Abstract

            The mechanisms of atrial fibrillation are complex, and have been the subject of intensive study for over fifty years.  There is likely a complex interplay between triggers and substrate that mediates the initiation and maintenance of AF.  Increasingly, atrial fibrosis has been recognized as a key component of that substrate, playing a critical role in conduction abnormalities in the left atrium that appear requisite to maintaining AF.  In the last several years, our abilities to quantify left atrial fibrosis – both through catheter- and MRI-based techniques – has shed important light on the underlying mechanisms of AF, and on therapeutic strategies to treat AF.  Whether our increased appreciation of the role of atrial fibrosis in AF translates into improved efficacy of catheter ablation or anti-arrhythmic therapy, though, remains to be seen.