Why does atrial fibrillation occur?

Abstract

Atrial fibrillation is often associated with atrial enlargement and stretch is known to cause electrophysiological alterations. Acute stretch may, depending on the moment at which it is applied, cause action potential shortening or induce both early and delayed afterdepolarizations which, when large enough, may initiate triggered premature action potentials. The effects of acute stretch may be very different from those of chronic stretch. In fact, in dogs with mitral valve disease in which progressive atrial enlargement, leading to atrial fibrillation, developed over a period of years, hardly any changes in transmembrane potential characteristics were found. In contrast, marked fibrosis developed which could favour re-entry because of slow fragmented conduction. A number of electrophysiological changes have been found in isolated preparations from human atria that had been fibrillating. Action potentials had a shorter duration and a triangular configuration in contrast to action potentials from normal atria that mostly showed a distinct plateau. Refractory periods were also shorter and the normal rate adaptation of the refractory period disappeared, so that, following a slowing of the heart rate, the refractory period did not prolong. These changes largely seem to be the result of prolonged episodes of rapid atrial activity and may be called electrophysiological remodelling. In addition, a marked dispersion refractoriness has been found which might be due to different factors, such as fibrosis and local denervation. It is likely that atrial dilatation and fibrosis are important factors in the occurrence and maintenance of atrial fibrillation. In an enlarged atrium, multiple re-entrant circuits can co-exist. Fibrosis leads to inhomogeneities in both conduction and refractoriness. Finally, the arrhythmia itself causes persistent shortening of refractoriness. All of these changes favour re-entry.