Atrial fibrillation: the tip of the iceberg

Atrial fibrillation (AF) usually results from profound alterations of the functional properties and structure of the atrial myocardium. For instance, at the cellular level AF is associated with a marked shortening of the action potential (AP) also seen in dilated atria in sinus rhythm. Drastic down-regulation of the I-type Ca2+ current that activates during the plateau phase is one of the main mechanisms responsible for this AP shortening. The down-regulation could be due to a variety of mechanisms including decreased channel expression and alteration of their camp-dependent phosphorylation. There are also alterations of repolarizing currents such as the transient outward potassium current or acetylcholinegated-inward rectifier potassium current. The electrical remodeling of diseased atria is most often associated with severe tissular and cellular alterations including: fibrosis, myocyte dystrophy with myolysis and dedifferentiation, apoptosis and gap junction disorganization. These abnormalities could result from a common and non specific adaptive response to changes in the working conditions of the atrial myocardium. The main goal of research in this field is now to link up the various abnormalities observed during AF and to determine their respective roles in atrial vulnerability to arrhythmia.