CLINICAL STUDIES
Transverse conduction capabilities of the crista terminalis in patients with atrial flutter and atrial fibrillation
Burghard Schumacher, MDa,
Werner Jung, MD, FACCa,
Harald Schmidta,
Christoph Fischenbecka,
Thorsten Lewalter, MDa,
Andreas Hagendorff, MDa,
Heyder Omran, MDa,
Christian Wolpert, MDa and
Berndt Lüderitz, MD, FACCa
a Department of Cardiology, University of Bonn, Bonn, Germany
Manuscript received September 21, 1998;
revised manuscript received March 6, 1999,
accepted April 15, 1999.
Reprint requests and correspondence: Dr. Burghard Schumacher, University Hospital Mannheim, University of Heidelberg, Theodor-Kutzer-Uber 1-3, 68167 Mannheim, Germany.
burghard.schumacher{at}med2.ma.uni-heidelberg.de
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Abstract
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OBJECTIVES
In this study, the transverse conduction capabilities of the crista terminalis (CT) were determined during pacing in sinus rhythm in patients with atrial flutter and atrial fibrillation.
BACKGROUND
It has been demonstrated that the CT is a barrier to transverse conduction during typical atrial flutter. Mapping studies in animal models provide evidence that this is functional. The influence of transverse conduction capabilities of the CT on the development of atrial flutter remains unclear.
METHODS
The CT was identified by intracardiac echocardiography. The atrial activation at the CT was determined during programmed stimulation with one extrastimulus at five pacing sites anteriorly to the CT in 10 patients with atrial flutter and 10 patients with atrial fibrillation before and after intravenous administration of 2 mg/kg disopyramide. Subsequently, atrial arrhythmias were reinduced.
RESULTS
At baseline, pacing with longer coupling intervals resulted in a transverse pulse propagation across the CT. During shorter coupling intervals, split electrograms and a marked alteration of the activation sequence of its second component were found, indicating a functional conduction block. In patients with atrial flutter, the longest coupling interval that resulted in a complete transverse conduction block at the CT was significantly longer than that in patients with atrial fibrillation (285 ± 49 ms vs. 221 ± 28 ms; p < 0.05). After disopyramide administration, a transverse conduction block occurred at longer coupling intervals as compared with baseline (287 ± 68 ms vs. 250 ± 52 ms; p < 0.05). Subsequently, a sustained atrial arrhythmia was inducible in 15 of 20 patients. This was atrial flutter in three patients with previously documented atrial fibrillation and in eight patients with history of atrial flutter. Mapping revealed a conduction block at the CT in all of these patients.
CONCLUSIONS
It was found that the CT provides transverse conduction capabilities and that the conduction block during atrial flutter is functional. Limited transverse conduction capabilities of the CT seem to contribute to the development of atrial flutter.
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Abbreviations and Acronyms
| | CT | = crista terminalis | | ERPtrans | = effective refractory period for transverse conduction |
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It is well established that typical atrial flutter is a macroreentrant rhythm localized to the right atrium (1–4). In animal models as well as in humans, it has been demonstrated that the atrial flutter reentrant circuit is determined by right atrial barriers to conduction (5–13). One of the conduction barriers during atrial flutter that has been identified is the crista terminalis (CT) (14). It has been suggested that this is anatomically fixed. However, mapping studies in animal models provide evidence that transverse conduction across the CT occurs in normal hearts (15,16). The transverse conduction capabilities of the CT have not been investigated in patients with history of atrial flutter.
In contrast to atrial flutter, the mechanism of atrial fibrillation has not been fully elucidated. However, recent studies support the multiple wavelet hypothesis of Moe (17) and the concept that atrial fibrillation involves a critical number of re-entrant wavelets (18,19).
It has long been recognized that some patients with recurrent atrial arrhythmias exhibit exclusively episodes of atrial flutter and others exclusively episodes of atrial fibrillation. Limited data are available concerning potential electrophysiologic conditions that are prone to the development of either atrial flutter or atrial fibrillation. Conversely, spontaneous or drug-related organization of atrial fibrillation into atrial flutter is well known (20). Studies in the sterile pericarditis canine model have provided evidence that the spontaneous conversion of atrial fibrillation to atrial flutter is determined by an increase in length of the line of functional block in the right atrial free wall (21).
The present study was performed to determine potential conduction across the CT in patients with history of atrial flutter and atrial fibrillation and to clarify a potential role of the CT in predisposing for the development of atrial flutter. Specifically, the CT was identified using intracardiac echocardiography (14,22,23). Subsequently, the transverse conduction capabilities of the CT were determined during pacing in normal sinus rhythm in patients with history of either atrial flutter or atrial fibrillation.
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Methods
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Study population.
This study included 26 patients (8 women, 18 men; mean age, 62 ± 7 years; range, 51 to 72 years) with atrial tachyarrhythmias who were referred to our institution for electrophysiologic study and catheter ablation of typical atrial flutter or atrioventricular node modification/ablation in drug-resistant atrial fibrillation. Eight patients had atrial enlargement, defined as a right atrial mediolateral diameter >3 cm in the apical view or a left atrial posteroanterior diameter >4 cm in the parasternal view. All patients had undergone coronary angiography. Seven patients had hypertensive heart disease and two patients had coronary artery disease. Left ventricular ejection fraction was normal in all patients. None of the patients had evidence of intracardiac thrombus formation, as assessed with transesophageal echocardiography. Ten patients (3 women, 7 men; mean age, 63 ± 8 years; range, 51 to 72 years) had documented recurrent typical type I atrial flutter (24). They had experienced at least two episodes of atrial flutter throughout the last six months. The flutter cycle length was 230 ± 22 ms (range, 210 to 280 ms). None of these patients had evidence of additional atrial fibrillation. Sixteen additional patients (5 women, 11 men; mean age, 62 ± 5 years; range, 54 to 69 years) had recurrent episodes of atrial fibrillation. At least one episode had been documented. None of the patients had evidence of additional arrhythmias.
Electrophysiologic study.
All patients gave informed written consent according to the protocol approved by the local Committee on Human Research. Antiarrhythmic drug therapy was discontinued for a duration of at least five half-lives. None of the patients was administered amiodarone for the last six months. All patients were in a fasting state and mildly sedated with midazolam. Twenty-two patients were in sinus rhythm at the onset of the electrophysiologic study; four patients were in typical atrial flutter.
If atrial flutter was present, sinus rhythm was re-established by atrial overdrive pacing. In normal sinus rhythm, a baseline electrophysiologic study was performed. Subsequently, a 10-F 10-MHz intracardiac ultrasound catheter (Cardiovascular Imaging System, San Jose, California) was inserted through a femoral vein and advanced to the right atrium to identify the CT. Images were obtained with a Vingmed ultrasound system (Santa Clara, California) and recorded on videotape. Two steerable 7-F decapolar catheters with an interbipole spacing of 5 mm and an interelectrode spacing of 2 mm were inserted in the femoral vein and advanced through an 8-F long introducer sheath (SRO, Daig, Minnesota) into the right atrium. One of these catheters was positioned under echocardiographic guidance along the CT. This catheter was used for determination of transverse conduction across the CT and is referred to as the CT catheter. The distal bipole was designated as Pair 1. The subsequent bipoles were numbered 2 through 5 in sequence. Pair 1 referred to the superior aspect of the CT, Pair 5 to the inferior aspect. The second decapolar catheter was positioned under fluoroscopic guidance parallel and 0.5 to 1.5 cm anteriorly to the CT catheter. This catheter was used for pacing. A typical catheter position is illustrated in Figure 1.
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Figure 1 A 60° right anterior oblique (A) and a 30° left anterior oblique (B) fluoroscopic view of the heart showing typical positions of the intracardiac echocardiographic catheter (ICE), the mapping catheter along the crista terminalis (CTMap) and the pacing catheter approximately 0.5 to 1.0 cm anteriorly to the crista terminalis (Pace).
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Endocardial bipolar electrograms were recorded from each catheter with a filter bandwidth of 30 to 500 Hz simultaneously with 12-lead surface electrocardiograms and stored digitally on a Lab System (Bard, Boston, Massachusetts). Pacing maneuvers were performed with a rectangular stimulus pulse of 1-ms duration at twice diastolic threshold amplitude (UHS20, Biotronik, Berlin, Germany). During normal sinus rhythm, programmed atrial stimulation was performed with one extrastimulus (10-ms decrement) at six different pacing cycle lengths (700, 600, 500, 400, 333, 300 ms) at each bipole of the pacing catheter positioned anteriorly to the CT. Accordingly, five pacing sites were used for analysis. For each pacing site, atrial activation at the CT was determined at each bipole of the CT catheter. Subsequently, a dose of 2 mg/kg disopyramide was administered intravenously. The pacing protocol was repeated then to determine drug-related changes of transverse conduction parameters. Finally, the pacing catheter was advanced into the coronary sinus. Atrial tachyarrhythmia was reinduced by programmed atrial stimulation at the coronary sinus orifice. During atrial tachyarrhythmia, pulse propagation at the CT and the coronary sinus was documented. After acquisition of all data, catheter ablation of atrial flutter, atrioventricular node modification or total atrioventricular junction ablation was performed.
Definitions.
During pacing, atrial activation at the CT was continuously recorded at the CT catheter. During baseline pacing, we determined the transverse conduction time by measuring the interval between the onset of atrial activation at corresponding opposite bipoles of the pacing and the mapping catheter and the longitudinal conduction time by measuring the interval between the onset of atrial activation at two subsequent bipoles of the mapping catheter. Split potentials were defined as two discrete deflections per beat separated by an isoelectric interval. When split potentials were found, separate measurements were made for each component. When the occurrence of split potentials was associated with a late activation of the second component of this split potential, this was interpreted as functional conduction block at the given site. In contrast, a continuous local activation with an activation sequence from the pacing site toward both ends of the CT or a simultaneous activation at all CT mapping sites was interpreted as transverse conduction across the CT. The effective refractory period for transverse conduction (ERPtrans) of the CT was defined as the longest coupling interval during programmed stimulation that resulted in a complete functional conduction block at the CT. The ERPtrans at a given bipole of the CT catheter was determined by pacing via the corresponding opposite bipole of the pacing catheter.
Statistical analysis.
All data are reported as the means ± 1 SD except when noted otherwise. Continuous variables were analyzed with a Student t test for paired or unpaired data and categorical variables by Fisher exact test. A p value <0.05 was considered statistically significant.
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Results
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Twenty-six patients were enrolled in this study. In six patients with previously documented atrial fibrillation, pacing during sinus rhythm resulted in sustained atrial fibrillation. These patients were excluded. The complete pacing protocol was performed in 20 patients who were used for analysis. In all patients, an adequate catheter position along the CT was documented by intracardiac echocardiography (Fig. 2).
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Figure 2 Intracardiac ultrasound images demonstrating the localization of the crista terminalis (CT) as well as an adequate (A) and an inadequate (B) position of the crista terminalis mapping catheter (Map) during a typical investigation. Images were obtained at the mid-right atrium inferior to the entrance of the right atrial appendage. Orientation of the images is labeled on top. IAS = interatrial septum; ICE = artifact of the intracardiac ultrasound catheter.
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Transverse conduction across the CT.
During pacing with longer pacing cycle lengths anteriorly to the CT, continuous endocardial activation could be recorded at all CT mapping bipoles in all patients. The activation showed a sequence from the pacing site toward both ends of the CT, which was identical on both sides of the CT. Accordingly, the intervals between atrial activation at a given pacing bipole and the corresponding opposite mapping bipole were almost identical along the entire length of the CT, giving no evidence of a localized conduction block resulting in a spread of activation on the posterior side of the CT, and thus, indicating the presence of a transverse conduction across the crista. An example is shown in Figure 3A. In some patients with progressive shortening of the coupling interval, the width of the potentials was progressively prolonged (Fig. 3B). During baseline pacing, the transverse conduction time between two opposite bipoles was considerably longer (35 ± 17 ms) than the longitudinal conduction time between two subsequent bipoles of the mapping catheter (14 ± 10 ms), despite the fact that the distances were comparable (11 ± 5 mm vs. 11 mm) (Table 1). This gave strong evidence for anisotropy at the CT with a fast pulse propagation conduction in the longitudinal direction and a slow pulse propagation in the transverse direction.
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Figure 3 Recordings obtained during programmed stimulation in sinus rhythm (baseline cycle length S1–S1, 500 ms) approximately 0.5 cm anterior to the crista terminalis at bipole 1/2 of the pacing catheter (Patient #10). The surface leads I, II and III and the intracardiac electrograms recorded at successive bipoles of the pacing (Pace) and the crista terminalis (CT) mapping catheter are shown. Bipole 1/2 refers to the most superior and bipole 9/10 to the most inferior pair of electrodes. Catheter position as in Figure 1. (A) Baseline pacing with a pacing cycle length S1–S1 of 500 ms as well as an atrial premature beat with a coupling interval S1–S2 of 430 ms resulted in continuous electrograms at all bipoles of the CT catheter. The width of local activation was relatively short, for example, 50 ms at bipole CT1/2. The atrial activation at the CT showed a sequence from the pacing site at the superior aspect of the right atrium toward the inferior right atrium (arrows). (B) A decrease of the coupling interval S1–S2 from 430 to 310 ms resulted in a significant prolongation of local activation, for example, from 50 ms to 80 ms at bipole CT1/2, indicating a conduction delay. Two components (A and B) of the fractionated potentials could be distinguished. However, no isoelectric interval was present and the activation sequence remained unchanged. (C) After extrastimulus testing with a further 20 ms decrement of the coupling interval (S1–S2, 290 ms), local electrograms at the CT mapping catheter showed a marked prolongation, for example, 105 ms at bipole CT1/2, and the two components became separated by an isoelectric interval. With the occurrence of split potentials, a marked alteration of the activation sequence of the second component of split potentials was found. As can be appreciated from these findings, a conduction block developed at the CT mapping catheter that was not present during atrial premature beats with longer coupling intervals.
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Table 1 Interval (Mean ± SD) Between the Onset of Atrial Activation at Two Subsequent Bipoles of the Crista Terminalis Mapping Catheter (Top) and at Two Opposite Bipoles of the Pacing and the Mapping Catheter (Bottom)
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Conduction block at the CT.
With further shortening of the coupling interval, split potentials were recorded at the CT catheter (Fig. 3C). The occurrence of split potentials was always associated with a marked shift of the activation sequence of the second component of the split potentials, whereas the activation sequence of the first component and the longitudinal conduction time remained unchanged. The interval between atrial activation at a given pacing bipole and the second component of the corresponding mapping bipole was long at mapping sites where split potentials were present, whereas it was short at sites with continuous activation, indicating an activation sequence from areas with continuous activation toward areas with split potentials (Fig. 4). Accordingly, each component of the split potentials could be interpreted as atrial activation on both sides of a functional conduction block at the CT that was not present during baseline pacing. Split potentials were found in 18 of 20 patients. In the presence of a functional block, activation sequences from low to high (Fig. 4), as well as from high to low (Fig. 5), were found on the posterior side of the CT. However, when split potentials occurred, they were not necessarily found along the entire extent of the CT (Fig. 6). When a localized conduction block had occurred, progressive shortening of the coupling intervals resulted in an increase of the length of the functional block. The longest coupling interval that was followed by a complete conduction block at the CT was defined as ERPtrans. The individual ERPtrans are presented in Table 2.
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Figure 4 Recordings obtained during programmed stimulation in sinus rhythm (baseline cycle length S1–S1, 600 ms; coupling interval S1–S2, 250 ms) at bipole 1/2 of the pacing catheter (Patient #6). Surface leads I, II and III and intracardiac electrograms recorded at successive bipoles of the pacing (Pace) and the crista terminalis (CT) mapping catheter are shown. Bipole 1/2 refers to the most superior pair of electrodes, bipole 9/10 to the most inferior. Catheter position as in Figure 1. Baseline pacing resulted in the occurrence of broad but continuous atrial activation at all CT mapping bipoles, suggestive for transverse pulse propagation across the CT. After extrastimulus testing with a coupling interval of 250 ms, split potentials with an isoelectric interval were recorded, indicating a functional conduction block at the CT. The first component of the split potentials represents the depolarization of the anterior aspect of the CT, the second component that of the posterior aspect, respectively. In the presence of conduction block, the pulse propagation at the posterior right atrium shows a sequence from low to high (arrow). Two components (A and B) of the fractionated potentials could be distinguished.
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Figure 5 Recordings obtained during programmed stimulation in sinus rhythm (baseline cycle length S1–S1, 500 ms; coupling interval S1–S2, 190 ms) at bipole 9/10 of the pacing catheter (Patient #11). Recordings, abbreviations and catheter position as in Figure 4. In this example, occurrence of a functional conduction block at the CT resulted at the posterior right atrium in a pulse propagation from high to low (arrow).
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Figure 6 Recordings obtained during programmed stimulation in sinus rhythm (baseline cycle length S1–S1, 500 ms; coupling interval S1–S2, 330 ms) at bipole 5/6 of the pacing catheter (Patient #7). Recordings, abbreviations and catheter position as in Figure 4. This figure illustrates a typical example of a localized conduction block at the central aspect of the CT. As can be seen, baseline pacing at bipole 5/6 results in a spread of activation from the pacing site toward both edges of the CT mapping catheter. After extrastimulus testing with a coupling interval of 330 ms, split potentials were recorded at bipole 5/6 and bipole 7/8 of the CT mapping catheter. The activation sequence of the first component of split potentials was identical to that during baseline pacing. However, the activation sequence of the second component indicated two wavefronts colliding at bipole 5/6. The descending wavefront emerges from bipole 1/2, the ascending wavefront from a site inferior to bipole 9/10.
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Table 2 Longest Coupling Interval That Resulted in a Functional Conduction Block at the Crista Terminalis During Programmed Atrial Stimulation
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Transverse conduction in patients with atrial flutter and atrial fibrillation.
The ERPtrans were analyzed separately for patients with history of atrial flutter and those with history of atrial fibrillation. The ERPtrans of the CT were longer in patients with atrial flutter, as compared with those with atrial fibrillation. The mean ERPtrans of the CT was 285 ± 49 ms in patients with atrial flutter and 221 ± 28 ms in patients with atrial fibrillation (p < 0.05). Correspondingly, at a given coupling interval, the length of the line of functional block in patients with atrial flutter exceeded that observed in patients with atrial fibrillation. However, the overall incidence of localized conduction block did not differ significantly with regard to the underlying arrhythmia. For both patient groups, the ERPtrans at each mapping bipole are listed in Table 3.
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Table 3 Longest Coupling Interval That Resulted in a Conduction Block at the Crista Terminalis in Patients With Atrial Flutter Versus Atrial Fibrillation
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Transverse conduction after disopyramide administration.
Intravenous administration of disopyramide resulted in an increase of ERPtrans in all patients. No differences in the amount of increase were found regarding the underlying arrhythmia. The average ERPtrans before and after disopyramide administration are listed in Table 4. After disopyramide administration, a sustained atrial tachyarrhythmia was inducible by programmed stimulation in 15 of 20 patients. This was typical atrial flutter with inverted flutter waves in leads II, III and a ventricular fibrillation in three patients with previously documented atrial fibrillation and in eight patients with history of atrial flutter. Mapping revealed a conduction block at the CT in all of these patients.
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Table 4 Longest Coupling Interval That Resulted in a Conduction Block at the Crista Terminalis Before and After Administration of 2 mg/kg Disopyramide
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Discussion
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Main findings.
In this study, pulse propagation across the CT was investigated during pacing in sinus rhythm. The findings were compared between patients with history of sole atrial flutter and those with atrial fibrillation. Four sets of results can be distinguished. Initially, the CT provides transverse conduction capabilities in patients with history of atrial fibrillation as well as in those with atrial flutter. Second, the development of a rate-dependent, progressively lengthening functional block is a characteristic electrophysiologic finding at the CT. Third, during previously recognized or drug-related atrial flutter, a conduction block was present at the CT. Finally, the coupling intervals resulting in a functional conduction block at the CT were significantly longer in patients with atrial flutter, as compared with those observed in patients with atrial fibrillation.
Transverse conduction across the CT.
In patients with typical atrial flutter, split potentials indicating a line of complete conduction block have been documented at the CT during atrial flutter (10,25). It has been suggested that this is anatomically fixed. However, mapping studies in animal models provide evidence that transverse conduction across the CT occurs in normal hearts (21). Yamashita et al. (15) found pulse propagation across the CT during pacing at the high right atrium in the isolated dog atrium. This result was supported recently by findings of Matsuo et al. (16), who found transverse activation across the CT in the canine model. In this study, transverse conduction across the CT could be demonstrated also during pacing in sinus rhythm in patients with history of atrial flutter.
Conduction block at the CT.
As demonstrated, pacing with shorter coupling intervals resulted in electrograms with split potentials and a marked alteration of activation sequence suggestive of a functional conduction block. This finding adds to the observation of several working groups that split potentials are present at the CT or the lateral right atrium during atrial flutter (14,21,25–28) or right atrial pacing (15,16). In this study, a functional conduction block was found in 18 of 20 patients investigated. Despite the high incidence, the electrophysiologic characteristics of the functional block showed a wide variation among individual patients. In some patients when conduction block occurred, it was apparent immediately along the entire extent of the CT mapping catheter. This resulted in depolarization of the posterior right atrium via a single ascending or descending wave front deriving from the inferior or superior right atrium. Both the descending and the ascending activation sequence were found to be equally frequent providing no evidence of a preferred propagation route. In addition to the observation of an immediate conduction block along the entire CT, a primarily circumscribed conduction block or a persistent gap was found in some patients. With progressive shortening of the coupling interval, the functional conduction block progressively lengthens.
Mechanism of conduction block.
The cause of slowed conduction and conduction block is very likely to be anisotropy rather than specific differences in local refractoriness. The methods used in this study did not allow accurate determination of conduction velocities. However, with known distance between the recording electrodes, determination of transverse and longitudinal conduction times gave strong evidence for a faster pulse propagation along the CT and a slower pulse propagation across the CT. Anisotropy at the CT with a high conduction velocity in the longitudinal direction and a low conduction velocity in the transverse direction due to a high gap junction density at end-to-end connections and a low density at side-to-side connections is well known (15,16,29–31). Yamashita et al. (15) found that the local effective refractory periods did not show any systematic pattern at the CT, whereas a marked anisotropic conduction was found at the intercaval region. High rate stimulation resulted in a functional conduction block at the lateral edge of the CT as well as at the border zone between the CT and the pectinate muscles. These findings were recently supported by Schoels et al. (32), who determined right atrial conduction velocity and dispersion of refractory periods at the CT by epicardial high density mapping in the canine model. Anisotropy might also explain the finding that a single propagation wavefront around the tricuspid annulus is found during low lateral or coronary sinus pacing after catheter ablation of atrial flutter (33–36) without evidence of additional activation emerging from the posterior right atrium. After atrial flutter ablation, pacing and mapping are performed adjacent to the tricuspid annulus. Due to a circumferential fiber orientation (37), the tricuspid annulus is a preferred propagation route (15). In contrast, a pulse to propagate around the inferior vena cava has to cross or pass at least two areas of slow conduction or block (when leaving and when entering the posterior border of the atrial flutter reentrant circuit), which are the CT and the eustachian ridge. Nakagawa et al. (38) could demonstrate that the eustachian ridge is a barrier to conduction and our findings, as others, give evidence that the CT is an area of slow conduction. Thus, the activation time around the tricuspid annulus might be shorter than the activation time around the inferior vena cava. However, this has to be clarified in further mapping studies.
Conduction in patients with atrial flutter versus atrial fibrillation.
During programmed stimulation in patients with history of atrial flutter, the occurrence of a functional conduction block was found at longer coupling intervals, as compared with that observed in patients with history of atrial fibrillation. Correspondingly, during stimulation with a given coupling interval, the length of the line of block in patients with atrial flutter exceeded that in patients with atrial fibrillation. In addition, a facilitation of conduction block at the CT by disopyramide resulted in 3 of 10 patients with previously documented atrial fibrillation in typical atrial flutter. It has long been recognized that some patients with recurrent atrial arrhythmias exhibit exclusively episodes of atrial flutter and others exclusively episodes of atrial fibrillation. It is well known (39–48) that a long linear lesion in the lateral right atrium by surgical incisions contributes to the development of atrial flutter. The findings of this study provide evidence that the occurrence of an extended functional conduction block at the CT may have similar effects, and thus may be one of the electrophysiologic conditions that are prone to develop atrial flutter. This hypothesis is supported by the observation from Waldo and Cooper (49) that before the spontaneous onset of atrial flutter in men a short episode of a transitional, progressively organizing rhythm, usually atrial fibrillation, can be found. The authors suggest that this rhythm is mandatory for the initiation of atrial flutter because it evolves the requisites for development of the atrial flutter reentry circuit. In addition, the same working group found a progressively lengthening line of functional conduction block at the lateral right atrium when mapping the spontaneous conversion from atrial fibrillation to atrial flutter in the canine sterile pericarditis model (50,51). Our findings suggest that the functional conduction block observed by these authors originates at the CT.
Study limitations.
The methodologic limitations of "low density" in vivo mapping in humans, however, should not be underestimated. Though the observation of split potentials associated with an alteration of the activation sequence of the second component strongly suggests conduction block, a marked conduction delay cannot be excluded. Actually, conduction delays have been proved to be the cause of double potentials in different settings (i.e., intrahisian "block"). However, the alteration of the activation sequence of the second component gives further evidence of conduction block and findings from experimental studies with high density epicardial mapping support the interpretation of our observations (15,16,32).
Aside from that, conduction was determined during pacing in the lateral right atrium adjacent to the anterior edge of the CT in patients with documented atrial tachyarrhythmias. Pulse propagation in the opposite direction (from posterior to anterior) or in healthy subjects or after pacing apart from the CT need not necessarily match the presented findings. The latter is especially true for conduction times and individual refractory periods since the conduction delay observed at the CT may be aggravated by the proximity of pacing and mapping site (52).
Finally, the effects of class I antiarrhythmic agents on right atrial activation during atrial fibrillation have not been fully elucidated. It is well known that atrial fibrillation organizes to typical atrial flutter in selected patients treated with these drugs (20,53–55). The antiarrhythmic effect of disopyramide results from a prolongation of atrial refractoriness and a decrease of intra-atrial conduction velocity. Prolongation of atrial refractoriness will lengthen excitation wavelength and thus prevent reentry. However, it is thought to mainly extinguish smaller reentrant circuits or reentrant circuits in areas of high conduction velocity. A decrease of intra-atrial conduction velocity may prevent reentrant circuits by producing complete block in the area of slow conduction. In this study after disopyramide administration, a conduction block at the CT was found at longer coupling intervals than during baseline. This observation gives evidence that a transformation of slow transverse conduction across the CT into a conduction block is facilitated by disopyramide. Subsequently, in selected patients with previously documented atrial fibrillation, programmed atrial stimulation resulted in atrial flutter, suggesting that this is the result of the disopyramide action at the CT. However, this study was not designed to clarify the effects of disopyramide and additional targets of its antiarrhythmic action are likely.
Conclusions.
In summary, it is concluded that limited transverse conduction capabilities of the CT may contribute to the development of atrial flutter.
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Acknowledgments
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We are indebted to Priv.-Doz. Dr. W. Schoels, University of Heidelberg, Germany for his comments.
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Footnotes
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This study was supported by the University of Bonn, BONFOR grant No. 107/13.
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