Trial reportNaunyn-Schmiedeberg's archives of pharmacology2010
Inhibition of IK,ACh current may contribute to clinical efficacy of class I and class III antiarrhythmic drugs in patients with atrial fibrillation.
Trial report in Naunyn-Schmiedeberg's archives of pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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.
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
23 citing papers in PubMed, 58 citations in OpenAlex.
- From allergy to arrhythmia - electrophysiological basis for the antiarrhythmic properties of antazoline.Frontiers in pharmacology · 2026Article
- Genetics and Pharmacogenetics of Atrial Fibrillation: A Mechanistic Perspective.JACC. Basic to translational science · 2024Review
- Tic-Tac: A Translational Approach in Mechanisms Associated with Irregular Heartbeat and Sinus Rhythm Restoration in Atrial Fibrillation Patients.International journal of molecular sciences · 2023Review
- Oxidation Driven Reversal of PIPFunction (Oxford, England) · 2023Article
- New Strategies for the Treatment of Atrial Fibrillation.Pharmaceuticals (Basel, Switzerland) · 2021Review
- The Small Conductance Calcium-Activated Potassium Channel Inhibitors NS8593 and UCL1684 Prevent the Development of Atrial Fibrillation Through Atrial-Selective Inhibition of Sodium Channel Activity.Journal of cardiovascular pharmacology · 2020Article
- Structural basis for the antiarrhythmic blockade of a potassium channel with a small molecule.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Muscarinic type-1 receptors contribute to IInternational journal of cardiology · 2018Article
- Voltage-gated and stretch-activated potassium channels in the human heart : Pathophysiological and clinical significance.Herzschrittmachertherapie & Elektrophysiologie · 2018Review
- Article
- [New developments in the antiarrhythmic therapy of atrial fibrillation].Herzschrittmachertherapie & Elektrophysiologie · 2014Review
- Calcium dysregulation in atrial fibrillation: the role of CaMKII.Frontiers in pharmacology · 2014Review
- NOS1AP modulates intracellular Ca(2+) in cardiac myocytes and is up-regulated in dystrophic cardiomyopathy.International journal of physiology, pathophysiology and pharmacology · 2014Article
- Atrial selectivity of antiarrhythmic drugs.The Journal of physiology · 2013Review
- Isolation of human atrial myocytes for simultaneous measurements of Ca2+ transients and membrane currents.Journal of visualized experiments : JoVE · 2013Article
- Pleiotropic effects of antiarrhythmic agents: dronedarone in the treatment of atrial fibrillation.Clinical Medicine Insights. Cardiology · 2013Article
- Safety and efficacy of vernakalant for acute cardioversion of atrial fibrillation: an update.Vascular health and risk management · 2013Review
- Novel electrophysiological properties of dronedarone: inhibition of human cardiac two-pore-domain potassium (K2P) channels.Naunyn-Schmiedeberg's archives of pharmacology · 2012Article
- Novel molecular targets for atrial fibrillation therapy.Nature reviews. Drug discovery · 2012Review
- Atrial-selective sodium channel block by dronedarone: sufficient to terminate atrial fibrillation?Naunyn-Schmiedeberg's archives of pharmacology · 2011Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inward rectifier potassium currents I(K1) and acetylcholine activated I(K,ACh) are implicated in atrial fibrillation (AF) pathophysiology. In chronic AF (cAF), I(K,ACh) develops a receptor-independent, constitutively active component that together with increased I(K1) is considered to support maintenance of AF. Here, we tested whether class I (propafenone, flecainide) and class III (dofetilide, AVE0118) antiarrhythmic drugs inhibit atrial I(K1) and I(K,ACh) in patients with and without cAF. I(K1) and I(K,ACh) were measured with voltage clamp technique in atrial myocytes from 58 sinus rhythm (SR) and 35 cAF patients. The M-receptor agonist carbachol (CCh; 2 microM) was employed to activate I(K,ACh). In SR, basal current was not affected by either drug indicating no effect of these compounds on I(K1). In contrast, all tested drugs inhibited CCh-activated I(K,ACh) in a concentration-dependent manner. In cAF, basal current was confirmed to be larger than in SR (at -80 mV, -15.2 +/- 1.2 pA/pF, n = 88/35 vs. -6.5 +/- 0.4 pA/pF, n = 194/58 [myocytes/patients]; P < 0.05), whereas CCh-activated I(K,ACh) was smaller (-4.1 +/- 0.5 pA/pF vs. -9.5 +/- 0.6 pA/pF; P < 0.05). In cAF, receptor-independent constitutive I(K,ACh) contributes to increased basal current, which was reduced by flecainide and AVE0118 only. This may be due to inhibition of constitutively active I(K,ACh) channels. In cAF, all tested drugs reduced CCh-activated I(K,ACh). We conclude that in cAF, flecainide and AVE0118 reduce receptor-independent, constitutively active I(K,ACh), suggesting that they may block I(K,ACh) channels, whereas propafenone and dofetilide likely inhibit M-receptors. The efficacy of flecainide to terminate AF may in part result from blockade of I(K,ACh).
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