ArticleNaunyn-Schmiedeberg's archives of pharmacology2010
Novel pharmacological approaches for antiarrhythmic therapy.
Article 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 10 papers.
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Who cites it
10 citing papers in PubMed.
- Identification and validation of five hypoxia- and immune-related hub targets in atrial fibrillation.Journal of cardiothoracic surgery · 2026Article
- KPharmaceuticals (Basel, Switzerland) · 2026Review
- Current Drug Treatment Strategies for Atrial Fibrillation and TASK-1 Inhibition as an Emerging Novel Therapy Option.Frontiers in pharmacology · 2021Review
- Advances in Cardiac Pacing: Arrhythmia Prediction, Prevention and Control Strategies.Frontiers in physiology · 2021Review
- Pharmacologic TWIK-Related Acid-Sensitive K+ Channel (TASK-1) Potassium Channel Inhibitor A293 Facilitates Acute Cardioversion of Paroxysmal Atrial Fibrillation in a Porcine Large Animal Model.Journal of the American Heart Association · 2020Article
- Modulation of K2P 2.1 and K2P 10.1 K(+) channel sensitivity to carvedilol by alternative mRNA translation initiation.British journal of pharmacology · 2014Article
- Novel electrophysiological properties of dronedarone: inhibition of human cardiac two-pore-domain potassium (K2P) channels.Naunyn-Schmiedeberg's archives of pharmacology · 2012Article
- In silico optimization of atrial fibrillation-selective sodium channel blocker pharmacodynamics.Biophysical journal · 2012Article
- Carvedilol targets human K2P 3.1 (TASK1) K+ leak channels.British journal of pharmacology · 2011Article
- The pathology and treatment of cardiac arrhythmias: focus on atrial fibrillation.Vascular health and risk management · 2011Review
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Arrhythmias are caused by the perturbation of physiological impulse formation, impaired conduction, or disturbed electrical recovery. Currently available antiarrhythmic drugs-perhaps with exception of amiodarone-are not sufficiently effective and are burdened by cardiac and extracardiac side effects that may offset their therapeutic benefits. Detailed knowledge about electrical and structural remodelling may provide a better understanding of the mechanisms leading to generation and maintenance of arrhythmias especially in the setting of underlying heart disease and accompanying autonomic dysfunction. Thus, targets for new pharmacological interventions could include atrial-selective ion channels (e.g. atrial I(Na), I(Kur) and I(K,ACh)), pathology-selective ion channels (constitutively active I(K,ACh), TRP channels), ischemia-uncoupled gap junctions, proteins related to malfunctioning intracellular Ca(2+) homeostasis (e.g. "leaky" ryanodine receptors, overactive Na(+),Ca(2+) exchanger) or risk factors for arrhythmias ("upstream" therapies). In ventricular arrhythmias implantable cardioverter-defibrillator devices rather than antiarrhythmic drugs are the safest treatment option. The domain for new approaches to drug treatment is atrial fibrillation.
Indexed as
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20082192What OpenQuestion holds
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.