Antiarrhythmic therapy in atrial fibrillation.
Currently available antiarrhythmic drugs for the management of AF are not sufficiently effective and are burdened with cardiac and extracardiac side effects that may offset their therapeutic benefits. Better knowledge about the mechanisms underlying generation and maintenance of AF may lead to the discovery of new targets for pharmacological interventions. These 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 Ca2+ homeostasis (e.g., "leaky" ryanodine receptors, overactive Na+, Ca2+ exchanger) or risk factors for arrhythmias ("upstream" therapies). The review will briefly summarize the current pathophysiological and therapeutic concepts of AF. A description of recently developed antiarrhythmic drugs and their proposed pharmacological action will follow. The final section will speculate about some putative targets for antiarrhythmic drug action in the context of the remodelled atria.
Ravens
Ursula
U
Department of Pharmacology und Toxicology, Medical Faculty Carl Gustav Carus, Dresden University of Technology, Fetscherstrasse 74, D-01307 Dresden. Ravens@rcs.urz.tu-dresden.de
D000889:Anti-Arrhythmia Agents / Q000009:adverse effects / Q000627:therapeutic use*; D001145:Arrhythmias, Cardiac / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism / Q000517:prevention & control; D001281:Atrial Fibrillation / Q000188:drug therapy* / Q000235:genetics / Q000503:physiopathology / Q000517:prevention & control; D002986:Clinical Trials as Topic; D015507:Drugs, Investigational; D017629:Gap Junctions / Q000378:metabolism; D006325:Heart Atria / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D007473:Ion Channels / Q000378:metabolism / Q000494:pharmacology
D000889:Anti-Arrhythmia Agents; D015507:Drugs, Investigational; D007473:Ion Channels