Differential Inhibition by Cenobamate of Canonical Human Nav1.5 Ion Channels and Several Point Mutants.International journal of molecular sciences · 2025Article
- Inhibitory Effects of Cenobamate on Multiple Human Cardiac Ion Channels and Possible Arrhythmogenic Consequences.Biomolecules · 2024Article
- Graphene-integrated mesh electronics with converged multifunctionality for tracking multimodal excitation-contraction dynamics in cardiac microtissues.Nature communications · 2024Article
- New insights on cardiac Na channel block by an atypical anti-arrhythmic drug.Nature cardiovascular research · 2023Article
- Hyperglycaemia-induced impairment of the autorhythmicity and gap junction activity of mouse embryonic stem cell-derived cardiomyocyte-like cells.Histochemistry and cell biology · 2023Article
- Reduction ofFrontiers in neuroscience · 2023Article
- Cardiac sodium channel inhibition by lamotrigine: In vitro characterization and clinical implications.Clinical and translational science · 2022Article
- Veratridine Can Bind to a Site at the Mouth of the Channel Pore at Human Cardiac Sodium Channel NaInternational journal of molecular sciences · 2022Article
- Characterization of cardiac bradyarrhythmia associated with LGI1-IgG autoimmune encephalitis.Frontiers in immunology · 2022Article
- The Citrus Flavonoid Hesperetin Has an Inadequate Anti-Arrhythmic Profile in the ΔKPQ NaBiomolecules · 2020Article
- Amiodarone-induced Hyponatremia: A Case Report and a Review of the Literature.The Journal of innovations in cardiac rhythm management · 2018Article
- Article
- Computational Analysis of the Mode of Action of Disopyramide and Quinidine on hERG-Linked Short QT Syndrome in Human Ventricles.Frontiers in physiology · 2017Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Although cardiac sodium channel blocking drugs can exert antiarrhythmic actions, they can also provoke life-threatening arrhythmias through a variety of mechanisms. This review addresses the way in which drugs interact with the channel, and how these effects translate to clinical beneficial or detrimental effects. A further understanding of the details of channel function and of drug-channel interactions may lead to the development of safer and more effective antiarrhythmic therapies.
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Registered trials
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 OpenQuestion graph.