Atrial fibrillation (AF) is one of the most common and dangerous arrhythmias and one of the main problems of medicine all over the world. The disease is characterised with rapid and disordered atrial depolarization, which leads to the disorganized contraction of atrial myocardium. The article deals with the mechanisms of AF from the first ideas to the modern data. AF is a complex pathology with several etiopathogenetic mechanisms. Many investigations show that this arrhythmia needs a trigger for its induction and anatomical or electrophysiological changes for its preservation. Fist G. Mines in 1914 advanced the theory of wave reentry and much more later a group of scientists headed by ?. Haissaguerre found trigger activity of pulmonary veins orifices, which may contribute to the formation of one or several macro-reentry circuits in one or both atriums and launch arrhythmia. After that many articles were dedicated to the anatomical and electrophysiological characteristics of pulmonary veins orifices. An important aspect of understanding of the mechanisms of persistence of AF is electrical remodeling. During this process, the cells involved into the of macro-reentrant circuits undergo changes in the characteristics of their repolarization, manifested as shortening of the action potential duration and consequently shortening of the refractoryness period. These changes contribute to the preservation of reentry circles. That means the more atrium is fibrillating, the more it tends to support fibrillation due to processes of electrical remodeling. Thus, AF becomes persistent, when the macro-reentry circles are able to support themselves without the participation of the triggers. Later other focuses of ectopic activity were found. Among them were sites of myocardium near superior vena cava, coronary sinus, posterior wall of left atrium, interatrial septum and left atrial appendage. Also the role of genes, which can take part in AF genesis in some cases, was established. For example, this can be genes encoding the ion channels or the proteins of the slot connections of the cardiomyocytes, named connexins. From all the above can be established the complexity of the pathogenesis of AF, many components of which require further studying to achieve more great success in its treatment.
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Author Name: Bockeria L.A., Shengelia L.D.
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Keywords: atrial fibrillation, ectopic activity, macro-reentry, electrical remodeling