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A Basket Full of Mechanistic Insights into Pulmonary Vein Arrhythmogenicity: Reentry, Focal Activity, or Fibrillatory Conduction?

Since the pioneering work of Haissaguerre et al.1,2 revealed the pulmonary veins (PVs) as the dominant source of atrial fibrillation (AF) almost a decade ago, numerous experimental and clinical electrophysiologists focused their research on mechanisms of PV arrhythmogenicity. Furthermore, the PVs as well as the PV-left atrial junction have become a target for morphological studies in both animal and human hearts. Reviewing the literature, we have learned that left atrial (LA) multilayer myocardial sleeves extend in a variable arrangement and distance into each PV resulting in a complex three-dimensional fiber orientation3,4 and that the “PV musculature” consist of specialized conduction cells similar to those found in the sinus node.5 In consideration of these anatomical findings, it is not surprising that PV conduction delay, nonuniform anisotropy, and fractionated electrograms correlate with myocardial fiber orientation and areas of discrete connective tissue.6,7 Moreover, distinctive electrophysiological properties have been described in human PVs with very short effective refractory periods (ERP), significantly shorter ERPs in the distal PVs than in the adjacent LA, and decremental conduction properties.8-10 Interestingly, these specific morphological and electrophysiological characteristics were found to be more pronounced in patients with AF than in those without.8,11 Since these distinctive PV properties support electrophysiologic mechanisms of both automaticity and reentry, experimental and clinical mapping studies have been performed to investigate by which mechanism(s) the PVs are arrhythmogenic. Zhou et al.12 demonstrated in canine PVs, using highdensity computerized mapping, repetitive focal activations with nonreentrant wavefronts originating from the middle of the PV, and propagating to the LA and distal PV with conduction block. Arora et al.13 performed high-resolution optical mapping of the PV and the PV-LA junction in a coronaryperfused canine atrium and demonstrated reentry within the vein, which could be sustained with isoproterenol. However, also nonreentrant focal activity has been observed under isoproterenol localized near the vein ostium. There are less data available on mapping of PV arrhythmogenicity in humans. Kumagai et al.14 demonstrated unstable reentrant activation fronts of up to two rotations with entry and exit at the PV-LA junction by the use of a 64-pole basket catheter. Takahashi