title: [Non-channel drugs to prevent atrial fibrillation].
abstract: Atrial fibrillation is the most prevalent sustained cardiac arrhythmia. To terminate or prevent atrial fibrillation, conventional "channel-blocking antiarrhythmics" are generally administered, which directly inhibit current flows through transmembrane sodium, calcium and/or potassium channels that give rise to the atrial action potential. However, prospective, randomized clinical trials have demonstrated that cardiomyocyte ion channel blocking antiarrhythmic drugs have limited long-term-efficacy for preventing recurrences of atrial fibrillation, their safety is far from ideal (because of the high incidence of proarrhythmic and extracardiac side-effects), and do not reduce mortality. Researchers during the last 10 years have revealed that the pathogenetic basis of the recurrence, persistence or permanence of atrial fibrillation is electrical and structural remodelling established by profound alterations in the electrophysiological, contractile and (ultra)structural properties of the myocardium (atrial remodelling). Accordingly, recent interest has shifted from ion channel blockers to the development of drugs that target underlying arrhythmogenic substrates by interference with receptors and specific signal transduction pathways involved in electrical and structural remodelling (non-channel drugs). They include antifibrotic angiotensin-converting enzyme inhibitors, angiotensin II AT1 receptor and aldosterone antagonists, beta-adrenergic blockers, anti-inflammatory statins and glucocorticoids, and a series of new atrioselective antifibrillatory agents that are currently undergoing clinical trials.
authors.affiliation: Szegedi Tudományegyetem, Szent-Györgyi Albert Orvos- es Gyógyszerésztudományi Centrum, Altalános Orvostudományi Kar, I. Belgyógyászati Klinika, Szeged. fat@in1st.szote.u-szeged.hu
authors.forename: Tamás
authors.initials: T
authors.lastname: Fazekas
authors.forename: Gizella
authors.initials: G
authors.lastname: Liszkai
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000450:Aldosterone / Q000378:metabolism; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology / Q000627:therapeutic use*; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D001281:Atrial Fibrillation / Q000188:drug therapy*; D006325:Heart Atria / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D026902:Potassium Channel Blockers / Q000627:therapeutic use; D044140:Receptor, Angiotensin, Type 1 / Q000187:drug effects; D055502:Secondary Prevention; D026941:Sodium Channel Blockers / Q000627:therapeutic use
chemical_list: D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D000889:Anti-Arrhythmia Agents; D000893:Anti-Inflammatory Agents; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D026902:Potassium Channel Blockers; D044140:Receptor, Angiotensin, Type 1; D026941:Sodium Channel Blockers; D000450:Aldosterone