Nonantiarrhythmic drug therapy for atrial fibrillation.

Murray KT, Mace LC, Yang Z
Heart Rhythm. 2007 4 (3 Suppl): S88-90

PMID: 17336893 · DOI:10.1016/j.hrthm.2006.12.027

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.

MeSH Terms (21)

Angiotensin-Converting Enzyme Inhibitors Angiotensin II Type 1 Receptor Blockers Animals Anti-Arrhythmia Agents Anti-Inflammatory Agents Antioxidants Atrial Fibrillation Calcium Channel Blockers Connexins Drugs, Investigational Fatty Acids, Omega-3 Gap Junctions Humans Hydroxymethylglutaryl-CoA Reductase Inhibitors Mineralocorticoid Receptor Antagonists Oligopeptides Oxidative Stress Receptors, Serotonin, 5-HT4 Renin-Angiotensin System Serotonin 5-HT4 Receptor Antagonists Serotonin Antagonists

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