الفهرس 
Insights from Pathophysiology of AFOnly 14 pages are availabe for public view
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Abstract
Although atrial fibrillation (AF) is the most prevalent arrhythmia, the fundamental mechanisms underlying AF remain poorly understood. AF contributes to a greatly increased risk of stroke, heart failure, and mortality, and available therapies are suboptimal. Conventional antiarrhythmic treatments that block cardiac ion channels have been largely ineffective at maintaining normal sinus rhythm or preventing stroke, and many have the potential for proarrhythmia. Failure of these drugs to maintain sinus rhythm may be due to adaptive changes in response to persistent arrhythmia and/or concomitant comorbidities (diabetes, hypertension, heart failure, etc.) that minimize the role of ion channel activity as primary determinants of arrhythmia persistence. These adaptive changes are collectively termed electrical and structural remodeling.
Electrical remodeling underlies changes in ion channel activity and expression in human AF [1.2]; analysis of the changes in ion channel activity after induction of AF in experimental animal models3 suggests that these changes may be secondary to the disease. Structural remodeling encompasses changes in atrial chamber dimension, extracellular matrix (ECM) content, and the relative distribution of cell types in the atria (eg, myocytes, fibroblasts, vascular). In view of the failure of conventional antiarrhythmic drugs, it may be desirable to consider the pathways that contribute to the substrate for persistent AF.
This review focuses on AF in the clinical practice and on the evidence supporting inflammatory mechanisms in AF.