Document Detail


Recent insights into the pathophysiology of atrial fibrillation.
MedLine Citation:
PMID:  17403452     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Although the problem of atrial fibrillation is now widely appreciated, the fundamental mechanisms that lead to arrhythmia onset and persistence have been difficult to elucidate. As a result, available pharmacologic therapies have focused more on modifying ion channel activity than on the underlying mechanisms. Recent studies suggest an important role for alterations in autonomic regulation, neurohormonal activation, and a systemic inflammatory state in the genesis and persistence of atrial fibrillation. The relative contributions of these distinct pathways to atrial fibrillation likely vary from patient to patient, and within a patient, as a function of age. Tailored therapies, together with patient-specific ablative interventions, may increase the success with which atrial fibrillation is treated and minimize the occurrence of life-threatening thromboembolic complications.
Authors:
David R Van Wagoner
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review    
Journal Detail:
Title:  Seminars in thoracic and cardiovascular surgery     Volume:  19     ISSN:  1043-0679     ISO Abbreviation:  Semin. Thorac. Cardiovasc. Surg.     Publication Date:  2007  
Date Detail:
Created Date:  2007-04-03     Completed Date:  2007-07-17     Revised Date:  2007-12-03    
Medline Journal Info:
Nlm Unique ID:  8917640     Medline TA:  Semin Thorac Cardiovasc Surg     Country:  United States    
Other Details:
Languages:  eng     Pagination:  9-15     Citation Subset:  IM    
Affiliation:
Department of Molecular Cardiology, Cleveland Clinic, Cleveland, Ohio 44195, USA. VANWAGD@ccf.org
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MeSH Terms
Descriptor/Qualifier:
Atrial Fibrillation / etiology,  physiopathology*,  surgery
Atrial Premature Complexes
Disease Progression
Humans
Postoperative Complications
Pulmonary Veins / pathology*,  surgery
Risk Factors
Grant Support
ID/Acronym/Agency:
R01 HL-65412/HL/NHLBI NIH HHS

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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