Role of Functional Block Extension in Lesion-Related Atrial Flutter
Background—A line of block in the right atrium (RA) between the venae cavae is necessary to obtain classic atrial flutter (AFL). We tested the hypothesis that the location of that line of block would determine whether the AFL reentrant circuit would be due to single-loop reentry or figure-of-8 reentry.
Methods and Results—Simultaneous mapping from 392 sites (both atria and the atrial septum) was performed in 13 normal dogs before and after creating a linear lesion on the RA free wall. The lesion was 1 to 1.5 cm anterior and parallel to the crista terminalis (7 dogs) or posterior and close to the crista terminalis region (6 dogs). Sustained AFL (>2 minutes) was then induced. In 4 dogs with an anterior lesion, the AFL reentrant circuit traveled around the lesion (lesion reentry). In 9 dogs (3 with anterior lesions and 6 with posterior lesions), the AFL reentrant circuit included the anterior RA free wall, the atrial septum, and Bachmann’s bundle (single-loop reentry). In these 9 dogs, the fixed line of block was extended to the superior and/or inferior vena cava by a functional line of block, thereby preventing lesion reentry. No figure-of-8 reentry was induced.
Conclusions—In this model, the location of a fixed line of block and its functional extension determine the type of AFL reentry. These data provide an explanation for the chronic AFL that occurs in some patients after surgical repair of congenital heart lesions.
Aline of block, functional or fixed anatomic, in the right atrial free wall between the venae cavae is recognized as being necessary to obtain stable classic atrial flutter (AFL).1 This was first shown by Rosenblueth and Garcia Ramos,2 who created a crush injury between the venae cavae in the canine heart and then were able to induce stable AFL. Since that time, others3 4 5 have studied the same or a similar model to investigate AFL in an otherwise normal heart. When this model was modified by Frame et al6 to form a Y-shaped lesion in the right atrial free wall, the AFL reentrant circuit was confined to the tricuspid ring. When a crush lesion was made to form a line of block in the anterior right atrial free wall by Feld and Shahandeh-Rad,7 AFL limited to reentry around the line of fixed block was induced. The model of Feld and Shahandeh-Rad can be likened to AFL due to incisional reentry, ie, reentry around a fixed anatomic obstacle, which is sometimes seen after surgical repair of a congenital lesion in which at least 1 incision was made in the right atrial free wall.8 9 10 11
Nevertheless, in a series of 21 episodes of AFL that occurred chronically in 19 patients after surgical repair of congenital heart disease, we have shown that most often (in 15 of the 21 episodes), the AFL was due to a classic AFL reentrant circuit rather than incisional reentry.12 Also, we have shown in the canine sterile pericarditis AFL model that when the line of functional block between the venae cavae is posterior in the right atrial free wall, generally parallel to and close to the crista terminalis, it is associated with the presence of classic single-loop reentry AFL.13 However, when the line of functional block between the venae cavae is more anterior in the right atrial free wall, it is associated with figure-of-8 reentry AFL. We designed a study in normal canine atria to help clarify these relationships and to test the hypothesis that a posterior location of the line of block in the right atrial free wall would result in induced single-loop reentrant AFL, whereas an anterior location would result in figure-of-8 reentrant AFL.
All studies were performed in accordance with guidelines of our Institutional Animal Care and Use Committee, the American Heart Association Policy on Research Animal Use, and the US Public Health Service Policy on Use of Laboratory Animals. In 13 normal adult mongrel dogs weighing 17 to 24.5 kg, the heart was exposed under general anesthesia and mechanical ventilation as previously described.13 14 Stainless-steel wire electrodes for pacing, recording, or monitoring were sutured on the right ventricle, right atrial appendage, and posterior-inferior left atrium. Radiofrequency catheter ablation of the His bundle was then performed to create complete atrioventricular block,13 14 followed by ventricular pacing at a rate of 60 to 100 bpm.
Creation of Right Atrial Free Wall Lesion
In each dog, an attempt to induce AFL was made before the creation of any lesion. A linear lesion in the right atrial free wall was then created by epicardial cryoablation (10 dogs), crush (1 dog), or surgical incision with suture repair (2 dogs). The lesion was 1 to 1.5 cm anterior and parallel to the crista terminalis (anterior lesion group) in 7 dogs and in the crista terminalis region (posterior lesion group) in 6 dogs (Figure 1⇓). Before cryoablation was performed, two 4-0 Prolene stay sutures were placed 2 to 2.5 cm apart both to mark the location and the length of the lesion to be created and to lift the atrial free wall to permit placement of a DeBakey-Satinsky vena cava clamp. To create a cryolesion in the beating heart, an ≈5-mm width of atrial tissue was first gently clamped over the extent (length 3 cm) of the clamp. After the tissue was clamped in all 11 dogs, induction of AFL was attempted. In 1 dog (No. 9, Table⇓), because sustained AFL was induced after the tissue was clamped, no cryoablation was performed, and this was considered a crush lesion. In the other 10 dogs, a series of cryoablation lesions were performed with the use of a 5-mm-diameter cryoprobe and cryosurgical system at a temperature of −80°C for 5 minutes each. The first cryoablation application was placed at the site of one of the stay sutures. After 3 side-by-side applications of the cryoprobe (cryolesion ≈1.5 cm long), an attempt was made to induce AFL. If unsuccessful, the length of the lesion was extended by the diameter (5 mm) of the cryoprobe from the initial length until either sustained AFL was induced or at least 6 applications with the cryoprobe were made and completed. To create a surgical lesion with the heart beating, an ≈5-mm width of atrial tissue was gently clamped by using the vena cava clamp (DeBakey-Satinsky). A surgical incision was made on the clamped tissue, which then was repaired with continuous suture (4-0 Prolene). This was extended in 1 dog until AFL could be induced.
Simultaneous mapping from 392 sites in both atria was performed. An epicardial electrode array containing 372 unipolar electrodes arranged in 186 bipolar pairs (95 for the right atrium, 77 for the left atrium, and 14 for Bachmann’s bundle) was used as previously described13 14 (Figure 1⇑). The interatrial septum was also mapped simultaneously with the epicardial sites by using a single 24-polar electrode catheter (Bard) with an interelectrode distance of 1 mm, placed as previously described13 14 (Figure 1⇑). We recorded from the proximal 20 electrodes of the 24-polar electrode catheter during septal recording.
Data were recorded and processed by our cardiac mapping system.14 15 16 Atrial electrograms from both atria and the interatrial septum along with ECG lead II were recorded during sinus rhythm and induced sustained AFL after creating the right atrial free wall lesion. AFL was induced by rapid atrial pacing from one of the atrial stainless-steel electrode sites at a rate of 400 to 600 bpm for at least 2 seconds.13 The length of fixed block was measured during a paced or spontaneous atrial rhythm first by mapping the sequence of atrial activation, then by identifying the line of block,14 and then by establishing its length by using the known distances between the electrode recording sites.17 Then the shortest distance between the superior and inferior ends of the line of block and the superior vena cava (SVC) and inferior vena cava (IVC), respectively, were measured.
Data were expressed as the mean±SD (range). Statistical analysis was performed with an unpaired t test for comparison of means. A value of P<0.05 was considered statistically significant.
Definitions are as follows: (1) line of fixed block, a line of block created by cryoablation, clamping, or a surgical incision and present during sinus rhythm or atrial pacing; (2) line of functional block, a line of block not caused by a lesion or another anatomic obstacle and not present during a sinus or paced atrial rhythm; (3) sustained AFL, AFL lasting ≥2 minutes; (4) single-loop reentry AFL, AFL due to a reentrant circuit consisting of the anterior right atrial free wall, atrial septum, and Bachmann’s bundle; (5) lesion reentry AFL, AFL due to a reentrant circuit consisting of activation around a right atrial free wall lesion; and (6) figure-of-8 reentry AFL, AFL in which 2 reentrant circuits (single-loop reentry and lesion reentry) are present and share the anterior right atrial free wall as a common pathway.
Before creating a lesion, no sustained AFL was induced. After a lesion of sufficient length was made, sustained AFL was induced in all dogs.
Effects of a Posterior Lesion
Figure 2A⇓ shows a representative example of an activation map and selected atrial electrograms during sinus rhythm after a posterior right atrial lesion was created by cryoablation (dog 12, Table⇑). The earliest atrial activation began in the sinus node region close to the SVC. Wave fronts traveled from the earliest activation site toward the right atrial appendage and toward the IVC. The later wave front turned around the inferior aspect of the lesion, advanced upward, and merged with the wave front crossing the superior aspect of the lesion. Electrograms a through d, recorded from recording sites a through d shown on the activation map, show conduction across the inferior aspect of the lesion, no double potentials, and a low amplitude potential at a site (site b) very close to the cryolesion.
Figure 2B⇑ shows the activation map and atrial electrograms recorded from the same sites from the same dog as shown in Figure 2A⇑ during induced AFL due to single-loop reentry. The AFL reentrant circuit travels up the anterior right atrial free wall and down the atrial septum, with breakthrough to the epicardium in the peri-IVC region and reentry into the septum at Bachmann’s bundle. Double potentials were recorded at sites b and c, indicating the presence of a line of block. Note also that each potential of the double potential corresponds to activation on either side of the area of block (sites a and d). The line of block that extended from the inferior end of the fixed anatomic lesion to the IVC was functional, inasmuch as there was no line of block there during sinus rhythm (Figure 2A⇑). In this example (Figure 2B⇑), a similar line of functional block extended from the superior end of the fixed anatomic lesion to the SVC. Thus, during induced AFL, each end of the line of fixed anatomic block became extended to the IVC and SVC by a line of functional block.
In all the posterior lesions, the induced AFL reentrant circuit consisted of single-loop reentry. In 2 dogs, the reentrant impulse traveled around the reentrant circuit in either direction during induced AFL episodes (Table⇑, bidirectional). In all, the fixed line of block was extended to the SVC and/or IVC by a line of functional block (Table⇑). In 4 of 6 dogs, the line of functional block extended from each end of the lesion to the SVC and IVC, respectively; in 1 of 6, it extended from the superior end of the lesion to the SVC; and in 1 of 6, it extended from the inferior end of the lesion to the IVC (Table⇑).
Effects of an Anterior Lesion
Figure 3⇓ shows a representative example of an activation map and selected atrial electrograms during AFL due to a reentrant circuit that traveled around an anterior lesion. Another potential reentrant circuit (denoted by a dashed line with arrows) consisted of activation from the right atrial free wall, entry to the atrial septum in the peri-IVC region (black asterisk), inferior-to-superior septal activation, and epicardial breakthrough at Bachmann’s bundle (Figure 3⇓, white asterisk). This potential figure-of-8 reentry did not develop, because the activation wave front that traveled around the inferior aspect of the lesion (solid black line) arrived at the superior pivot point relatively early compared with activation from the atrial septum via Bachmann’s bundle. Also shown are atrial electrograms from selected sites recorded during AFL: a through g from epicardial sites around the lesion, h through j from sites in the atrial septum, and k and l from sites in Bachmann’s bundle. Activation arrives at site e before it arrives at site k, preventing figure-of-8 reentry.
In 4 of 7 dogs in the anterior group (Table⇑), only lesion reentry AFL was induced, with another potential reentrant circuit present as just described. However, in 3 of 7 dogs in this group (Table⇑), single-loop reentry AFL was induced just as in the posterior group. This occurred because a line of functional block extended from each end of the lesion to the SVC and IVC, respectively, in 1 dog and from the superior end of the anatomic lesion to the SVC in the other 2 dogs. In sum, in the anterior group, the AFL was due to lesion reentry in 4 dogs and single-loop reentry in 3 dogs. In the 3 latter dogs, a line of functional block extending from the lesion to one or both venae cavae was present, preventing lesion reentry.
Comparison of Selected Characteristics of Induced AFL
The Table⇑ shows the characteristics of the lesions and the induced AFL in each group. There was no significant difference in the length of the lesions or AFL cycle lengths between groups. However, the mean cycle length of AFL due to single-loop reentry was significantly longer than that of AFL due to lesion reentry (152±16 versus 128±7 ms, respectively; P<0.05). The mean length of the line of functional block (9 dogs with single-loop reentry) between the lesion and the closest vena cava was 1.2±0.3 cm (range 0.4 to 1.6 cm). In the dogs with lesion reentry AFL, the mean gap between the end of the lesion and the closest vena cava was 1.6±0.3 cm (range 1.2 to 2.2 cm). Although there was overlap in the range between these measurements (lines of functional block length in single-loop reentry AFL versus gap length in lesion reentry AFL), the mean of 1.6±0.3 cm for lesion reentry was significantly longer than the mean of 1.2±0.3 cm for single-loop reentry (P<0.05).
Critical Role of Functional Block
The present study demonstrates once again that a line of block between the venae cavae is critical for the development of classical AFL. However, the present study also provides important new and clinically useful insights into the nature of that block in the presence of a lesion. First, single-loop reentrant AFL occurred when the line of fixed block was extended to either or both venae cavae by a line or lines of functional block. This occurred regardless of whether the fixed block was anterior or posterior in the right atrial free wall and prevented an activation wave from turning around the fixed lesion, thereby preventing either figure-of-8 reentry or lesion reentry.
Second, although figure-of-8 reentry did not develop in the presence of an anterior right atrial free wall lesion in this model, the potential for figure-of-8 reentry was there (Figure 3⇑). However, the lesion reentry circuit had a cycle length sufficiently shorter than the activation time of the wave front of the potential reentrant circuit using the atrial septum, so that daughter wave fronts from the lesion reentry circuit collided with the former wave front, which traveled via the atrial septum. Therefore, no figure-of-8 AFL was present. This is clearly different from that described for the sterile pericarditis model.13 The reason for this difference is suggested from comparisons with the data from previous studies of induced AFL in the latter model. In those studies, the mean AFL cycle length in figure-of-8 AFL was 157 and 159 ms, respectively.13 18 However, in the present study, the mean cycle length of AFL due to lesion reentry was 128 ms. This difference between models may be explained by differences in the length of the line of block, conduction velocity around the line of block, or both. Review of the data suggests that it is primarily, if not entirely, explained by differences in conduction velocity as a result of the pericarditis. Thus, this difference between the results in the canine sterile pericarditis model and the lesion model in normal atria serves to emphasize the importance of substrate in the pathophysiology of arrhythmias.
Mechanism of Development of Functional Block Extension
The mechanism of functional extension of the line of fixed block is not explained in the present study. It is known from experimental and simulation studies that many factors may play a role, including anisotropic conduction, the rapid atrial rate during induction of the arrhythmia, and curvature of the activation wave front around the ends of the fixed line of block.19 20 21 We know that conduction across the isthmus between either end of the lesion and its respective vena cava was possible because it occurred during sinus rhythm or atrial pacing at rates in the range of sinus rhythm. However, when a wave front has to turn around the end of a line of block, the arc of curvature determines the nature of conduction at this pivot point.19 20 21 We suggest that it is likely, if not probable, that at the high rate of pacing used to induce AFL in the present study, the arc of curvature around the end or ends of the line of block was so severe that conduction around it could not be sustained. In any event, a definitive explanation requires further study.
Implications for AFL Associated With Surgical Repair of Congenital Lesions
We believe that these observations have important clinical and theoretical implications. For a long time, it has been recognized that several open-heart surgical procedures to repair congenital heart lesions, including the complex (Mustard, Senning, Fontan) and the simple (ASD repair), are associated with an important incidence of chronic postoperative AFL.22 23 24 AFL in these instances sometimes may be due to incisional reentry.8 9 10 11 However, as we have recently shown,12 in these circumstances, AFL is probably more often due to reentry involving the classic AFL isthmus. The present study provides insight into why the latter often happens. Surgical incisions and/or suture lines placed as part of the surgical repair in the right atrial free wall in the region between the venae cavae may not, of themselves, be long enough to create the critical line of block between the cavae, which leads to the development of AFL. However, when a line of functional block between one or both ends of the lesion and one or both of the venae cavae develops, eg, as the result of activation from ≥1 premature atrial beats or a run of atrial fibrillation, the substrate to support stable AFL may then be realized.
There are still further clinical implications that logically follow the insights from the present study. One is to modify the nature of incisions and suture lines placed as part of the surgical repair so that a functional line of block from the “surgical lesion” to one or both of the venae cavae will not develop. For example, this could include modifying the atriotomy (length, direction, or both). A second implication is that perhaps a prophylactic ablation of the AFL isthmus between the inferior venae cavae and the tricuspid ring should be performed to avoid the subsequent development of classic AFL.12 Another implication is that in the presence of incisional reentry, simply extending the atriotomy lesion to one or both venae cavae may eliminate incisional reentry only to promote classic AFL using the flutter isthmus.
Finally, there is the implication for ablative treatment of incisional reentry AFL. Although an option may be to prevent lesion reentry by extending the line of fixed block with a radiofrequency line of block to one of the venae cavae, one may thereby simply change lesion reentry to single-loop reentry AFL.
This study was supported in a part by grant RO1-HL-38408 from the US Public Health Service, National Institutes of Health, National Heart, Lung, and Blood Institute, Bethesda, Md.
- Received February 18, 2000.
- Revision received August 25, 2000.
- Accepted August 31, 2000.
- Copyright © 2001 by American Heart Association
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