Author + information
- Philipp Sommer, MD∗ ()
- ↵∗Address for correspondence:
Dr. Philipp Sommer, Department of Electrophysiology, Heart Center, University of Leipzig, Struempellstrasse 39, 04289 Leipzig, Germany.
In an era of rapidly increasing numbers of procedures for managing atrial fibrillation, ablation of atypical atrial flutters has become a relevant topic in our clinical practice. Atypical flutters are a common secondary tachycardia, especially after complex ablation procedures with ablation of fragmented potentials or placement of linear lesions, as well as after surgical interventions using atriotomies. Understanding the mechanism and detecting the anatomical regions involved in the tachycardia circuit are mandatory for an effective and successful treatment of these arrhythmias. Multiple approaches have been described in the past, such as identification of the re-entry circuit by local activation time (LAT) mapping by using manual point-by-point annotation, use of entrainment maneuvers for identification of the tachycardia circuit (1), or empirical connection of nonconductive tissue by linear lesions. Strategies using manual annotation of signals are limited by the spatial resolution of the map; usually these conventional maps consist of 50 to 100 points, which are more or less equally distributed over both atria (surface areas: 80 to 120 cm2 for right atrium and 70 to 110 cm2 for left atrium) (2), resulting in a point density of approximately 1 signal/4 cm2 of tissue. With this limited coverage of atrial tissue, relevant information (e.g., characteristic electrograms with fractionation or late potentials but also visualization of wave-front propagation with adequate spatial and temporal resolution) could be missed.
Two major innovations have changed our approach to mapping these tachycardias: multielectrode mapping catheters, which allow simultaneous registration of multiple signals, and algorithms for 3-dimensional (3D) mapping systems, which enable automated annotation of these signals according to predefined criteria. When these 2 innovative approaches are used in combination with each other, they facilitate acquisition of true high-density maps within reasonable procedure times. In the current issue of JACC: Clinical Electrophysiology, Xue et al. (3) describe their experience with treating post-surgical atrial flutters by using 1 of the mapping technologies in combination with a 64-electrode basket catheter. In addition, the authors describe the step in which an adjustment is made to the window of interest to discriminate between true macro-re-entries and focal tachycardias with pseudomacro patterns (3). This maneuver is possible in the era of modern mapping systems where a relevant number of signals can automatically be reannotated, that is mapping criteria can be adjusted, and the new mapping information using the “old” points is available within seconds. By doing so, most tachycardias can be mapped, understood, and successfully ablated with excellent outcome during follow-up as previously described (4).
One of the questions arising from this study is whether these new tools are true innovations in the field of ablation for atypical flutters. The answer is yes and no. The answer is yes if by using these new options we can annotate thousands of electrograms and acquire fascinating mechanistic insights (Figure 1). The autoannotation algorithms work well, and multielectrode mapping catheters are easy and safe to use. However, the answer is no if just putting a 64-electrode basket in both atria and collecting 5,000 points will not result in a red arrow on the display of our 3D mapping systems that points at a spot where ablation will terminate all tachycardias within 10 s. The operator still must understand the mechanistic aspects of the tachycardia by looking at electrograms, analyzing post-pacing-intervals, assessing scar regions in the atria, and deciding about the potential mechanism of the tachycardia. In contrast to pulmonary vein isolation procedures using cryoablation, for example, in which even operators with limited understanding and experience with electrophysiology could achieve quite satisfying results, ablation of atypical atrial flutters requires a fully educated and experienced operator.
In the paper by Xue et al. (3), the main mechanism of macro-re-entry tachycardia was typical, isthmus-dependent right atrial flutter in 53% of patients, an arrhythmia which probably also could have been identified by analyzing coronary sinus activation and performing entrainment maneuvers using distal and proximal coronary sinus bipoles.
Clearly, having access to these new tools offers great opportunities to better understand tachycardia mechanisms, both in the atria and in the ventricles. However, these innovations will not automatically generate answers to our clinical questions. Patient histories, results of pacing maneuvers, and well-educated electrophysiology specialists still are mandatory ingredients for successful therapies, even in times of high-density mapping. In addition to descriptive studies like the one by Xue et al. (3), we clearly need convincing data that demonstrate clinical benefits in terms of hard endpoints in prospective studies comparing “old-school mapping” with the new tools. These endpoints will not be the number of mapping points or duration of radiofrequency applications but nothing else than periprocedural complication rates and rhythm stability during follow-up, the only endpoints that matter to our patients. Clarification certainly is needed if maps with several thousand mapping points really do translate into improved patient outcomes, especially if the economic aspects of multipolar mapping tools are taken into account.
Also, we must be aware of differences between the technological platforms, perhaps even comparisons among mapping systems could make sense. Some of the unique algorithms may be of clinical benefit in ablation of premature ventricular complexes but not in ablation of atypical atrial flutters. It is all about personalized treatment strategies!
↵∗ Editorials published in JACC: Clinical Electrophysiology reflect the views of the authors and do not necessarily represent the views of JACC: Clinical Electrophysiology or the American College of Cardiology.
Dr. Sommer has received research support from Abbott; and is a member of the advisory boards for Abbott and Biosense Webster.
The author attests he is in compliance with human studies committees and animal welfare regulations of the author’s institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the JACC: Clinical Electrophysiology author instructions page.
- 2018 American College of Cardiology Foundation
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