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Atrial fibrillation (AF) is the most prevalent arrhythmia in western countries and it is estimated that its prevalence will increase further over the coming decades. AF affects 1% of the general population and up to 17% of patients aged >84 years.1 Until recently, pharmacological therapy has been the only treatment, but its efficacy is limited in terms of maintenance of sinus rhythm and control of symptoms.2 Over the last decade catheter based ablation of AF has proved to be more efficacious in comparison to medical treatment,3 especially in the paroxysmal form. Moreover, the catheter ablation strategy has evolved considerably, leading to significant improvements in efficacy and reductions in the procedural complication rate. Initially, linear lesions were performed in the atria mimicking the surgical Maze procedure4 which, however, resulted in limited success and significant complications. Haissaguerre et al5 and Chen et al6 found that AF is most commonly initiated by a premature beat from the orifices of the pulmonary veins (PVs). As a result, the procedure initially targeted elimination of foci inside the triggering vein (the earliest PV electrogram that initiates tachycardia), but this strategy was not effective enough to prevent recurrences which originated from the same or other veins. Therefore, electrical disconnection of all four PVs from the atrium became the proposed treatment option. The antral (also called circumferential) isolation of the veins is the approach that is most frequently used nowadays,7 and in many cases cures the disease.
As the atrium becomes more dilated and fibrotic, other structures in addition to PVs are increasingly being recognised as a possible source of AF initiation and/or are key in the perpetuation of AF. Typical locations of triggers and the micro-reentry circuit are one or more of the following atrial structures: left lateral ridge (LLR), left …
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