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Author + information
- Philipp Sommer, MD,
- Andreas Bollmann, MD, PhD and
- Gerhard Hindricks, MD∗ ()
- ↵∗Reprint request and correspondence:
Dr. Gerhard Hindricks, Department of Electrophysiology, University of Leipzig-Heart Center, Struempellstrasse 39, 04289 Leipzig, Germany.
Many approaches for ablation of persistent atrial fibrillation (AF) have been introduced in the past decade—many with promising initial results. However, most failed to be confirmed in larger, multicenter studies. Recently the STAR AF II (Substrate and Trigger Ablation for Reduction of Atrial Fibrillation II) trial demonstrated that more complex approaches are not superior to a “simple” pulmonary vein isolation (PVI)—even in persistent AF patients (1). A new idea for increasing success rates is to identify and ablate cores of rotating electrical activity, and the presence and potential importance of rotors in AF patients is currently heavily discussed. Several approaches with different technologies are available—one of them is the Topera system (FIRMap, Abbott, Abbott Park, Illinois). Here, a 64-electrode basket catheter is used for AF recordings sequentially in both atria—identified rotors or focal impulses are then targeted by conventional radiofrequency ablation.
In this issue of the Journal, Mohanty et al. (2) present the OASIS (Outcome of Different Ablation Strategies in Persistent and Long-Standing Persistent Atrial Fibrillation) study that addresses the question of whether focal impulse and rotor modulation (FIRM) alone is enough to treat patients with persistent or even long-standing persistent AF. In this prospective multicenter trial, they compared 3 different strategies: FIRM only, FIRM+PVI and PVI + posterior wall ablation + non-PV triggers. Three centers with experienced operators performed the procedures and an excellent follow-up with symptom-based event recordings and 7-day Holter monitoring at 3, 6, and 12 months was provided. A total of 113 patients were enrolled; the FIRM-only arm was prematurely stopped due to an interim data analysis and low success rates (this subgroup with 5.7 months of follow-up has been recently published by the same investigators ). The results seem clear: both FIRM arms are associated with longer procedure times compared with group 3: 222 min versus 233 min versus 131 min. In contrast, ablation time is highest in group 3: 35 min versus 42 min versus 54 min. The procedural data of the FIRM groups seem to confirm the findings of previous studies (4,5) using this technology: 1.5 rotors in the right atrium, 2.5 in the left atrium, with a typical distribution of rotor sites in both atria. The outcome of these patients shows freedom from AF/atrial tachycardia after 12 months in 14% versus 52% versus 76% while off antiarrhythmic drugs. The messages from OASIS are the following: 1) FIRM ablation only is not enough for persistent or even long-standing persistent AF patients; and 2) PVI+FIRM has acceptable results, but takes longer compared with empiric posterior wall ablation + ablation of non-PV triggers. Is it that easy? No, many questions have been raised by this important study.
The Problem of Reproducibility and the Role of Left Atrial Appendage Isolation
FIRM procedures are quite demanding in terms of signal interpretation (Figure 1). At this stage of development, there still might be a relevant interobserver variability in determining the sites of interest. The strategy that showed the best results in terms of procedure time and success rate will be difficult to be reproduced: PVI + ablation of the posterior wall with complete isolation of the “box” (crossing the esophagus usually 2 times), then delivering isoproterenol for 20 min to identify non-PV triggers with consecutive ablation in a total procedure time of 131 min. This will only be achievable in very experienced hands.
Furthermore, in 38% of the patients of group 3 the investigators found triggers in the left atrial appendage (LAA), which then was isolated. What about the thromboembolic risk in these patients? Some groups even recommend implantation of LAA occlusion devices or epicardial ligature of the LAA because anticoagulation alone might not be sufficient to prevent strokes after isolation of the LAA. What about the transport function of these atria after ablating the posterior wall and non-PV targets? In our experience, ablating the posterior wall with 35 W is rather aggressive, usually leading to significant temperature rises and esophageal lesions. The number of patients in this study (n = 42) is much too low to draw any conclusions on the safety aspect of this approach. But we would expect that problems with atrio-esophageal fistulas might occur if this approach were to be in widespread application.
“More is More”?
The findings of OASIS are in line with earlier studies by the Austin group showing benefits by adding the posterior wall ablation to PVI alone (6) and by targeting the LAA as a potential trigger in redo procedures (7). This is in a way contradictory to what was found in the STAR AF II trial, which showed almost identical outcome for the groups PVI versus PVI + complex fractional atrial electrogram (CFAE) versus PVI + lines (1), and to the Minimax trial, which also revealed that a straightforward PVI is not inferior to other ablation regimens (8). In the OASIS trial, the strategy delivering most ablation energy was the most effective with a combination of empiric (posterior wall) and mapped (non-PV triggers) targets.
We probably are forgetting an important factor in exploring our strategies: the patient. What if persistent AF does not require 1 uniform ablation approach? What if there are different types of AF irrespective of the clinical phenotype (paroxysmal and persistent)? Perhaps there is PV-dependent and non-PV-dependent AF. Perhaps there is a role of rotors that needs to be adequately addressed in a subset of patients. Perhaps antral isolation is more effective if ganglionated plexi are incidentally modulated; maybe CFAE ablation can be effective because fractionated electrograms are ablated in the border zone between normal tissue and fibrotic areas. Maybe we will even be able to visualize the substrate that needs to be addressed by mapping or by imaging modalities such as magnetic resonance imaging (DECAAF [Determinant of successful radiofrequency Catheter Ablation in Atrial Fibrillation] and DECAAF II study) (9).
Many open questions remain: which approach is the key to success and which approaches do merely incidentally hit the right spots? The candidates are PVI, rotors (mapped endo- or epicardially (10)), CFAE, ganglionated plexi, low voltage areas, empiric linear lesions, and non-PV triggers. The study by Mohanty et al. (2) gives us the following answer: the solution probably is a combination of these, but perhaps there is no single solution for all patients.
↵∗ Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology.
Dr. Sommer has received lecture fees and/or travel grants from St. Jude Medical, Biosense Webster, and Abbott Medical; and is a member of the advisory board of St. Jude Medical. Dr. Bollmann has received lecture fees and/or travel grants from Boston Scientific; and is a member of the advisory board of Boston Scientific. Dr. Hindricks has received research grants from St. Jude Medical and Boston Scientific.
- 2016 American College of Cardiology Foundation
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