title: Non-ion channel blockers as anti-arrhythmic drugs (reversal of structural remodeling).
abstract: Approximately 90% of patients with atrial fibrillation have concomitant cardiovascular disease, such as hypertension, heart failure or valve disease. These diseases have been found to substantially affect the structure of atrial tissue, and thereby the occurrence of atrial fibrillation. At the molecular level, angiotensin II, oxidative stress and pro-inflammatory mediators are of particular importance in the induction of pro-arrhthymic atrial dilation, myocardial hypertrophy and interstitial atrial fibrosis. Elucidating the signalling pathways responsible for the process of structural atrial remodeling has helped to define novel non-ion channel drug targets for atrial fibrillation.
authors.affiliation: Division of Cardiology, University Hospital Magdeburg, Leipziger Str 44, Magdeburg, Germany. andreas.goette@medizin.uni-magdeburg.de
authors.forename: Andreas
authors.initials: A
authors.lastname: Goette
authors.forename: Alicja
authors.initials: A
authors.lastname: Bukowska
authors.forename: Uwe
authors.initials: U
authors.lastname: Lendeckel
mesh_terms: D000804:Angiotensin II / Q000378:metabolism; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology / Q000627:therapeutic use*; D001281:Atrial Fibrillation / Q000188:drug therapy* / Q000503:physiopathology; D002318:Cardiovascular Diseases / Q000150:complications; D016503:Drug Delivery Systems; D006325:Heart Atria / Q000187:drug effects / Q000503:physiopathology; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D018384:Oxidative Stress; D015398:Signal Transduction
chemical_list: D000889:Anti-Arrhythmia Agents; D018836:Inflammation Mediators; D000804:Angiotensin II