title: Nonantiarrhythmic drug therapy for atrial fibrillation.
abstract: Recent studies have begun to elucidate the molecular mechanisms that promote the generation and progressive nature of atrial fibrillation. Evidence from both experimental and clinical investigations has implicated an important role for the renin-angiotensin-aldosterone system, inflammation, and oxidative stress, with data that suggest a potential beneficial effect for angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, aldosterone receptor antagonists, antiinflammatory agents, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins), and omega-3 polyunsaturated fatty acids. In addition, compounds that increase gap junctional conductance or that block 5-hydroxytryptamine-4 receptors have also shown promise in the experimental setting. Large-scale, prospective clinical trials will clarify the utility of these new therapeutic approaches to prevent atrial fibrillation in specific clinical settings.
authors.affiliation: Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-6602, USA. kathy.murray@vanderbilt.edu
authors.forename: Katherine T
authors.initials: KT
authors.lastname: Murray
authors.forename: Lisa C
authors.initials: LC
authors.lastname: Mace
authors.forename: Zhenjiang
authors.initials: Z
authors.lastname: Yang
mesh_terms: D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology* / Q000627:therapeutic use; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D000975:Antioxidants / Q000494:pharmacology; D001281:Atrial Fibrillation / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D017630:Connexins / Q000378:metabolism; D015507:Drugs, Investigational / Q000494:pharmacology* / Q000627:therapeutic use; D015525:Fatty Acids, Omega-3 / Q000494:pharmacology; D017629:Gap Junctions / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology; D000451:Mineralocorticoid Receptor Antagonists / Q000494:pharmacology; D009842:Oligopeptides / Q000494:pharmacology; D018384:Oxidative Stress / Q000187:drug effects; D044422:Receptors, Serotonin, 5-HT4 / Q000378:metabolism; D012084:Renin-Angiotensin System / Q000187:drug effects; D058832:Serotonin 5-HT4 Receptor Antagonists; D012702:Serotonin Antagonists / Q000494:pharmacology
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D000889:Anti-Arrhythmia Agents; D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D002121:Calcium Channel Blockers; D017630:Connexins; D015507:Drugs, Investigational; D015525:Fatty Acids, Omega-3; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D000451:Mineralocorticoid Receptor Antagonists; D009842:Oligopeptides; D058832:Serotonin 5-HT4 Receptor Antagonists; D012702:Serotonin Antagonists; D044422:Receptors, Serotonin, 5-HT4; C477643:rotigaptide