Abstract
Atrial fibrillation (AF) is the commonest cardiac rhythm disorder, affecting about 5% of elderly patients.1 Despite the wide spread prevalence of AF, treatment options for the condition up until recently, were limited. Antiarrhythmic drug therapy which for a long time had been and to some extent still is the cornerstone for treating these patients, has shown a disappointing (≤ 40%) efficacy for long-term maintenance of sinus rhythm.2 The seminal observations by Haissaguerre and colleagues demonstrating AF initiation from electrical depolarizations in the pulmonary veins (PV) and cure of AF in these patients by radiofrequency ablation (RFA) of the PV focus, has led to the emergence of percutaneous catheter based AF ablation.3 Since its original description in 1998, the AF ablation procedure has evolved considerably.4-7 This evolution was the result of several short comings of the original technique (focal ablation) including the inability to expeditiously target multiple evanescent PV foci effectively and the long term consequences of delivering RF energy within the PVs i.e., occurrence of vein stenosis.8-12 Thus an alternative approach was developed where instead of ablating individual foci within the veins, RF lesions are delivered around the circumference of the PV ostium in order to interrupt PV-left atrial (LA) electrical connections and thus achieve PV isolation (PVI).8 Compared with focal AF ablation, PVI has shown a significant enhancement in long term arrhythmia control while dramatically reducing the occurrence of PV stenosis.11, 13 both of which are welcome developments. A potential reason for the enhanced success of PVI may be that the triggers of AF are clustered in close proximity to the vein ostia. However, an alternative explanation for the enhanced success of PVI is that the procedure inadvertently targets LA tissue (around PV os) and so results in modification of the underlying substrate. This hypothesis has been supported by the observation that anatomically guided circumferential PV ostial ablation without necessarily achieving true PVI (entry / exit block) is equally efficacious in achieving long term AF control.5,6 In fact, this observation has led to the development of an anatomically guided incremental ablation strategy which attempts to substantially modify the AF substrate by extensive LA ablation.14-16 However, such an approach has not consistently demonstrated a significant improvement in long term AF control rates as compared with PVI alone, which would suggest that PVs may be critical to the initiation and / or maintenance of AF.18,19 The purpose of this editorial is to provide the readers with a concise overview on the arrhythmogenic potential of PVs and to discuss how best we can identify and target such veins and whether that translates into long term control of AF.
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