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Ann Thorac Surg 1996;61:1666-1678
© 1996 The Society of Thoracic Surgeons
Division of Cardiothoracic Surgery, Department of Surgery, and Division of Pediatric Cardiology, Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri
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Abstract |
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 TopFootnotes Abstract IntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Methods. After cardiopulmonary bypass, adult dogs (n = 18) underwent a simulated classic Fontan operation. This included a longitudinal right atriotomy and an incision from the base of the right atrial appendage toward the dome of the left atrium, representing the atriopulmonary connection. In 6 of 18 dogs, an atrial septal defect was created at the level of the fossa ovalis. Unipolar 253-point biatrial endocardial mapping electrodes were placed via bilateral ventriculotomies. Induction of AFL was attempted by atrial burst pacing. If AFL could not be induced, isoproterenol was administered and pacing repeated. Activation sequence maps of the pathways of atrial reentry were generated. In 8 dogs with inducible AFL, an incision was made from the atriotomy to the atriopulmonary connection and burst pacing repeated.
Results. Sustained AFL could not be induced after bypass alone in any case. After the simulated Fontan operation, sustained AFL was reproducibly induced in all 18 dogs, 6 of which required isoproterenol. The mean cycle length of all cases was 177 ± 20 ms. During AFL, atrial activation sequence maps demonstrated lines of conduction block created by both the atriotomy and the atriopulmonary connection. The isthmus of tissue between these two lines of block was essential for propagation of the reentrant wavefront. Interruption of this isthmus with an incision successfully terminated AFL in 8 of 8 dogs.
Conclusions. In an acute canine model, the Fontan suture lines alone, in the absence of atrial hypertension or stretch, permit the induction of AFL. An essential electrophysiologic substrate is an isthmus of myocardium between the atriotomy and the atriopulmonary connection. Interruption of conduction through this isthmus terminates the AFL in this model and suggests a technique for ablation of AFL in patients who have undergone a classic Fontan operation.
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Introduction |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Atrial flutter (AFL), or intraatrial reentrant tachycardia, is a common early and late postoperative complication of the classic Fontan operation, which uses a direct atriopulmonary connection (APC). A prevalence of atrial tachyarrhythmias approaching 40% has been reported with 10-year follow-up [1–4]. Although surgical modifications of the Fontan procedure that incorporate an intraatrial cavopulmonary baffle [5, 6] now comprise the primary forms of repair in children with a functional single ventricle, characterization of AFL after the Fontan procedure remains very important for numerous affected individuals. Atrial flutter is not well tolerated in patients with single-ventricle physiology. It may precipitate a reduction in cardiac output or sudden arrhythmogenic death [7]. The medical management of these arrhythmias is often ineffective and is associated with substantial side effects [8].
The electrophysiologic substrates for AFL after the Fontan operation have not been well defined. The development of reliable invasive ablative techniques mandates an intimate understanding of the reentrant circuit [9]. We have previously demonstrated in an acute canine model of total cavopulmonary connection that the suture lines alone were adequate to produce AFL [10]. Thus, we hypothesized that surgically induced barriers to atrial conduction after the Fontan operation, in the absence of hemodynamic alterations, provide the essential electrophysiologic substrates for AFL in this circumstance. The objectives of this study were to determine if the suture lines alone in the classic Fontan operation are sufficient to permit sustained AFL and to characterize any resulting reentrant circuits to surgically terminate the AFL.
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Material and Methods |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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). A right atriotomy was made from the mid-atrial appendage to proximal to the level of the sinus node artery, which, in the dog, arises in the lower right atrial free wall. The APC was mimicked with an incision extending from the base of the right atrial appendage toward the dome of the left atrium; no vascular anastomosis was performed, avoiding any circulatory alterations. In 6 of 18 dogs, an atrial septal defect (ASD) was created at the level of the fossa ovalis. The atriotomy and APC were closed with continuous 4-0 polypropylene suture.
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All animals received humane care in compliance with the ``Principles of Laboratory Animal Care'' formulated by the National Society for Medical Research and the ``Guide for the Care and Use of Laboratory Animals'' prepared by the National Academy of Science and published by the National Institutes of Health (NIH publication 86-23, revised 1985). In addition, the study protocol was approved by the Washington University Animal Studies Committee.
Pacing Protocol
Programmed extrastimulation and burst pacing were performed using a programmable pulse generator (Bloom Inc, Reading, PA). Stimulus input was set at twice pacing threshold. Atrial burst pacing was conducted at cycle lengths of 100 to 250 ms. Programmed extrastimulation was done using drive trains at cycle lengths of 200 to 300 ms with premature intervals of 100 to 200 ms. In all cases, attempts to induce AFL were made (1) after bypass alone and (2) after the atriotomy and APC were closed and the mapping electrodes inserted. Attempts to induce AFL were also made after only the atriotomy was performed, before completing the APC, in 3 cases. In 3 additional cases, the APC was made first and the induction of AFL attempted before creating the atriotomy. Sustained AFL was defined as a stable tachycardia of greater than 30 seconds in duration that exhibited a fixed atrial cycle length less than 250 ms. Termination of AFL was either by overdrive pacing or premature stimulation. Reproducibility was determined by reinduction of the tachyarrhythmia using the same extrastimulus pattern that originally induced it. In instances when sustained AFL was not inducible, isoproterenol (3 to 6 µg/kg) was administered and the pacing protocol repeated.
Surgical Ablation of Arrhythmias
In 14 dogs with inducible AFL, an effort was made to surgically ablate the arrhythmia. In 2 cases, a cryothermal lesion was placed in a linear and stepwise fashion from the atriotomy to the APC. In 8 cases, including those 2 in which a cryolesion was initially attempted, an incision was made from the atriotomy to the APC. A cryolesion followed by an incision was made from the inferior aspect of the atriotomy to the inferior vena cava (IVC) in another 2 cases. In 2 additional animals, an incision was made from the inferior extent of the atriotomy to the tricuspid annulus. An incision was placed between the inferior margin of the APC and the superior vena cava (SVC) in the 2 remaining animals. All incisions were closed with continuous 4-0 polypropylene suture. After each attempt at ablation, burst pacing was repeated.
Data Acquisition and Analysis
Atrial activation sequence data were obtained by simultaneously recording 253 unipolar electrograms from the endocardial multipoint electrodes. A limb lead electrocardiogram and a bipolar left atrial electrogram were simultaneously recorded. Data were recorded during spontaneous rhythm and during any sustained arrhythmia using a 256-channel computerized data acquisition and analysis system based on a VaxStation II/GPX graphics workstation (Digital Equipment Corp, Maynard, MA) connected to two 128-channel PDP 11/23+-based data acquisition subsystems. The system is run with in-house developed software (GLAS). Unipolar electrograms were recorded at a gain of 1,000 with a frequency response of 50 to 500 Hz. Each channel was digitized at 1,000 Hz with a 12-bit resolution. Local endocardial activation times were determined from the time of the maximum negative derivative of the unipolar electrogram. Computer generated activation sequence maps were reconstructed from all recordings. Data processing and three-dimensional interactive display were performed on a Silicon Graphics Iris 4D/320GTX high performance graphic workstation (Silicon Graphics Inc, Mountain View, CA). Activation sequence maps were displayed as real-time images on a three-dimensional surface model of the canine atria [11]. From these images, two-dimensional isochronous maps were created using previously established criteria [12].
Statistical Analysis
All values for each group are expressed as mean ± standard deviation. Statistical significance of all paired data was determined by Student's paired t test (SYSTAT 5.0; SYSTAT Inc, Evanston, IL). A p value less than 0.05 was considered statistically significant.
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Results |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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). The mean cycle length of all cases was 177 ± 20 ms. In animals in which an ASD was created, its presence did not alter the inducibility of AFL nor did it significantly affect the resultant cycle length (187 ± 15 ms with ASD versus 171 ± 20 ms without ASD; p = 0.08). No differences in cycle length or activation sequence patterns were present in those cases that required isoproterenol for the induction of AFL (173 ± 21 ms with isoproterenol versus 178 ± 19 ms without isoproterenol; p = 0.6). The tachycardia demonstrated the conventional clinical criteria of AFL. It was of fixed atrial cycle length, did not require ventricular participation, and could be induced and terminated by an atrial premature extrastimulus (Fig 2).
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Atrial Activation Sequence Maps During Sinus Rhythm and Atrial Flutter
During sinus rhythm, the endocardial site of earliest activation was near the sinoatrial node (Fig 3). The impulse spread in a centrifugal fashion toward both appendages. Conduction was not uniform on either side of the atriotomy, being somewhat more rapid in the isthmus of myocardium between the atriotomy and the tricuspid annulus. Activation propagation was uniformly equivalent on both sides of the ASD. The latest site of right atrial activation was located in the superomedial aspect of the right atrium.
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). The direction of rotation did not alter cycle lengths (182 ± 12 ms for clockwise rotation and 174 ± 22 ms for counterclockwise rotation; p = 0.38) or activation sequence patterns.
During AFL, lines of conduction block created by both the atriotomy and the APC were necessary for sustaining the tachycardia (Fig 4). The atriotomy created a corridor on the free wall between it and the tricuspid annulus. This corridor effectively lengthened the tachycardia circuit. The APC and a contiguous line of functional conduction block that extended to the tricuspid annulus created a blind alley, which blocked the wavefront from circulating around the tricuspid annulus. These lines of conduction block created an isthmus of myocardium between the atriotomy and APC, which was essential for propagation of the reentrant wavefront. The AFL impulse most often passed in the intercaval region. In certain instances, the pathway incorporated the IVC. In some cases, distinguishing whether the reentrant circuit used a path superior or inferior to the IVC was not possible from the activation sequence maps. Wavefront propagation across the septum was rapid and uniform. The ASD was not involved in the reentrant circuit.
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). The premature impulse, after colliding with the reentrant circuit on the septum, continued down the free wall and back onto the septal surface. It encountered a zone of refractory tissue proximal to the SVC, extinguishing the tachycardia.
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). When a premature depolarization from the right atrial appendage was delivered 130 ms after an eight-beat drive train, it encountered refractory tissue on the free wall distinct from either the APC or atriotomy. The wavefront subsequently conducted in a unidirectional fashion down the septum. By the time the unopposed rostrally moving wavefront traveled around the SVC, passed through the isthmus between the atriotomy and the tricuspid annulus, and arrived at the previously refractory region, the myocytes had recovered excitability, resulting in the onset of AFL. A premature interval of 140 ms in the same case was sufficiently long that refractory tissue was not encountered on the free wall. No functional unidirectional block occurred and the wavefront propagated simultaneously down the free wall and septum. The two impulses extinguished each other and reentry was not initiated (Fig 7).
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). In 2 of 2 cases, an incision between the inferior aspect of the atriotomy and the tricuspid annulus successfully terminated AFL. The same result was attained in 2 of 2 dogs with an incision between the inferior margin of the APC and the SVC.
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). An incision between the atriotomy and IVC similarly failed to ablate the AFL.
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Comment |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Although hemodynamic factors are probably important in the genesis of postoperative AFL, the present model of the classic Fontan repair supports the contention that surgically created barriers to conduction, independent of hemodynamic variables, are the fundamental electrophysiologic substrates of reentrant circuits. This has been manifested in numerous other animal models, including simulations of the total cavopulmonary connection [10] and the Mustard procedure [18], and also has been implicated clinically [19].
Substrates for Atrial Flutter After the Simulated Classic Fontan Operation
ANATOMIC AND FUNCTIONAL CONDUCTION BLOCK.
The atriotomy and the APC were both necessary components of the electrophysiologic substrate required for AFL. Atrial flutter could not be induced when either incision was created alone. These anatomic barriers resulted in conduction of the reentrant wavefront through a focal isthmus of myocardium between them. The surgically created ASD had no role in the tachycardia.
In addition to these anatomic boundaries, functional block was also critical in producing macroreentry. There was an area of functional block between the APC and the tricuspid annulus that could not entirely be accounted for by the position of the atrial incisions. Functional block occurs as a consequence of anisotropy of the cardiac muscle bundles or unequal dispersion of refractoriness [20]. The area of functional block served as an external barrier, which prevented convergent impulses from short circuiting the leading reentrant wavefront.
The boundaries of the reentrant pathway incorporate aspects of previous animal models of AFL. Rosenblueth and Garcia Ramos [21] produced reentrant excitation around a barrier consisting of an intercaval lesion in continuity with both caval orifices. Frame and associates [22] created a model of stable AFL by adding a Y-extension to the intercaval lesion with a contiguous incision in the right atrial free wall, which forced preferential localization of the reentrant circuit to the atrial tissue around the tricuspid ring [23]. In our model, similar to that of Frame and associates, the tricuspid annulus forms an integral anterior component of the circular reentrant surface, bounded superiorly by the inexcitable atriotomy. It is the posterior discontinuity that distinguishes the present model from those of Frame and associates and Rosenblueth and Garcia Ramos. The lack of an intercaval lesion eliminates the need of the reentrant pathway to necessarily travel around the IVC. The presence of the APC and continuous line of functional block to the tricuspid annulus forces the circuit to travel between the APC and the SVC, instead of taking the shorter route around the septal perimeter of the tricuspid annulus.
SLOW CONDUCTION.
Slow conduction was encountered around the free wall aspect of the SVC. Similar areas of slow conduction have been documented in other animal models of AFL [20, 24] and postoperatively in the atria of patients who have undergone a Fontan repair [25]. The zone of slow conduction, although crucial for reentry, was exterior to the actual reentrant circuit. It functioned as a region of passive discontinuity, permitting preferential conduction of the wavefront between the atriotomy and the tricuspid annulus. Were it not for this slow conduction, the resultant path between the atriotomy and the SVC would have been too short to sustain AFL. Rapid conduction of the circus wave in a shorter pathway encircling only the SVC was also prevented by a zone of slow conduction around the SVC in the canine with spontaneous AFL described by Boineau and colleagues [20].
DISPERSION OF REFRACTORINESS.
The temporal dispersion and spatial pattern of refractoriness have been implicated as the basis of functional conduction block integral in precipitating supraventricular tachyarrhythmias [20]. Repolarization inhomogeneity of adjacent atrial fibers can result in functional unidirectional conduction block if a premature stimulus is applied to the site of shorter refractory periods, permitting the initiation of reentry. Although this canine model presumably did not alter dispersion of refractoriness, initiation of reentry was dependent on it (see Fig 6). The functional conduction block, ie, the refractory myocardium, present at the inception of AFL was unrelated to the anatomic zones of conduction block created by the surgical procedure. Variation in the location of this block between dogs may explain the clockwise and counterclockwise rotation patterns of AFL.
Surgically created substrates provide areas of myocardial discontinuity that generate circuits able to sustain intraatrial reentrant tachycardia after the Fontan operation. However, the spontaneous initiation of postoperative AFL relies on factors superseding these fixed anatomic barriers. Atrial depolarizations may be the triggering events that, when combined with the asymmetric recovery of myocardial excitability, initiate reentry. Atrial refractory periods are prolonged by increased right atrial pressure [26]. It has also been demonstrated that the spatial distribution of refractoriness is markedly pronounced in enlarged canine atria with inducible AFL [16]. In patients who have undergone the Fontan operation, chronic atrial stretch and hypertension may alter dispersion of refractoriness [27] and increase the frequency of atrial premature depolarizations. The additive impact of these factors over time may account for the consistent decrease in arrhythmia-free survival that is so typical of this patient population [1–3].
Surgical Ablation of Atrial Flutter
By creating a line of conduction block between two nonconducting barriers that border a reentrant circuit, circus movement will be terminated. Elucidation of the flutter circuit in this canine model revealed four potential anatomic locations where the arrhythmia was susceptible to eradication (Fig 10): (1) between the atriotomy and the APC, (2) between the APC and the SVC, (3) between the atriotomy and the tricuspid annulus, and (4) between the atriotomy and the IVC.
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Although potential disadvantages accompany the other possible sites, they were used in several cases as a confirmation of the described pathway of atrial reentry. Although an incision from the atriotomy to the tricuspid annulus was successful in ablating the tachycardia, this technique must be viewed with caution in cases of AFL in postoperative Fontan patients, as their underlying pathology often involves atresia of the tricuspid valve, rendering accurate identification of the remnant annulus difficult. An incision from the SVC to the APC, although also successful as an ablative approach, may be technically more difficult.
Clinical Implications
Experience with the catheter ablation of AFL after the Fontan operation is limited, and the results have been modest. Several groups have used radiofrequency point lesions at the exit sites of slow conduction and have experienced high rates of arrhythmia recurrence [25, 28]. Anatomically guided approaches have yielded more success in the ablation of other forms of postoperative intraatrial reentrant tachycardia [19, 29]. The present study emphasizes that it is not necessarily the site of slowest conduction but rather the anatomic site of an isthmus between nonconductive barriers that is critical for successful interruption of a reentrant circuit. Clinical investigations are often hindered by the absence of true sequential atrial activation sequence mapping with an electrode density sufficient to clearly delineate areas of conduction disturbance, thereby making it difficult to rationally propose the length and orientation of a linear ablative lesion that will effectively interrupt the reentrant circuit.
There are no published reports of the surgical ablation of AFL after the Fontan operation. Operative strategies have generally focused on methods by which to alleviate the degree of right atrial enlargement and hypertension [5, 17]. The present study introduces the possibility that reentrant tachyarrhythmias after the classic Fontan may be terminated surgically. Our failure with the cryolesion, secondary to incomplete conduction block, and the high recurrence rates experienced by others after radiofrequency ablation raise questions concerning the inherent limitations of these less invasive approaches. In patients with AFL recalcitrant to pharmacologic therapy, an anatomically guided incision might be warranted.
Limitations of the Study
Caution must be exercised in extrapolating data from this study to patients with AFL after the classic Fontan. The animals in our model had normal cardiac anatomy. It is difficult to speculate how the anatomic and physiologic influences of complex congenital cardiac malformations, such as tricuspid atresia and hypoplastic left heart syndrome, may have influenced the results. Atrial flutter was induced by burst pacing and premature extrastimulation, raising the possibility that it was an artifact of stimulus technique.
As this was an acute study design, none of the alterations in atrial structure, such as hypertrophy and fibrosis, present chronically in patients who have undergone the Fontan operation were present. These histologic changes may also contribute to abnormalities in atrial conduction.
Finally, a large number of variations have been used to establish nonvalved continuity between the right atrium and the pulmonary arterial circulation in children with univentricular pathology [30–32]. These include varieties of anterior and posterior anastomoses of the right atrial appendage and the use of synthetic grafts and native pericardium. Such differences in technique would influence the boundaries of any resulting reentrant circuit. Unfortunately, specifics of surgical technique are not often included or compared in clinical discussions of AFL after the Fontan operation. That these specifics may be critically important is illustrated by the present study.
Conclusions
In an acute canine model, the Fontan suture lines alone, in the absence of atrial hypertension or stretch, permit induction of AFL. An essential electrophysiologic substrate is an isthmus of myocardium between the atriotomy and the APC. Interruption of conduction through this isthmus terminates the AFL in this model and suggests a technique for ablation of AFL in patients who have undergone a classic Fontan operation.
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Acknowledgments |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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This work was supported by National Institutes of Health grants HL 32257 and HL 33722.
Doctor Gandhi is a research fellow at Washington University. He is completing the clinical portion of his general surgery residency at St. Louis University.
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Footnotes |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Address reprint requests to Dr Huddleston, Department of Surgery, St. Louis Children's Hospital, One Children's Place, Suite 5W24, St. Louis, MO 63110.
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References |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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