title: Role of angiotensin system and effects of its inhibition in atrial fibrillation: clinical and experimental evidence.
abstract: Atrial fibrillation (AF) is a common arrhythmia that is difficult to treat. Anti-arrhythmic drug therapy, to maintain sinus-rhythm, is limited by inadequate efficacy and potentially serious adverse effects. There is increasing interest in novel therapeutic approaches that target AF-substrate development. Recent trials suggest that angiotensin converting-enzyme (ACE)-inhibitors and angiotensin-receptor blockers (ARBs) may be useful, particularly in patients with left ventricular hypertrophy or failure. The clinical potential and mechanisms of this approach are under active investigation. Angiotensin-II is involved in remodelling and may have direct electrophysiological actions. Experimental studies show protection from atrial structural and possibly electrical remodelling with ACE-inhibitors and ARBs, as well as potential effects on cardiac ion-channels. This article reviews information pertaining to the clinical use and mechanism of action of ACE-inhibitors and ARBs in AF. A lack of prospective randomized double-blind trials data limits their application in AF patients without another indication for their use, but studies under way may alter this in the near future. This exciting field of investigation may lead to significant improvements in therapeutic options for AF patients.
authors.affiliation: Division of Clinical Electrophysiology, J.W. Goethe University, Theodor Stern Kai 7, 60590 Frankfurt, Germany. j.ehrlich@em.uni-frankfurt.de
authors.forename: Joachim R
authors.initials: JR
authors.lastname: Ehrlich
authors.forename: Stefan H
authors.initials: SH
authors.lastname: Hohnloser
authors.forename: Stanley
authors.initials: S
authors.lastname: Nattel
mesh_terms: D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use*; D001281:Atrial Fibrillation / Q000188:drug therapy*; D004554:Electric Countershock; D006801:Humans; D009200:Myocardial Contraction / Q000187:drug effects; D009203:Myocardial Infarction / Q000209:etiology; D015221:Potassium Channels / Q000502:physiology; D011379:Prognosis; D012008:Recurrence; D012084:Renin-Angiotensin System / Q000502:physiology
chemical_list: D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D000889:Anti-Arrhythmia Agents; D015221:Potassium Channels