[Mechanisms of atrial fibrillation: recent advances]

Atrial fibrillation (AF) is due to the presence of multiple reentry pathways. Although this mechanism has been known for some time, new information has recently been acquired about the factors of atrial vulnerability 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 to be taken into consideration. The abnormalities of the refractory periods liable to increase atrial vulnerability are their shortening, spatial dispersion and poor adaptation to the heart rate. All these changes may be demonstrated at cellular level. The product of the intra-atrial conduction velocity and the duration of the refractory period defines 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 fibrillation giving rise to atrial fibrillation. Histological lesions of the atrial tissue may be demonstrated, even in the absence of underlying cardiac disease. They mainly consist of fibrosis, fatty degeneration and myocytic hypertrophy. In the long-term, atrial fibrillation leads to a number of structural abnormalities of the atrial, and sometimes ventricular tissues, progressing to cardiomyopathy in some cases.