| Literature DB >> 26701216 |
Larissa Fabritz1,2, Eduard Guasch3,4, Charalambos Antoniades5, Isabel Bardinet6, Gerlinde Benninger7, Tim R Betts5, Eva Brand8, Günter Breithardt2,7, Gabriela Bucklar-Suchankova9, A John Camm10,11, David Cartlidge12, Barbara Casadei5, Winnie W L Chua1, Harry J G M Crijns13,14, Jon Deeks15, Stéphane Hatem16, Françoise Hidden-Lucet16, Stefan Kääb17,18, Nikos Maniadakis19, Stephan Martin6, Lluis Mont3,4, Holger Reinecke20, Moritz F Sinner17, Ulrich Schotten13,14, Taunton Southwood21, Monika Stoll13,14, Panos Vardas22, Reza Wakili17,18, Andy West12, André Ziegler9, Paulus Kirchhof1,2,7,23,24.
Abstract
Despite remarkable advances in antiarrhythmic drugs, ablation procedures, and stroke-prevention strategies, atrial fibrillation (AF) remains an important cause of death and disability in middle-aged and elderly individuals. Unstructured management of patients with AF sharply contrasts with our detailed, although incomplete, knowledge of the mechanisms that cause AF and its complications. Altered calcium homeostasis, atrial fibrosis and ageing, ion-channel dysfunction, autonomic imbalance, fat-cell infiltration, and oxidative stress, in addition to a susceptible genetic background, contribute to the promotion, maintenance, and progression of AF. However, clinical management of patients with AF is currently guided by stroke risk parameters, AF pattern, and symptoms. In response to this apparent disconnect between the known pathophysiology of AF and clinical management, we propose a roadmap to develop a set of clinical markers that reflect the major causes of AF in patients. Thereby, the insights into the mechanisms causing AF will be transformed into a format that can underpin future personalized strategies to prevent and treat AF, ultimately informing better patient care.Entities:
Mesh:
Year: 2015 PMID: 26701216 DOI: 10.1038/nrcardio.2015.194
Source DB: PubMed Journal: Nat Rev Cardiol ISSN: 1759-5002 Impact factor: 32.419