title: Novel pharmacological approaches for antiarrhythmic therapy.
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.
authors.forename: Ursula
authors.initials: U
authors.lastname: Ravens
mesh_terms: D000889:Anti-Arrhythmia Agents / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D001145:Arrhythmias, Cardiac / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism; D055724:Electrophysiological Phenomena; D006325:Heart Atria / Q000187:drug effects* / Q000378:metabolism; D006352:Heart Ventricles / Q000187:drug effects* / Q000378:metabolism; D006801:Humans; D007473:Ion Channels / Q000378:metabolism
chemical_list: D000889:Anti-Arrhythmia Agents; D007473:Ion Channels