Atrial fibrillation may be a vascular disease: the role of the pulmonary vein.

Recent years have seen an enormous amount of experimental and clinical research into role of the pulmonary veins (PVs) in atrial fibrillation (AF). The PVs contain cardiomyocytes with easily inducible arrhythmogenic activity due to the enhanced automaticity, induction of triggered activity, and genesis of microreentrant circuits. The enhanced automaticity, induced triggered activity, either alone or in combination with the reentrant mechanisms, may play a role in the initiation of PVs AF. Detailed mapping studies suggest that reentry within the PVs is most likely responsible for their arrhythmogenicity. There is no doubt that the PVs represent the most important source of arrhythmogenic activity in patients with paroxysmal AF. In AF patients with risk factors for development of AF, the presence of the pathological situation is important in enhancing the PV arrhythmogenic activity. Coronary sinus or superior vena cava may also be a source of rapid repetitive electrical activity during AF. Thus, AF should be considered a kind of vascular disease. Moreover, in patients with paroxysmal AF originating from the PVs, a wide spectrum of atrial arrhythmias may coexist, including paroxysms of atrial premature, tachycardia, flutter and fibrillation. This kind of arrhythmias should be named as PV atrial arrhythmias. These new views will help understand the mechanism, diagnosis and treatment method for AF.

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