Three things you should know when considering the atria: location, location, location.

Abstract

Atrial fibrillation (AF) is an arrhythmia of varied phenotypes, yet we continue to classify it under one heading. In an attempt to demystify it, the AF phenotype has been subdivided not by mechanism but by duration; that is, we acknowledge that AF comes in three not-so-simple varieties: paroxysmal, persistent, and permanent.1 2 Our knowledge of the mechanism underlying the progression from the paroxysmal to persistent form and then onto the permanent form is still limited, but it recently has been expanded with the study by Wijffels et al,3 which showed that AF begets AF. Now we are comfortable with the idea that rapid pacing per se can alter atrial cell/ionic electrophysiology as well as wall/cellular morphology (remodeling), which subsequently causes changes in atrial refractoriness. Here the basic assumption is that changes in atrial action potential duration and refractoriness track each other (but this is not always the case; for example, see Reference 44 ). Importantly, an increase in heterogeneity of refractoriness plays a significant role in both animal and human forms of AF.5 6 7 This increased heterogeneity could result from either a different response of regions of atrial cells to mediators of remodeling or from different initial or starting conditions of myocytes of different atrial locations. It has long been appreciated that normal, nonremodeled atrial cell transmembrane voltage profiles vary considerably and depend on the anatomical location of cells …