Abstract
In concert with many other areas of cardiovascular pathophysiology, our understanding of atrial fibrillation (AF), which not all that long ago seemed to be essentially devoid of any major unexplored domains, nonetheless continues to evolve, often in rather unpredictable directions. Novel mechanisms and operational postulates seem to be evolving continuously: new terms such as “electrical remodeling” (denominating the shortened atrial action potential) and “atrial fibrosis and atrial ionic remodeling” (simply, “structural remodeling”) are being introduced into the description of chronic AF.
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