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Driver Regions in Atrial Fibrillation Associated with Congestive Heart Failure: Where Are They, and What Are They Telling Us?

The most widely held concept of the mechanism of atrial fibrillation (AF) has been the idea of multiple-circuit reentry, first espoused by Mines1 and Garrey2 and later refined by Gordon Moe and co-workers.3 This notion holds that AF is based on multiple propagating wavefronts that course more or less randomly through the atria and maintain continuous activity by always being able to find enough excitable tissue through which to propagate. Moe acknowledged that rapid, irregular atrial activation could result from single or multiple rapidly firing ectopic foci, from a single rapid circus movement tachycardia or from multiple-circuit reentry, as suggested by multiple investigators early in the 20th century,4 but distinguished between “true fibrillation” that he considered multiple-circuit reentry and the other mechanisms that he considered rather to be initiators.3 Central to Moe’s conceptualization was the idea that the wavefronts that maintain AF are formed randomly and die out as a function of tissue properties, with AF being maintained if the rate of formation exceeds the rate of wavefront extinction.3