The following activity is supported by an unrestricted educational grant from Biosense Webster a Johnson and Johnson company. Atrial fibrillation (AF) affects up to 5% of the population over the age of 65,1 and it is associated with manifestations ranging from palpitations to heart failure. The prevalence of this arrhythmia is increasing over time, with some projections estimating that by the year 2050, a total of 5.6 million Americans will suffer from AF.2 Thromboembolic events are the most feared complication of this disease; approximately 30% of strokes occurring in patients over the age of 65 can be attributed to AF. Furthermore, data from the Framingham study has shown that AF is an independent predictor of mortality, with a relative risk 1.5-1.9 times greater than that of patients without arrhythmia.3 The difficulty in treating patients with paroxysmal AF is that contrary to patients with a persistent form of the arrhythmia, they tend to be particularly symptomatic of abrupt rhythm changes. In these patients in whom rhythm control appears to be more desirable, pharmacologic treatment has traditionally been the first-line approach. The efficacy of antiarrhythmic drug therapy for the maintenance of sinus rhythm in AF patients ranges from 37-65% (when using amiodarone4), although often at the expense of significant side effects and cost. Even when some measure of control is achieved, approximately half of the patients will experience recurrences within a year. Additionally, all antiarrhythmics carry the potential risk of inducing proarrhythmia, which ranges from 1 to 6 percent.5 For these reasons, alternative methods of treatment have been sought. Different trials attempting to suppress AF with atrial pacing or more sophisticated overdrive pacing algorithms have shown mixed results with this form of therapy providing, at best, a reduction in the AF burden. Palliative measures such as ablation of the atrioventricular node and pacing have been effective in reducing the symptoms related to AF. However, it is important to bear in mind that this is by no means a curative strategy, and the persistence of AF requires that the patients remain anticoagulated. Furthermore, rendering patients completely pacemaker-dependent is not always an attractive proposition. Curative therapies are currently being developed both by surgeons and electrophysiologists based on either eliminating the initiating triggers for AF or modifying the substrate for its maintenance. Multiple reentrant wavelets are necessary for perpetuating AF. Surgical incisions (atriotomies) have been shown to prevent paroxysmal or chronic AF by depriving the wandering of wavelets of the spatial extent necessary for their persistence. The challenge for electrophysiologists has been to recreate the success of the surgical approach by using radiofrequency (RF) ablation catheters to create linear lesions in lieu of surgical incisions. However, linear ablation is limited by the fact that current catheters are designed to create point lesions, thus, the catheter must be dragged across the endocardium in order to create a complete line of block. This can be particularly difficult in the ridges and valleys of the posterior left atrium, and incomplete linear lesions may form the substrate for a reentrant arrhythmia.6 Recent studies have demonstrated that focal sources of ectopic activity are critical for patients with paroxysmal atrial fibrillation.7 In some patients, the sole abnormality consists of an ectopic focus that discharges for long periods (focally driven AF). In addition, these patients do not necessarily have the substrate for AF maintenance. In others, these ectopic foci act as triggers, which induce episodes of AF that subsequently continue independently of the initiating event (focally initiated AF). All these foci have one shared characteristic: a propensity to originate in the thoracic veins, particularly the four pulmonary veins (PV).8 These pulmonary vein foci can be targeted by percutaneous transcatheter techniques as well as isolating surgical atriotomies, thereby providing a curative therapy for AF. Though a surgical procedure creating lesions in the left atrium is clearly effective for PV isolation, this invasive approach is likely to be limited only to patients with other indications for cardiac surgery. Radiofrequency catheter ablation for the treatment of AF has evolved considerably over the last few years. The observation that, in the majority of cases, AF is initiated by foci from the myocardial sleeves of certain PVs (so-called arrhythmogenic PV) led to an ablation strategy targeting the site of earliest activity distally within the PV.8,9 However, if the patient had little spontaneous or inducible ectopy at the time of the ablation procedure, localizing this earliest site was time consuming.10 Multiple initiating triggers from the same or different veins were responsible for high recurrence rates and the need for repeated ablation procedures. Additionally, ablations performed as far as 5 centimeters within a narrow PV, carried an unacceptable risk of PV stenosis. For these reasons, this strategy has largely been abandoned in favor of a more systematic procedure targeting all PV ostia. In this instance, eliminating all PV potentials (PVPs) electrically, isolates the veins from the left atrium and carries a lower risk of inducing PV stenosis, while providing a more tangible electrophysiological endpoint to the procedure.11,12 Patient Preparation. Patients are anticoagulated orally for at least 1 month before the procedure, and a transesophageal echocardiogram is performed prior to the procedure in order to rule out left atrial (LA) thrombus. Procedural Setup. Our practice consists of placing a catheter in the coronary sinus (CS), which is used for pacing and recording. A circumferential decapolar catheter (Lasso, Biosense Webster, Diamond Bar, California) and an ablation catheter are used for the mapping and isolation of the PVs, and are introduced into the LA via transseptal catheterization or a patent foramen ovale. Selective PV angiography is performed by a hand injection of 5-10 mL of contrast, using an N.I.H. catheter, or a transseptal sheath to assess the size and to locate the ostia of all four PVs. Patients are anticoagulated during the procedure with a 50 IU/kg heparin bolus prior to ablation which is repeated after 3 hours. The transseptal sheath is continuously infused with heparinized saline (2,500 IU/250 mL) at a rate of 2.5 mL/minute, and is withdrawn to the right atrium whenever possible during the procedure, in order to minimize the potential risk of thromboembolic events. The circumferential mapping catheter is positioned as proximal as possible in each of the PVs. RF energy is controlled by a temperature setting of 50 °C with a power limit of 30W for right superior PV, left superior PV, right inferior PV; and a power limit of 25W for left inferior PV, because of the higher risk of PV stenosis in this vein. 1. Recognizing PV Potentials. Mapping catheters placed in the PVs may record local electrograms (PVPs) emanating from the muscular sleeve of tissue, as well as farfield potentials from adjacent cardiac structures. Farfield electrograms recorded in the left superior or left inferior PVs originate either from the left atrial appendage or the posterior LA.13 Similarly, potentials recorded in the right superior and right inferior PVs may include farfield potentials from the right atrium, superior vena cava, or posterior LA. During mapping of the left PVs, distinguishing between farfield and local PV activity can be difficult because the left PVs and the LA appendage are activated synchronously during sinus rhythm. In order to differentiate between the two, distal CS pacing is performed to separate PVPs from left atrial appendage activation. Thus, the pacing artifact is followed first by the atrial farfield potential and then by the PVP (Figure 1). Pacing maneuvers are of lesser importance in trying to distinguish between farfield potentials and right PVPs. This is because it is more difficult to separate the activation sequences, and the farfield signals are generally of lower amplitude, such that most of the potentials recorded are felt to originate within the vein. However, the timing of the potentials relative to the surface P wave is useful in that right atrial farfield potentials are synchronous with the first half of the P wave, while posterior LA farfield signals and PVPs occur later. Ultimately, one can distinguish farfield potentials recorded on a circumferential mapping catheter by placing the roving catheter at the suspected site of origin of the farfield potential. Signals recorded at this farfield site should be synchronous with those on the circumferential catheter. Pacing at this suspected farfield site will then make the potential recorded on the circumferential catheter synchronous with the pacing spike (Figure 2).14 The absence of proximal to distal activation, typically seen when dealing with true PVPs, can also be used as a distinguishing characteristic. Correctly identifying the PVPs is of primordial importance both in localizing the site of ablation and in recognizing the endpoint for PV electrical isolation. 2. Targeting PV potentials. Once properly identified, the PVPs can be targeted for ablation. A reasonable approach consists of first targeting the PV producing the most repetitive ectopy and/or inducing AF, in order to avoid initiations of sustained AF during the procedure. RF energy is then delivered to the other PVs sequentially. The goal of PV isolation is to electrically disconnect PVs from the left atrium, thus preventing propagation of triggering foci to the LA where they can initiate AF. Pulmonary vein isolation is performed during sinus rhythm for right-sided veins, and during distal coronary sinus pacing for left sided veins. This is achieved by targeting LA-PV breakthrough15 points, identified by the earliest PVPs recorded on the circumferential mapping catheter. Electrogram polarity reversal of the PVP can be used as an additional indicator of LA-PV breakthrough.16 The ablation catheter is then positioned as ostial as possible, and adjacent to the earliest PVP recorded on the circumferential mapping catheter. A fractionated activity bridging the interval between the atrial signal and earliest PVP is usually recorded on the ablation catheter, confirming the site of LA-PV breakthrough (Figure 3). Once again, it is important to note that the circumferential mapping catheter should be positioned as close to the PV ostium as possible, and RF delivery should be applied proximal to this to avoid PV stenosis. Application of RF energy at this site may be associated with an ablation artifact on the circumferential mapping catheter. When an ostial breakthrough point is successfully ablated, a change or a delay in the PV activation sequence is observed on the circumferential catheter (Figure 4). At this point, application of energy should continue for at least thirty seconds to ensure a complete ablation of this breakthrough site before displacing the ablation catheter to the next point. If ablation is rendered difficult by multiple early re-initiations of AF requiring electrical cardioversions, pulmonary vein isolation can alternatively be performed during ongoing AF.17 The activity recorded on the circumferential mapping catheter inside the vein typically varies but may be organized in up to 37% of cases with a consistent PV activation sequence, allowing for identification of ostial breakthrough sites either by targeting the earliest PV activity or a site of polarity reversal. When PV activation is chaotic, ablation is performed anatomically around the PV perimeter. During RF delivery, organization of the PV electrogram pattern occurs in about 75% of PVs, once again enabling direct targeting of breakthrough points using the PV activation sequence.18 Progressive or abrupt high-grade block of conduction between the LA and the PVs always occurs during ablation immediately preceding complete isolation, thus allowing for better distinction between farfield atrial signal and PV activity. Confirmation of PV isolation should always be obtained after the restoration of sinus rhythm (Figure 5). 3. Endpoints for PV isolation. Contrary to a purely anatomic approach, PV isolation using a circumferential mapping catheter has specific electrophysiological endpoints.12 There are two characteristic markers identifying electrical PV isolation: abolition or dissociation of PVPs. In the majority of cases, all the PVPs recorded on the circumferential mapping catheter are completely abolished (Figures 6, 7 and 8). It is important to bear in mind that farfield potentials may still be recorded within the PV after ablation, and the previously described maneuvers can be helpful in correctly differentiating any remaining PVPs from these farfield signals. A less frequently occurring event is PVP dissociation, which is encountered in 22% of superior PVs, and in 8% of inferior PVs. In these cases, electrical isolation has been achieved, and PV ectopic discharges can be seen on the recording catheters, but remain confined within the PV itself. These discharges have no relation to either atrial or ventricular activity (Figure 9). The extent of PV ablation required to obtain the aforementioned endpoints varies from a discrete PV segmental ablation in about 1020% of the veins (particularly in the left inferior PVs) to a fully circumferential ablation in 40% of the veins. These endpoints should always be reconfirmed at the end of the procedure. In certain cases, even after PV isolation has been successfully carried out, ectopic foci originating outside the PVs may also serve as triggers initiating AF.19 These non-PV foci are usually located in the posterior left atrium, the interatrial septum, the superior vena cava, the coronary sinus, and the right atrium. These can be mapped and ablated using standard activation mapping techniques. The potential complications for this procedure arise chiefly because of the risks associated with performing ablations in the left atrium. Significant complications related to PV isolation are thromboembolic events (14 Fortunately, these can be minimized through careful irrigation of the transseptal sheath, and whenever possible, withdrawing it to the right atrium, limiting the temperature at the catheter tip to 50 ºC, and judicious ablation at the PV ostium rather than more distally. Our practice consists of administering subcutaneous low-molecular weight heparin after the procedure, while oral anticoagulation is reinitiated. Patients are discharged on the third day following the procedure on oral anticoagulation. A CT-scan is performed at 6 months (or earlier in presence of symptoms) to assess the PV diameters. Additional ablation procedures for recurrence of AF are needed in about 50% of patients. These recurrences may be caused either by recovery of conduction in the PVs or by non-PV foci. Complete elimination of AF without drugs is observed in approximately 70% of patients using this approach. An additional 15% of patients remain free of AF using a previously ineffective antiarrhythmic drug, increasing the percentage of patients in sinus rhythm to about 85%.14 Anticoagulant treatment is stopped after three months of freedom from AF in the absence of other risk factors for thromboembolic events. Pulmonary veins play an important role in the pathogenesis of atrial fibrillation, and electrical isolation of these by catheter ablation can be curative in approximately 70% of patients. A careful analysis and understanding of pulmonary vein recordings is essential to successfully achieve PV isolation, as they can provide a clear endpoint to the procedure.