[The electrocardiology of atrial fibrillation]

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and it is associated mainly with a significant mortality and morbidity. The purpose of this report is to focus on the major electro-cardiological aspects of AF and to provide some elements useful in the understanding of its pathophysiology. Experimental and clinical studies have shown that AF is maintained by multiple reentrant wavelets within the atrial muscle. It has been estimated that a critical number of wavelets (from 3 to 6) is necessary for perpetuation of AF. The short duration of the atrial effective refractory period (ERP) usually favors the onset of AF. Two different kinds of reentry have been observed during AF: random reentry and leading circle reentry. The presence of an adequate substrate is critical for the beginning of AF. Although this event is possible even in a normal atrium, atrial dilation and/or structural heterogeneity enhance the atrial propensity to develop AF. Even uniform or non-uniform anisotropy is now believed to play an important role in the genesis of AF. Finally, ionic channel disorders, some of which are genetically transmitted, may represent a possible substrate of AF. An important modulating role of the autonomic nervous system in the genesis of AF is universally accepted. In particular, many observations support the hypothesis that patients without heart disease tend to have vagally-mediated AF, whereas patients with structural heart disease tend to have adrenergic-mediated AF. In the presence of an opportunely modulated substrate, a third prerequisite for the triggering of a multiple atrial reentry is the presence of an adequate "trigger" factor. This is represented, in most cases, by ectopic atrial beats, commonly originating in the pulmonary veins. AF may cause atrial changes, either in an electrophysiological behavior and anatomy or both, that may favor its irreversibility and/or its frequent recurrence. Some of these changes are: atrial ERP disease, paradoxical shortening of ERP at a lower rate (inversed rate adaptation), accumulation of glycogen within atrial cells, apoptosis, and cellular dedifferentiation. The ventricular rate during AF has a pivotal role in its pathophysiology. The ERP of the atrioventricular node, the concealed conduction through the atrioventricular node, the autonomic neural balance and the drug's action are the most important factors that regulate ventricular rate during AF. In the presence of an atrioventricular accessory pathway, with fast anterograde conduction, AF is a very dangerous arrhythmia. During AF, aberrant conduction may often be seen, especially after long cycles (Ashman phenomenon). In patients with dilated cardiomyopathy and AF, arrhythmia is not always a secondary phenomenon. In fact, there is current evidence that AF may be the cause of cardiomyopathy.