Electrogram-Guided Ablation
Evan Lockwood
Koonlawee Nademanee
In 1994, Swartz et al. (1) ushered in an era of incredible growth in the understanding and treatment of atrial fibrillation (AF) with their introduction of a catheter-based MAZE procedure. Astute observations, such as those made by Haïssaguerre et al. (2), in the recognition of the importance of the pulmonary veins (PVs), have helped develop and refine the catheter-based MAZE to instead target triggers arising from the PVs. Several other laboratories around the world have worked extensively to create the best approach for the ablation of AF while focusing on the important role played by the PVs (3, 4, 5, 6). However, the weakness in this strategy is the assumption that all patients with AF have the same underlying mechanism. Certainly PV-related triggers play a significant role in patients who have paroxysmal AF, but this does not address the increasing numbers of patients who have persistent or permanent AF and who are now seeking ablative therapies. It behooves us to seek and understand the multiple components of AF triggering, initiating, and perpetuation that will allow us to tailor our procedure to the individual.
Mechanisms of Atrial FibrillationIdeally, one would eradicate triggers and eliminate or modify the substrate that initiates and perpetuates AF. Focusing on the elimination of triggers that are electrically active at the time of ablation is not sufficient given the possible interplay of other mechanisms—and these strategies have had only moderate success (7, 8, 9).
Triggers of AF include ectopic beats, which may arise from any area of the left or right atria, the superior vena cava (SVC), inferior vena cava (IVC), the coronary sinus (CS), or any of the four PVs (2,10, 11, 12). These abnormal impulses “trigger” an initiating rhythm, which may include an atrial tachycardia (AT), atrioventricular nodal reentry tachycardia (AVNRT), atrioventricular re-entry tachycardia (AVRT), or atrial flutter (AFl). Any of these arrhythmias or the triggers themselves may lead to an unstable AF, which depends on electrically abnormal substrate (predominately involving the left atrium [LA] and CS to perpetuate as stable AF) (Fig. 11.1). Strategies to abolish or modify the final common pathway in the development of AF should be the most
successful, but challenges still exist. Current methods of substrate modification rely on debulking atrial tissue with catheter-based lines of scar formed by widely encircling endocardial lesions created around PVs by radiofrequency (RF) ablation (3, 4, 5, 6), or by an open-chest ablation (endocardial or epicardial) or cut-and-sew method (13). Most techniques for the less-invasive catheter-based procedures still rely primarily on the idea of PV isolation and substrate modification only results secondarily. The era of “burn and learn” is coming to an end and now we must target our ablations to address the mechanisms behind AF. To this end, areas of complex fractionated atrial electrograms have been identified as important substrate targets whose elimination can result in successful treatment of AF (14).
successful, but challenges still exist. Current methods of substrate modification rely on debulking atrial tissue with catheter-based lines of scar formed by widely encircling endocardial lesions created around PVs by radiofrequency (RF) ablation (3, 4, 5, 6), or by an open-chest ablation (endocardial or epicardial) or cut-and-sew method (13). Most techniques for the less-invasive catheter-based procedures still rely primarily on the idea of PV isolation and substrate modification only results secondarily. The era of “burn and learn” is coming to an end and now we must target our ablations to address the mechanisms behind AF. To this end, areas of complex fractionated atrial electrograms have been identified as important substrate targets whose elimination can result in successful treatment of AF (14).
 Figure 11.1. The development of AF depends on the complex interaction of triggering impulses (often from the PVs), which initiate abnormal arrhythmias including AT, AVNRT, AVRT, AFl, or unstable AF. The final step in the perpetuation of stable AF requires interplay between an initiating arrhythmia and abnormal substrate. |
Definition of Complex Fractionated Atrial ElectrogramsComplex fractionated atrial electrograms (CFAE) are low-voltage signals (0.04-0.25 mV) defined as either: (a) atrial electrograms that are fractionated and
composed of two deflections or more and/or have a perturbation of the baseline with continuous deflections from a prolonged activation complex; or (b) atrial electrograms with a very short cycle length (≤120 ms) with or without multiple potentials when compared with the atrial cycle length recorded from other parts of the atria (14) (Fig. 11.2).
composed of two deflections or more and/or have a perturbation of the baseline with continuous deflections from a prolonged activation complex; or (b) atrial electrograms with a very short cycle length (≤120 ms) with or without multiple potentials when compared with the atrial cycle length recorded from other parts of the atria (14) (Fig. 11.2).
 Figure 11.2. CFAEs are composed of two deflections or more and/or have a perturbation of the baseline with continuous deflections from a prolonged activation complex; or are associated with a very short cycle length (≤120 ms). The ablation catheter (ABL d) is used to map and ablate the CFAE. The most highly fractionated electrograms can be seen in this example to exist on the LA septal wall although they still exist in the CS os and LIPV antrum. The local electrograms at the RSPV antrum are less fractionated, but have a very short cycle length and this may represent a “driver.” CS, coronary sinus; LA, left atrium; LIPV, left inferior pulmonary vein; RSPV, right superior pulmonary vein. |
Mechanisms of Complex Fractionated Atrial ElectrogramsThe underlying etiology of CFAE has not yet been elucidated, but several theories are being investigated. Pioneering work by Wells et al. (15) identified four types of atrial electrograms that may be present in AF:
Type I: Discrete complexes separated by an isoelectric baseline free of perturbation.
Type II: Discrete complexes but with perturbations of the baseline between complexes.
Type III: Fractionated electrograms that fail to demonstrate either discrete complexes or isoelectric intervals.
Type IV: Electrograms of Type III alternating with periods characteristic of Type I and/or Type II electrograms.
Konings et al. (16) applied this knowledge during intraoperative studies and identified three types of AF based on their mechanism of propagation:
Type I: Single broad-wave fronts propagating without significant conduction delay, exhibiting only short arcs of conduction block or small areas of slow conduction not disturbing the main course of propagation.
Type II: Activation patterns characterized either by single waves associated with a considerable amount of conduction block and/or slow conduction or the presence of two wavelets.
Type III: Presence of three or more wavelets associated with areas of slow conduction (<10 cm/s) and multiple arcs of conduction block.
Despite the elaborate descriptions of CFAE, a true explanation for their existence did not exist until very recently.
The work in sheep by Kalifa et al. (17), has shown a key relationship between areas of dominant frequency and areas of fractionation. They were able to localize areas with regular, fast, spatiotemporally organized activity and map the regions around them. Waves propagating from these areas were found to break and change direction recurrently at a boundary zone and demonstrate fractionation of local electrograms. One of the key electrophysiologic mechanisms for AF that was confirmed by their work relates to the hypothesis that high-frequency re-entry at the boundary zones is responsible for the fractionation.
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