Atrial fibrillation (AF) is due to the presence of multiple reentry pa
thways. Although this mechanism has been known for some time, new info
rmation has recently been acquired about the factors of atrial vulnera
bility and the conditions of myocardial alteration. There are two main
factors of atrial vulnerability : intra-atrial conduction defects and
abnormalities of the refractory periods. In addition, the concept of
critical mass and the influence of the autonomic nervous system have t
o be taken into consideration. The abnormalities of the refractory per
iods liable to increase atrial vulnerability are their shortening, spa
tial dispersion and poor adaptation to the heart rate. All these chang
es may be demonstrated at cellular level. The product of the intraatri
al conduction velocity and the duration of the refractory period defin
es the wave length. The risk of developing reentry pathways increases
as the wave length shortens. Moreover, the more the atrium fibrillates
, the greater will be the decrease of the refractory periods, atrial f
ibrillation giving rise to atrial fibrillation. Histological lesions o
f the atrial tissue may be demonstrated, even in the absence of underl
ying cardiac disease. They mainly consist of fibrosis, fatty degenerat
ion and myocytic hypertrophy. In the long-term, atrial fibrillation le
ads to a number of structural abnormalities of the atrial, and sometim
es ventricular tissues, progressing to cardiomyopathy in some cases.