ArticleHeart rhythm2008
Can inhibition of IKur promote atrial fibrillation?
Article in Heart rhythm, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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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.
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Who cites it
34 citing papers in PubMed, 53 citations in OpenAlex.
- Oxidative stress and atrial fibrillation.Journal of molecular and cellular cardiology · 2024Review
- Immune response caused by M1 macrophages elicits atrial fibrillation-like phenotypes in coculture model with isogenic hiPSC-derived cardiomyocytes.Stem cell research & therapy · 2024Article
- Advances in basic and translational research in atrial fibrillation.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
- Design, synthesis, and biological evaluation of arylmethylpiperidines as Kv1.5 potassium channel inhibitors.Journal of enzyme inhibition and medicinal chemistry · 2022Article
- In silico assessment of genetic variation in KCNA5 reveals multiple mechanisms of human atrial arrhythmogenesis.PLoS computational biology · 2017Article
- Rate-Dependent Role of IBiophysical journal · 2017Article
- Potassium currents in the heart: functional roles in repolarization, arrhythmia and therapeutics.The Journal of physiology · 2017Review
- Synergistic Anti-arrhythmic Effects in Human Atria with Combined Use of Sodium Blockers and Acacetin.Frontiers in physiology · 2017Article
- Use of whole exome sequencing for the identification of Ito-based arrhythmia mechanism and therapy.Journal of the American Heart Association · 2015Article
- Evolution and pharmacological modulation of the arrhythmogenic wave dynamics in canine pulmonary vein model.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2014Article
- Pro-arrhythmogenic effects of atrial fibrillation-induced electrical remodelling: insights from the three-dimensional virtual human atria.The Journal of physiology · 2013Article
- Atrial selectivity of antiarrhythmic drugs.The Journal of physiology · 2013Review
- Article
- Atrial-selective prolongation of refractory period with AVE0118 is due principally to inhibition of sodium channel activity.Journal of cardiovascular pharmacology · 2012Article
- Rate-dependent effects of vernakalant in the isolated non-remodeled canine left atria are primarily due to block of the sodium channel: comparison with ranolazine and dl-sotalol.Circulation. Arrhythmia and electrophysiology · 2012Article
- Atrial-selective inhibition of sodium-channel current by Wenxin Keli is effective in suppressing atrial fibrillation.Heart rhythm · 2012Article
- Atrial-selective sodium channel block strategy to suppress atrial fibrillation: ranolazine versus propafenone.The Journal of pharmacology and experimental therapeutics · 2012Article
- Novel pharmacological targets for the rhythm control management of atrial fibrillation.Pharmacology & therapeutics · 2011Review
- American Heart Association atrial fibrillation research summit: a conference report from the American Heart Association.Circulation · 2011Article
- Advances in the Pharmacologic Management of Atrial Fibrillation.Cardiac electrophysiology clinics · 2011Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundBlock of ultrarapid delayed rectified potassium current (I(Kur)), present in atria but not in ventricles, is thought to be a promising approach for atrial-specific therapy of atrial fibrillation (AF). However, it has been shown that I(Kur) block may abbreviate atrial repolarization and that loss-of-function mutations in KCNA5, which encodes K(v) 1.5 channels responsible for I(Kur), is associated with familial AF.
objectiveOur objective in this study was to use low concentrations of 4-aminopyridine (4-AP, 10 to 50 microM), known to selectively block I(Kur), to assess the proarrhythmic and antiarrhythmic effects of I(Kur) block in healthy and remodeled atria.
methodsIsolated canine coronary-perfused right atrial preparations were used. Acetylcholine or ischemia/reperfusion was used to acutely remodel the atria. Transmembrane action potentials and a pseudo-electrocardiogram were simultaneously recorded.
resultsNormal (healthy) atria typically displayed action potentials (AP) with a prominent plateau, whereas remodeled atria displayed triangular-shaped APs (remodeled). In healthy atria, in which AF could not be induced with programmed stimulation, 4-AP abbreviated action potential measured at 90% repolarization (APD(90)) and effective refractory period (ERP), permitting the induction of AF in 4 of 12 preparations (33%). In remodeled atria, 4-AP produced little (50 microM) to no (10 to 25 microM) prolongation of APD(90) or ERP and was either ineffective or poorly effective in terminating AF or preventing its induction.
conclusionOur findings suggest that block of I(Kur) can provide the substrate for development of AF in healthy canine atria, presumably via abbreviation of APD and ERP.
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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.