Kadlec Regional Medical Center has opened the first-ever electrophysiology (EP) laboratory in the Tri-Cities area of Washington state, bringing a vital specialty to a population approaching 300,000. The new EP lab at Kadlec includes Carto 3 v3.2 (Biosense Webster, Inc., a Johnson & Johnson company), CardioLab v6.9 (GE Healthcare) with GE fluoroscopy, and the ACUSON SC2000 ultrasound system (Siemens Healthcare). From my prior position in Spokane, it was evident that the Tri-Cities area was underserved for EP services. Embraced by a very supportive group of referring cardiologists, and with Kadlec committed to building an outstanding facility, I welcomed the opportunity to relocate to the Tri-Cities and establish an EP program at Kadlec.
In designing the lab, we chose to partner with Biosense Webster and GE Healthcare because of the potential for integration of the electroanatomic mapping and recording systems, and intracardiac echo (ICE) with mapping and fluoroscopy. Even with the latest equipment, it is the outstanding staff who make our program successful. We have three dedicated EP technologists and designated nursing staff. Senior EP technologist Joe Dituri also moved from Spokane to build the Kadlec program, and his presence is vital to the smooth function of the lab as well as its capacity for complex ablation and high success rate with CRT. Our first ablation was performed February 26, 2014, and based on initial volumes, the lab is projected to perform 400 ablations within the first year of operation. We implanted the first subcutaneous ICD (S-ICD System, Boston Scientific) in the Tri-Cities on March 24, 2014, the first Reveal LINQ insertable cardiac monitor (Medtronic) in Washington state on March 24, 2014, and the first MRI-compatible single-chamber pacemaker (Entovis SR-T Pacemaker System, BIOTRONIK) implant in the United States on May 13, 2014.
Ablation of atrial fibrillation (AF) is our most frequently performed complex ablation. Our approach to ablation of persistent AF represents a confluence of the recent literature with evolving technical capability. Pulmonary vein isolation (PVI) may be considered the cornerstone of AF ablation for any AF pattern; however, recent studies identify the atrial substrate, rather than PVs, as a major source of persistent AF.1 This finding is consistent with identification of rotors as drivers of human AF.2 Recognition of the potential importance of substrate and rotors was easily anticipated, given that wavebreak occurs constantly during AF as high-frequency wavefronts encounter structural and functional heterogeneities, with fractionation resulting in localized conduction failure and the tendency for rotation.3 It seems self-evident that certain rotors may persist, acting as drivers of AF.
We recognize that the resolution of available mapping systems continues to be the Achilles heel of rotor mapping and ablation. Nevertheless, complex fractionated atrial electrograms (CFAEs) should be found in the core region of rotors,3 although CFAEs may also arise from other processes (discharging ganglionated plexi, heterogeneous conduction, wavelet collision). In this regard, ablation of CFAEs would likely interrupt the drivers of AF, with the most dense and tenacious CFAE nests being most important to AF maintenance.4 With this paradigm, Dr. Koonlawee Nademanee from White Memorial Medical Center in Los Angeles convincingly dismantles AF cases by systematically mapping and ablating CFAEs, with AF slowing, organizing and finally terminating. Considering the proven benefit of standard lesion sets5 and the ablation of certain CFAEs,4,6 tempered by the uncertain electrophysiologic origin of CFAEs, we have pursued a CFAE-guided approach to PVI and standard lesion sets during AF ablation. In this article, I would like to share our workflow for CFAE-guided PVI and AF ablation, which we anticipate will improve outcomes.
Techniques at Kadlec
We routinely acquire a pre-procedure CT of the LA and PV insertions. Unless patients have a cardiovascular implantable electronic device with monitoring ability for AF, I also strongly prefer to implant a Medtronic Reveal XT or LINQ ICM at least 4 weeks prior to ablation to obtain baseline AF burden, and subsequently to monitor the success of each ablation. This serves as an invaluable guide for discontinuation of antiarrhythmic medications, symptom correlation with any AF recurrence, and anticoagulation. We perform ablation with therapeutic INR; however, we prefer to hold the new oral anticoagulants (Xarelto, Eliquis, Pradaxa) pre-ablation, with the goal to resume full-dose therapy with the evening dose post-ablation. We do not use Pradaxa immediately post-ablation due to the lack of a reversal agent. All AF ablations are performed under general anesthesia, thereby minimizing patient motion for stable Carto mapping. Antiarrhythmic drugs are held at least 7 days prior to ablation, with amiodarone held as long as clinically reasonable. Antiarrhythmics are resumed immediately post-ablation, and discontinued following the 3-month blanking period unless significant breakthrough episodes are still occurring If so, discontinuation is considered based on the incidence of AF over the subsequent 3 months.
We use 4 Biosense Webster catheters, including the SoundStar ICE, CS, PentaRay, and Surround Flow (SF) ablation catheters, with SL1 transseptal sheaths. Patients with persistent AF typically present in AF; otherwise, AF is induced with burst pacing and maintained with low-dose isuprel as needed. The PentaRay catheter is first used to create RA geometry using fast anatomical mapping (FAM). During FAM, the Carto software is used to perform CFAE analysis of all EGMs recorded by the PentaRay, with simultaneous generation of an atrial scar map (<0.05 mV).7 The ablation catheter is advanced within the CS to incorporate this geometry, with the PentaRay subsequently used for CFAE mapping within the CS when proximal poles of the CS catheter display complex signals. Ablation targeting the most complex signals within the RA and CS is then performed (10-20W within the CS, 20-40W within the RA, 15 cc/min irrigation) with high-output pacing (10 mV, 10 msec) to assess for phrenic nerve capture along the lateral RA. Heparin bolus is given during RA studies, such that ACT >300 is achieved prior to transseptal puncture, minimizing the risk of thrombus formation within the arterial circulation. As a final step prior to transseptal puncture, ICE is used to create a preliminary LA geometry and localize the esophagus, and with care taken to mark the LPV carina.
As illustrated in Figure 1, the FAM of the CS and reference point at the LPV carina (Panel A) allow the CT image of the LA to be positioned precisely relative to the RA (Panel B). Following transseptal catheterization, generating the LA FAM (Panel C) is then like manipulating the PentaRay within a known geometry provided by the CT image. By preventing blind mapping of the LA, this workflow allows LA geometry to be obtained quickly and with certainty. We find the resulting geometry is often hardly distinguishable from the CT, likely due to less deformation artifact compared to traditional lasso catheters and the ability of the PentaRay splines to better align with LA contours. CT merge is therefore not needed and not performed. An added benefit of the PentaRay is less concern for entrapment in the mitral valve apparatus.
Figure 2 shows Carto displaying all left atrial EGMs meeting CFAE criteria (high [red dot] and medium [blue dot] confidence, default settings). We find CFAEs are typically scattered around the PV antra, with clusters found in 2-4 areas throughout the LA, which typically represents a combination of sites posterior to the LPVs, along the LA ridge, anterior to the LAA or RPVs, the interatrial septum, or along the LA floor adjacent to the CS. Comparison to the associated voltage map (not shown) indicates how CFAEs may correspond to regions of scar, serving as a further guide for effective ablation. After creation of the CFAE maps, the distribution of complex signals, as determined by the Carto software, suggests where antral PVI (Figure 3) and linear lesion sets (LA roof, mitral isthmus, CS isolation) may be placed to maximally interrupt CFAEs. By performing such CFAE-guided AF ablation, with creation of standard lesion sets as would otherwise be indicated by clinical circumstances, patients may also benefit from CFAE ablation without increased risk for macroreentrant tachycardias, as may sometimes occur after targeting CFAEs.6
If AF does not terminate during CFAE-guided ablation within the LA, the RA is revisited, with AF terminating on numerous occasions during ablation of remaining complex signals within the RA. Otherwise, ibutilide may be infused to simplify AF dynamics, allowing identification of remaining critical CFAE sites, which may then be revisited to complete the ablation. Following AF termination, block across ablation lines may be assessed. Figure 4 shows a successful case. The patient is a 64-year-old male originally referred for pacemaker implantation and AVJ ablation for permanent AF. Instead, dofetilide was started with implantation of a Reveal XT loop recorder to monitor AF, which demonstrated a paroxysmal AF pattern in the presence of an antiarrhythmic (Figure 4C). On this basis, AF ablation was performed in October 2013, with termination of AF occurring during ablation of CFAEs anterior to the LAA following CFAE-guided PVI (Panel A). Following termination, AF was completely non-inducible with atrial burst pacing, both under control conditions and following isuprel infusion. The Reveal XT continues to demonstrate no AF recurrence post-ablation (Figure 4C).
It is my belief that performing standard ablation lesion sets (PVI, linear lines) passing through regions of CFAEs is more effective than ablation performed on a purely anatomic basis. This CFAE-guided approach to AF ablation should be more effective, as it is more likely to neutralize non-PV mechanisms contributing to AF (GPs, rotors, regions of heterogeneity, atrial scar supporting focal ATs and micro-reentrant circuits). A randomized trial pursuing this hypothesis would be very interesting.
Disclosures: The author has no conflicts of interest to report regarding the article herein. Outside the submitted work, Dr. Kneller reports speaker bureau honoraria from Biosense Webster, BIOTRONIK, Boston Scientific, and Medtronic.
- Seitz J, Horvilleur J, Curel L, et al. Active or passive pulmonary vein in atrial fibrillation: is pulmonary vein isolation always essential? Heart Rhythm. 2014;11(4):579-586.
- Narayan SM, Krummen DE, Shivkumar K, Clopton P, Rappel WJ, Miller JM. Treatment of atrial fibrillation by the ablation of localized sources: CONFIRM (Conventional Ablation for Atrial Fibrillation With or Without Focal Impulse and Rotor Modulation) trial. J Am Coll Cardiol. 2012;60(7):628-636.
- Kneller J, Zou R, Vigmond EJ, Wang Z, Leon LJ, Nattel S. Cholinergic atrial fibrillation in a computer model of a two-dimensional sheet of canine atrial cells with realistic ionic properties. Circ Res. 2002;90(9):E73-E87.
- Nademanee K, McKenzie J, Kosar E, et al. A new approach for catheter ablation of atrial fibrillation: mapping of the electrophysiologic substrate. J Am Coll Cardiol. 2004;43(11):2044-2053.
- Haïssaguerre M, et al. Catheter ablation of long-lasting persistent atrial fibrillation: critical structures for termination. J Cardiovasc Electrophysiol. 2005;16(11):1125-1137.
- Oral H, Chugh A, Good E, et al. Radiofrequency catheter ablation of chronic atrial fibrillation guided by complex electrograms. Circulation. 2007;115(20):2606-2612.
- Verma A, Wazni OM, Marrouche NF, et al. Pre-existent left atrial scarring in patients undergoing pulmonary vein antrum isolation. J Am Coll Cardiol. 2005;45(2):285-292.