Many experimental and clinical studies have demonstrated that it is possible to trigger atrial fibrillation (AF) by vagal stimulation which reduces and disperses the atrial refractory periods and decreases the threshold of fibrillation. In order to induce fibrillation, it is necessary to deliver a stimulation near to the refractory period. It has also been shown that, in these conditions, there is a delay in atrial conduction. A temporal relationship between the preceding diastole and the coupling interval increases atrial vulnerability and plays an equally important role. The decrease in the effective atrial refractory period, especially when the values are widely dispersed, and the delay in conduction predisposing to atrial reentry, may be considered to be the two most important electrophysiological mechanisms of AF. However, in order to maintain AF, the atrium must be dilated, especially when there is a concurrent cardiac disease. The presence of a shorter "wave length" of activation allowing multiple reentry circuits is an essential condition for sustaining AF. All conductions of induction and maintenance of AF may be observed without participation of S.N.A.. When no cause of AF (atrial pathology, etc.) is apparent, a short atrial refractory period with dispersion of its values and slowing of atrial conduction in presence of an extrastimulus are the probable inducing factors.