During the past 50 years different theories have been proposed to explain the mechanism underlying atrial fibrillation, but many controversies surrounded these mechanisms. In the past decade it seems well accepted that both focal and reentrant mechanisms are involved, playing a different role in the initiation and perpetuation of the arrhythmia. Several recent human multielectrode mapping systems and other studies indicate that in atrial fibrillation the dominant mechanism incorporates multiple meandering wavelets, both in the acute and chronic form of this condition. Multiple wavelengths of excitation propagate around the atrial myocardium and the arrhyth¬mia is perpetuated because of an abnormal atrial tissue substrate, particularly in patients with structural heart disease and permanent atrial fibrillation. Patients with paroxysmal atrial fibrillation with no evidence of structural heart disease appear to have a trigger-predominant mechanism, but the two basic mechanisms reflect a large overlap. After very long periods of permanent atrial fibrillation, if sinus rhythm is restored, reverse remodeling usually fails to occur. This may explain why in patients with persistent atrial fibrillation for more than 12 months it is difficult to maintain sinus rhythm following cardioversion.

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