doi: 10.1161/CIRCULATIONAHA.106.686741
(Circulation. 2007;115:1698-1700.)
© 2007 American Heart Association, Inc.
Editorial |
The Fontan Right Atrium—In Context
From the Duke University School of Medicine, Durham, NC.
Correspondence to Ronald J. Kanter, MD, Duke University Medical Center, Duke North, Erwin Road, Room 7502, Box 3090, Durham, NC 27710. E-mail kante001{at}mc.duke.edu
Key Words: Editorials • ablation • atrial flutter • atrium • electrophysiology • Fontan procedure • tachyarrhythmias
The original vision for what is still eponymously called the Fontan operation was to provide a subpulmonary pumping chamber for patients who lack 2 functional ventricles.1 Thus began the era of the original atriopulmonary (or atrioventricular, in some patients who have tricuspid atresia) anastomosis. Beginning with de Leval’s seminal paper in 1988, which demonstrated that hydrodynamic advantage is conferred by surgical strategies that limit the interposition of atrial mass,2 the phylogeny of Fontan-style operations has gone through several iterations. Currently favored is the extracardiac conduit, which results in the case where the entire atrial mass serves as the low-pressure pulmonary venous receptacle. The occurrence of atrial tachyarrhythmias long-term after these operations seems to parallel the magnitude of right atrial dilatation and hypertension. Not surprisingly, comparisons of medium-term incidences of atrial tachyarrhythmias have shown that the total cavopulmonary connection (also known as the "lateral tunnel," in which only a posterolateral portion of the right atrium is at pulmonary artery pressure) is better than the atriopulmonary (or atrioventricular) connection,3,4 and that the extracardiac conduit is better than the total cavopulmonary connection.5,6 Consistent with these clinical series is evidence for mechanoelectrical interactions within the enlarged right atria. Compared with asymptomatic Fontan patients, patients who have atrial tachyarrhythmias have longer P wave durations, greater P wave dispersions, and larger atrial dimensions.7
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Abrams and colleagues report in the current issue of Circulation the story of electroanatomic mapping of the giant, high-pressure right atrium long-term after the atriopulmonary (or atrioventricular)-style Fontan operation.8 No histopathological-electrophysiological models of this entity exist in the literature. As the authors endeavor to compare a contact electroanatomic mapping (EAM) system to a non-contact mapping (NCM) system to define scar, viable myocardium, and reentrant circuits, they use results from animal models of experimental myocardial infarction9,10 and other series of human atrial flutter mapping11–13 for validation of definitions. The methodologies in this paper reflect the authors’ considerable experience with both systems, and they meticulously account for the putative strengths of each. The methods of comparison of reconstructed electrograms are based on well-validated algorithms or principles, and statistical analyses are appropriate. Before discussion of their conclusions, however, 2 aspects of this work deserve further comment: the definition and relevance of "scar" and "abnormal myocardium," and the practical limitations of the noncontact multielectrode array (MEA) for tachycardia circuit mapping.
There remains debate about the electrical definition of scar in the postoperative right atrium. When electrogram (EGM) amplitudes from the right atria of patients who have AV nodal reentrant tachycardia, focal atrial tachycardia, atrial flutter, or postoperative intra-atrial reentry tachycardia (IART) are compared, de Groot et al showed that only patients with IART had bipolar EGMs <0.1 mV in amplitude, which prompted that value as the scar cutoff.14 (As will be discussed later, unipolar EGMs <1.0 mV were present both in patients who have lone atrial flutter and in those who have IART.) Others have used 0.05 mV11–13 as the bipolar voltage cutoff,11–13 partially on the basis that this value is the noise limit of the CARTO contact EAM system (Biosense Webster, Diamond Bar, Calif). Only in the paper by Jaïs et al was the inability to pace capture those locations also used to validate the designation of scar.11 Unlike the infarcted left ventricle from animal models, in which there is a more homogeneous nature of the injury (and good electropathological correlates), the pathology of the Fontan right atrium is heterogeneous. Seven years after a total cavopulmonary connection in a patient, Yoshikawa et al showed that the high-pressure portion of the right atrium was thicker, contained fewer myocytes per volume, and had larger areas of interstitial fibrosis than in the lower-pressure portion.15 Whether such tissue can generate >0.05 mV of local endocardial bipolar voltage and also sustain conductivity is unclear. Nakagawa et al recorded voltages as low as 0.04 mV in a right atrial IART circuit from a Fontan patient and validated the conduction vitality of such sites with an interruption of IART with radiofrequency energy.16 Furthermore, the walls of these right atria tend to be heterogeneous in thickness, sometimes with regions up to 20 mm in depth. The propensity for conduction to be preserved epicardially versus endocardially in such sites is unknown, which makes the interpretation of very low-amplitude bipolar EGMs difficult.
The amplitudes of unipolar EGMs either from the contact electrode or as derived from the MEA are not as influenced by the direction of the conducting wavefront as bipolar EGMs, but they confer few other advantages for the definition of tissue viability. Although they are usually larger in amplitude than their associated bipolar counterparts and may be better able to identify a deeper conducting fiber, they are very much influenced by unwanted far-field events. Although unipolar EGMs were not thought to be useful in the definition of scar by de Groot et al,14 the specificity of EGMs <1.0 mV in this patient group has not been fully explored. In the present report by Abrams and colleagues, the poor correlation between "scar" and "abnormal tissue" as defined for the 2 mapping systems is appropriately explained by the geometric limitations of the NCM system, and not by the relative merit of its unipolar EGM-derived dynamic substrate mapping. That said, bipolar EGMs from EAM should not necessarily be crowned the gold standard for this particular task.
Few anatomic structures exist in postoperative congenital heart disease with dimensions as great as those of the Fontan right atrium. Likewise, few substrates can be identified that support multiple reentrant tachycardia circuits like the right atrium after the atriopulmonary connection. Therefore, a mapping system that provides accurate and rapid isopotential data from brief time segments of these tachycardias is highly desirable. As originally reported by Schilling and colleagues,17 the NCM system EnSite (St. Jude Medical, St. Paul, Minn) instantaneously computes >3300 endocardial points by mathematical resolution of far-field (intracavitary) unipolar potentials at the MEA. Though tantalizing for Fontan patients, this technique is frustrated by certain anatomic irregularities that create line-of-sight interference, and, germane to the Fontan patient, by blood-endocardial boundaries >4 cm from the MEA. Using previously validated methods, Abrams et al elegantly show that unipolar EGMs derived by this technique only correlate well with unipolar EGMs from the contact catheter at sites <4 cm from the MEA. (As acknowledged by the authors, the use of the contact catheter’s unipolar EGM as the control is only flawed in this study by failure to prove adequate endocardial contact with impedance monitoring.) Hence, in the giant right atrium, the NCM system can only provide accurate information within these geometric limits. Before the MEA is deployed, the practitioner is well advised to use magnetic resonance imaging or radiographic techniques to measure the right atrium in all dimensions. If the right atrium is >8 cm in diameter in any dimension, prior knowledge of the most likely sites of slow conduction critical to IART circuits may then direct proper positioning of the MEA. This amounts to a degree of circular reasoning. In fact, to enable accurate data acquisition from all portions of such a right atrium, the MEA may need to be repositioned multiple times with obligatory geometric reconstructions.
The authors conclude that contact mapping with bipolar electrograms is superior to the NCM technique for arrhythmias late after the Fontan procedure. Their contention is well supported by this work when applied to complete delineation of the arrhythmia’s anatomic circuit. Whether this should be the first priority of patient care relates more to the goals of electrophysiological testing in these patients. Complete circuit definition is rarely required for successful identification of zones of slow conduction as targets for IART ablation. After all, in the present report, successful ablation was achieved in 16 of 19 patients in whom NCM was "at least as good" as EAM. Even in early small experiences with the NCM system for IART in Fontan patients, Betts et al18 and Paul et al19 reported short-term success in 4 of 6 and in 2 of 3 patients, respectively. Therefore, even with previous comments as caveats, the spirit of the authors’ conclusions may be a bit harsh if it includes implied condemnation of the NCM technique.
In context, "early returns" suggest that the newer Fontan techniques will result in fewer atrial arrhythmias than the atriopulmonary connection. Analogous to arrhythmias associated with the now passé Mustard and Senning operations for simple transposition of the great arteries, the troublesome arrhythmias in classic Fontan patients described here will likely diminish in frequency as these patients age and pass on. However, the information gained from these patients will live in perpetuity, which will ultimately benefit those who suffer from currently unimagined arrhythmia substrates. In the words of Ralph Sockman: "The larger the island of knowledge, the greater the shoreline of wonder."
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Acknowledgments |
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Disclosures
None.
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Footnotes |
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The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.
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References |
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- Gelatt M, Hamilton RM, McCrindle BW, Gow RM, Williams WG, Trusler GA, Freedom RM. Risk factors for atrial tachyarrhythmias after the Fontan operation. J Am Coll Cardiol. 1994; 24: 1735–1741.[Abstract]
- Fishberger SB, Wernovsky G, Gentles TL, Gauvreau K, Burnett J, Mayer JE Jr, Walsh EP. Factors that influence the development of atrial flutter after the Fontan operation. J Thorac Cardiovasc Surg. 1997; 113: 80–86.
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