title: Atrial remodeling and novel pharmacological strategies for antiarrhythmic therapy in atrial fibrillation.
abstract: Atrial fibrillation (AF) is the most common arrhythmia in clinical practice. It can occur at any age, however, it becomes extremely common in the elderly, with a prevalence approaching more than 20% in patients older than 85 years. AF is associated with a wide range of cardiac and extra-cardiac complications and thereby contributes significantly to morbidity and mortality. Present therapeutic approaches to AF have major limitations, which have inspired substantial efforts to improve our understanding of the mechanisms underlying AF, with the premise that improved knowledge will lead to innovative and improved therapeutic approaches. Our understanding of AF pathophysiology has advanced significantly over the past 10 to 15 years through an increased awareness of the role of "atrial remodeling". Any persistent change in atrial structure or function constitutes atrial remodeling. Both rapid ectopic firing and reentry can maintain AF. Atrial remodeling has the potential to increase the likelihood of ectopic or reentrant activity through a multitude of potential mechanisms. The present paper reviews the main novel results on atrial tachycardia-induced electrical, structural and contractile remodeling focusing on the underlying pathophysiological and molecular basis of their occurrence. Special attention is paid to novel strategies and targets with therapeutic significance for atrial fibrillation.
authors.affiliation: Division of Cardiovascular Pharmacology, Hungarian Academy of Sciences and Department of Pharmacology & Pharmacotherapy, Faculty of Medicine, University of Szeged, Dóm tér 12, P.O. Box 427, H-6701 Szeged, Hungary. jost@phcol.szote.u-szeged.hu
authors.forename: N
authors.initials: N
authors.lastname: Jost
authors.forename: Z
authors.initials: Z
authors.lastname: Kohajda
authors.forename: A
authors.initials: A
authors.lastname: Kristóf
authors.forename: P P
authors.initials: PP
authors.lastname: Kovács
authors.forename: Z
authors.initials: Z
authors.lastname: Husti
authors.forename: V
authors.initials: V
authors.lastname: Juhász
authors.forename: L
authors.initials: L
authors.lastname: Kiss
authors.forename: A
authors.initials: A
authors.lastname: Varró
authors.forename: L
authors.initials: L
authors.lastname: Virág
authors.forename: I
authors.initials: I
authors.lastname: Baczkó
mesh_terms: D000889:Anti-Arrhythmia Agents / Q000737:chemistry / Q000494:pharmacology* / Q000627:therapeutic use; D001281:Atrial Fibrillation / Q000188:drug therapy* / Q000503:physiopathology; D016275:Atrial Function / Q000187:drug effects; D006325:Heart Atria / Q000503:physiopathology; D006801:Humans; D007473:Ion Channels / Q000037:antagonists & inhibitors / Q000378:metabolism
chemical_list: D000889:Anti-Arrhythmia Agents; D007473:Ion Channels