Author + information
- Received April 5, 1996
- Revision received September 23, 1996
- Accepted October 25, 1996
- Published online February 1, 1997.
- Jeffrey E. Olgin, MDA,2,2,
- Jonathan M. Kalman, MD, PhDA,
- Leslie A. Saxon, MD, FACCA,
- Randall J. Lee, MD, PhDA and
- FACC Michael D. Lesh, MD, FACCA,* ()
- ↵*Dr. Michael D. Lesh, University of California San Francisco, Department of Medicine and Cardiovascular Research Institute, Section of Cardiac Electrophysiology, Millberry Union East, Room 436, Box 1354, 500 Parnassus Avenue, San Francisco, California 94143-1354.
Objectives. Using a standardized induction protocol, we investigated the mechanism of initiation of atrial flutter, before ablation, to determine the site of initiating unidirectional block and to test the hypothesis that the direction of rotation of atrial flutter depends on the pacing site from which it initiates.
Background. The high recurrence rate of atrial flutter after presumed successful ablation may be due to difficulty in reinduction after termination. In addition, induction of clockwise flutter is currently of unknown clinical importance.
Methods. Ten patients with documented typical flutter were studied before ablation. A standard protocol consisting of single and double extrastimuli followed by burst pacing was performed from four sites in the right atrium (high and low trabeculated and smooth right atrium) to assess efficacy at inducing atrial flutter. A 20-pole halo catheter placed around the tricuspid annulus and a decapole catheter placed in the coronary sinus were used for mapping during initiation to determine type of flutter induced and the site of unidirectional block during initiation.
Results. Atrial flutter was induced in 52 (6.2%) of 838 attempted inductions. Of these, 33 were counterclockwise and 20 were clockwise. Of the 20 inductions resulting in clockwise flutter, 18 were from the trabeculated right atrium, whereas all the counterclockwise inductions were from the smooth right atrium. In all but the two inductions, the site of unidirectional block was identified between the os of the coronary sinus and the low lateral right atrium for both counterclockwise and clockwise flutter, in the same isthmus at which ablation is targeted.
Conclusions. Even in patients with clinical counterclockwise flutter, clockwise flutter is frequently induced before ablation and is dependent on the site of induction: Pacing from the smooth right atrium induces counterclockwise flutter, whereas pacing from the trabeculated right atrium induces clockwise flutter. The site of the unidirectional block during the initiation of either form of flutter is in the low right atrium isthmus.
(J Am Coll Cardiol 1997;29:376–84)
Atrial flutter is a right atrial reentrant arrhythmia that is now amenable to cure by radiofrequency catheter ablation ([1–7]). The anatomic substrate for typical flutter has been elucidated and has been shown ([6, 8, 9]) to rotate around the tricuspid annulus in a counterclockwise direction. This form of flutter uses a critical isthmus between the tricuspid annulus and the eustachian ridge, just anterior to the inferior vena cava (). Recent studies ([10, 11]) have suggested that another form of atrial flutter uses the same circuit as typical atrial flutter but rotates in a clockwise fashion around the tricuspid annulus. Although both forms can be induced in the same patient, it is not known why one form is induced in preference to the other. In addition, the clinical significance and mechanism of initiation of this form of atrial flutter when induced in the electrophysiology laboratory, and whether it is simply a byproduct of ablation, are unknown.
For reentry to occur, as in atrial flutter, there must be unidirectional block within the circuit at initiation. We previously identified ([6, 8]) the crista terminalis and eustachian ridge, which separate the posterior smooth from the anterior trabeculated right atrium, as posterior barriers and the tricuspid annulus as the anterior barrier in human atrial flutter. However, the site of unidirectional block during initiation has not been previously identified. Furthermore, the relative efficacy of inducing atrial flutter from either side of these barriers is unknown, and the site specificity of the direction of flutter rotation has not been defined.
The present study was performed to investigate the mechanism of initiation of atrial flutter in patients with clinical flutter before ablation. Specifically, we used a standardized induction protocol from specific sites in the right atrium during multisite endocardial recording to study the initiation of atrial flutter in humans. Because it is the narrowest portion of the flutter circuit and may be an area of discontinuous or anisotropic conduction, we hypothesized that unidirectional block occurs in the low right atrial tricuspid annulus–eustachian ridge isthmus and is independent of pacing site. If this were the case, then it follows that the site of pacing determines the type of flutter induced (i.e., counterclockwise rotation vs. clockwise rotation).
Ten consecutive patients referred for curative catheter ablation of typical atrial flutter were studied. All antiarrhythmic medications were stopped at least 5 half-lives before study. All patients had had atrial flutter documented on the 12-lead electrocardiogram (ECG), with flutter wave configuration consistent with counterclockwise flutter (see later), before the study. For patients presenting to the laboratory in atrial flutter, after confirmation with intracardiac recordings that counterclockwise flutter was present, pace termination of their flutter was performed before the study. Those presenting in atrial fibrillation underwent direct current (DC) cardioversion before the study. All data in this study were accumulated before any attempted ablation. Written informed consent was obtained from all patients, and the protocol was approved by the institutional review board.
An 8F, open lumen decapolar catheter (Daig) (2-mm interelectrode distance, 5-mm intraelectrode distance) was inserted into the coronary sinus through the internal jugular vein. Positioning of the proximal electrode pair at the os of the coronary sinus (CS) was confirmed with contrast injection viewed with fluoroscopy. A 7F, 20-pole halo catheter (Webster) with 2-mm interelectrode distance was positioned in the right atrium around the tricuspid annulus with its distal tip in the os of the CS and poles 1 and 2 at ∼7:00 on the tricuspid annulus (when viewed in the left anterior oblique view) (Fig. 1). Fluoroscopy in both the right and left anterior oblique projections was used to ensure that the halo lay along the anterior right atrium along the tricuspid annulus. An 8F steerable roving catheter (EP Technologies) was used for pacing from four sites: 1) the superior portion of the right atrium, posterior to the crista terminalis, referred to here as “high smooth”; 2) the inferoposterior smooth right atrium (just above the CS os), designated as “low smooth”; 3) the superior portion of the right atrium anterior to the crista terminalis, designated as the “high trabeculated” right atrium; and 4) the inferior portion of the right atrium anterior to the crista terminalis, designated as “low trabeculated.”
1.3 Induction protocol.
Pacing was performed at twice threshold with a pulse width of 2 ms. At each of the four sites, single and then double extrastimuli were introduced after an 8-beat drive train of cycle length 300 ms. The extrastimuli were introduced at coupling intervals of 50 ms greater than the cycle length of the clinical flutter and decremented by 10 ms down to refractoriness. After single and then double extrastimulation at each site, burst pacing from a cycle length of 50 ms greater than the flutter cycle length down to 180 ms was performed. The burst pacing protocol was performed three times at most sites. If flutter was induced at any time during this protocol, it was pace terminated, and the protocol continued. If atrial fibrillation was induced and did not spontaneously terminate after 10 min, the patient underwent electrical cardioversion. Ten minutes after cardioversion, the induction protocol was continued.
1.4 Electrogram analysis.
Bipolar intracardiac electrograms filtered between 30 and 500 Hz were recorded and stored digitally on a Cardiolab system (Prucka Engineering) simultaneously with 12-lead surface ECGs. All measurements were performed with the Cardiolab system using on-screen digital calipers at screen speeds of 400 to 1,600 mm/s.
Induced atrial flutter was characterized as either counterclockwise or clockwise according to the surface ECG, endocardial activation sequence and entrainment ([10, 11]). Counterclockwise flutterwas defined as a regular tachycardia having 1) the typical appearance of negative flutter waves on the 12-lead ECG in the inferior leads and lead V6; 2) a constant endocardial activation sequence, counterclockwise in direction around the tricuspid annulus; and 3) demonstrating concealed entrainment from the inferior vena cava–tricuspid annulus isthmus and manifest entrainment from the high right atrium ([10, 11]). Clockwise flutterwas defined as a regular tachycardia having 1) positive flutter waves in the inferior leads and lead V6, on the 12-lead ECG, with notching of the flutter waves in the inferior leads; 2) a constant endocardial activation sequence, clockwise in direction around the tricuspid annulus; and 3) demonstrating concealed entrainment from the inferior vena cava–tricuspid annulus isthmus and manifest entrainment from the high right atrium ([10, 11]). Inductions were defined as successful only if counterclockwise or clockwise atrial flutter was induced. Typical flutterwas defined as either counterclockwise or clockwise flutter, both of which use the typical flutter circuit. True atypical flutterwas defined as any atrial arrhythmia shown to be inconsistent with clockwise or counterclockwise atrial flutter on the basis of flutter wave configuration, endocardial activation sequence or entrainment criteria ([10, 11]). Inductions were excluded from analysis if typical flutter occurred in transition from an episode of induced atypical flutter or atrial fibrillation.
Electrograms and surface ECGs were analyzed during pacing to determine changes in activation sequence. Initiation was determined by an abrupt change in endocardial activation sequence or change in surface p wave configuration, or both, during pacing. Activation times from the stimulus (Stim Time) to each endocardial electrogram were determined on the beat before induction and on the beat of induction. The difference in Stim Time between the beat before (i − 1) and the beat of (i) induction (ΔStim Time) was calculated at each endocardial site: ΔStim Time = Stim Timei− Stim Timei−1. The site of unidirectional block was determined by comparing the ΔStim Time at each endocardial recording site. Block was determined to be between the two consecutive sites with the largest difference in ΔStim Times (Fig. 2).
1.6 Statistical analysis.
Results are expressed as mean value ± SD. Statistical comparisons were made using the Student ttest, Chi-square analysis and analysis of variance (ANOVA) when appropriate. Independence of induction attempts in all patients was analyzed using the Fisher exact test. A value of p < 0.02 was considered statistically significant.
The Fisher exact test was used to determine whether the proportion of successful inductions was the same in all patients. Our premise was that if there was a significant difference in the proportion (incidence) of successful inductions among the patients, then a “patient effect” might be present. If there was no difference, and all patients had the same proportion of successful inductions, then no patient effect would be present. That is, no one (or more) patient would account for the observed results when analyzed independent of patients.
The Fisher exact test was performed using the Stat Xact statistical program. This program allows the performance of Fisher exact tests in nonsquare (>2 × 2) contingency tables. This test is more appropriate than chi-square analysis in samples with small cells. The 10 × 2 table was set up with “patients” in the rows and “number of successful and unsuccessful inductions” in the columns. In this way, the Fisher exact test determines whether the proportion of successful induction attempts (or unsuccessful) is equivalent among all patients. The test demonstrated that that there was no difference in the proportion of successful inductions among the patients (p = 0.998). We therefore assumed that because the proportion of successful inductions was the same for all patients, there was no “patient effect.”
All patients (mean age 62 ± 16 years, range 45 to 76) had a documented clinical history of typical counterclockwise atrial flutter with a cycle length of 258 ± 8 ms. Two patients had a history of coronary artery disease and an ejection fraction of 45% and 50%, respectively; the remaining eight had no previous cardiac history. Only one patient had right atrial enlargement on echocardiography, defined as a diameter >5 cm. No patient had undergone previous ablation. Five patients presented to the electrophysiology laboratory in atrial flutter, all of whom underwent successful termination at the onset of the study. One patient presented to the electrophysiology laboratory in atrial fibrillation that was successfully cardioverted with a single 200-J DC shock. The remaining four patients presented in sinus rhythm.
2.2 Frequency of flutter initiation.
A total of 838 inductions (defined as any single drive train or pacing sequence) were attempted with a median of 90 induction attempts at four sites in each patient. There was no difference in the incidence of successful induction of flutter among patients (p = 0.998), and therefore induction of flutter was independent in each patient. Typical atrial flutter was induced 52 times (6.2%), or 5.8 ± 4.3 times (6.8 ± 4.9%) per patient. Typical flutter was induced at least once in every patient. The cycle length of induced atrial flutter (250 ± 24 ms) was not significantly different (paired ttest) from that of the clinical flutter. Atrial fibrillation or atypical atrial flutter was induced 44 times (5.2%), or 4.4 ± 5.1 times (8.4 ± 11%) per patient. For burst pacing, the pacing rate was significantly faster (p < 0.001, ANOVA) for those inductions producing atypical flutter/fibrillation (191 ± 21 ms) or flutter (202 ± 24 ms) compared with unsuccessful attempts (218 ± 29 ms). Similarly, for extrastimulation, the coupling interval of the last extrastimulus was significantly shorter (p = 0.02, ANOVA) for those inductions producing atypical flutter/fibrillation (175 ± 13 ms) and flutter (200 ± 8 ms) than for unsuccessful attempts (216 ± 34 ms). Double extrastimuli (10.4%) and burst pacing (7.2%) were significantly (p < 0.001, chi-square) better at inducing atrial flutter than single extrastimulus (2.1%). However, burst pacing was significantly (p < 0.001, chi-square) more likely to produce atypical atrial flutter or fibrillation (7.4%) than the other induction methods (2.1% for single, 0.9% for double extrastimuli). For burst pacing, the likelihood of inducing atypical flutter or fibrillation (7.4%) was not statistically different from that of inducing typical (clockwise or counterclockwise) flutter (7.2%, chi-square). The number of successful flutter inductions were not different at each of the sites. Typical flutter (clockwise or counterclockwise) was successfully induced 5.7% of attempts from the trabeculated right atrium and 6.5% from the smooth right atrium (chi-square).
2.3 Site specificity of type of flutter.
Of the 52 episodes of typical atrial flutter induced, 33 were counterclockwise and 20 were clockwise. The cycle length of induced counterclockwise flutter (239 ± 24 ms) was not significantly different (paired ttest) from that of induced clockwise flutter (249 ± 31 ms). The type of flutter induced—clockwise or counterclockwise—was almost exclusively dependent on the site of induction. Of the 20 inductions of clockwise flutter, 18 (90%) were induced from the trabeculated right atrium, whereas all 33 inductions of counterclockwise flutter were induced from the smooth right atrium (p < 0.0001, chi-square).
For attempted inductions with burst pacing, the pacing cycle lengths were not significantly different (ANOVA) for those that induced clockwise flutter (207 ± 24 ms) from those that induced counterclockwise flutter (201 ± 26 ms). Similarly, for extrastimuli, the coupling intervals that induced clockwise flutter (180 ± 28 ms) were not significantly different (ANOVA) from those that produced counterclockwise flutter (181 ± 16 ms). Induction method (burst vs. extrastimulation) was also not related to the type of flutter induced (p = 0.5, chi-square). Induction from the high or low right atrium was not related to the type of flutter induced (p = 0.6, chi-square, trabeculated vs. smooth right atrium only).
2.4 Site of unidirectional block.
During successful induction of flutter, the beat of induction was readily identified by an abrupt change in endocardial activation sequence. Examples of induction of clockwise flutter from the trabeculated right atrium and counterclockwise flutter from the smooth right atrium are shown in Fig. 3and Fig. 4. In most inductions, the change in endocardial activation sequence occurred in a single beat. However, in six inductions (four resulting in counterclockwise flutter and two resulting in clockwise flutter), this change occurred over a period of several beats with a “Wenckebach-type” prolongation of stimulus times (Fig. 4). In several successful inductions with burst pacing, flutter was initiated early during the pacing drive, with subsequent entrainment of the flutter during the remainder of the drive. Such entrainment was determined to occur when the surface p wave changed abruptly during induction and was different from the flutter wave configuration after pacing ceased (i.e., fusion was present). In addition, in a few instances, the flutter was induced and entrained, then terminated and reinduced during a single drive.
2.4.1 Clockwise flutter.
During induction of clockwise flutter, which occurred during pacing from the trabeculated right atrium, ΔStim Time at the CS os was significantly greater than that at the low lateral right atrium (LLRA) (p < 0.0001, ANOVA) (Fig. 3and Fig. 5). The ΔStim Time at the LLRA was 18 ± 6 ms, indicating counterclockwise capture at all times during induction (Fig. 5). In contrast, the ΔStim Time at the CS os was 115 ± 21 ms, indicating counterclockwise capture before initiation and clockwise capture on the beat of initiation (Fig. 3and Fig. 5[block diagram]). The greatest difference in ΔStim Times in consecutive sites occurred between the CS os and the LLRA, indicating that the site of unidirectional block was located between these sites (Fig. 3and Fig. 5). This location was confirmed by the overall activation sequences of the halo and CS catheters during initiation (Fig. 3).
The site of unidirectional block was located between the CS os and the LLRA in all but two episodes. In two episodes of clockwise flutter, no clear unidirectional block was identified.
2.4.2 Counterclockwise flutter.
During induction of counterclockwise flutter from the smooth right atrium, the ΔStim Time at the LLRA was significantly greater than that at the CS os (p < 0.0001, ANOVA) (Fig. 4and Fig. 5). In fact, the ΔStim Time at the CS os was only 9 ± 11 ms, indicating that it was activated from a clockwise wavefront (antidromically as related to the typical counterclockwise flutter circuit), both before induction and on the beat of induction (Fig. 4). However, the ΔStim Time at the LLRA was 102 ± 39 ms, indicating that before flutter induction this site was captured from a clockwise wavefront, whereas on the beat of flutter initiation it was activated from a counterclockwise wavefront (orthodromically as related to the typical counterclockwise flutter circuit) (Fig. 4). These clockwise and counterclockwise activations were confirmed by the overall activation sequence of the halo and CS catheters (Fig. 4). The greatest difference in ΔStim Times existed between the LLRA and the CS os, indicating that the site of unidirectional block occurred between these sites (Fig. 5), which was confirmed by the overall activation sequence in the halo and CS catheters during induction (Fig. 4).
In our study, careful, prospective attempts were made to induce atrial flutter before ablation was performed. We found that induction of atrial flutter is difficult even in patients who have clinical atrial flutter before ablation. Although flutter was induced in all patients studied, typical flutter (either counterclockwise or clockwise) was induced in only 6.2% of pacing sequences, slightly more than was true for atypical flutter or atrial fibrillation (5.2%). Double extrastimuli and burst pacing were significantly superior to single extrastimulus at inducing flutter; however, burst pacing was equally likely to induce atypical flutter/fibrillation as it was to induce atrial flutter. Although the site of induction did not affect the success rate of inducing flutter, it was significantly related to the type of flutter induced—pacing from the smooth right atrium resulted in counterclockwise flutter, and pacing from the trabeculated right atrium resulted in clockwise flutter. Analysis of electrograms during induction demonstrated that unidirectional block during induction of either clockwise or counterclockwise flutter occurred in the isthmus between the CS os and the LLRA.
3.1 Comparison with other studies.
Brignole et al. () and Watson and Josephson () reported that the induction of atrial flutter with programmed stimulation is highly sensitive and specific. Brignole et al. () found that only patients with a clinical history of flutter or risk factors could be induced with programmed stimulation. Watson and Josephson () found that single and double atrial extrastimuli were equally effective in inducing flutter and that pacing from the high right atrium was more effective than from the CS, although the direction of rotation was not analyzed. Of note, Watson and Josephson () reported a period of irregularity (fibrillation) before most episodes of induced flutter, whereas our analysis excluded such episodes. However, we did also observe induced atrial fibrillation and atypical flutter “organize” into typical flutter.
Yamashita et al. (), using a crista ligation animal model, found that during initiation of atrial flutter, unidirectional block occurred in a region of slow conduction in the low right atrium. In addition, this area exhibited atrioventricular node like properties with rate-dependent conduction delay and Wenckebach periodicity (). In a sterile pericarditis model of flutter, Schoels et al. () similarly identified the site of unidirectional block in the low right atrium, between the inferior vena cava and tricuspid annulus. These findings in animal models are similar to ours for flutter in humans, identifying the site of unidirectional block during the initiation of atrial flutter to the low right atrium in the reputed slow zone of conduction ([2, 16]). In addition, we also observed the Wenckebach conduction noted by Yamashita et al. ().
3.2 Site of block and relation to direction of rotation.
Regardless of whether counterclockwise or clockwise flutter was induced, the site of unidirectional block was identified in the same area—between the CS os and the LLRA in the isthmus between the tricuspid annulus and the inferior vena cava and eustachian ridge. This finding explains the site specificity of the form of flutter induced. Pacing from the smooth right atrium produces counterclockwise flutter because, if the “clockwise” limb blocks in the flutter isthmus, the “counterclockwise” limb is free to propagate. Because isthmus block in this case results in the longest possible conduction time to the lateral margin of the isthmus, recovery of excitability at the site of unidirectional block can occur, and counterclockwise flutter is initiated. Conversely, during pacing from the trabeculated right atrium, if the “counterclockwise” limb blocks in the flutter isthmus, the “clockwise” limb to is free to propagate. The longest possible delay is then to the medial border of the isthmus (near the CS os), and if recovery of excitability of the site of unidirectional block in the isthmus occurs, clockwise flutter is induced.
One can speculate why counterclockwise flutter is more commonly seen clinically. Clockwise flutter is induced only from the trabeculated right atrium (the anterolateral right atrium) and counterclockwise flutter from the smooth right atrium (septum and posterior wall). Because the trabeculated right atrium occupies a smaller total area than the smooth atrium and the entire left atrium, statistically it is more likely that an initiating premature atrial depolarization will arise from the septal side of the flutter isthmus, making counterclockwise flutter the most likely direction of rotation. Furthermore, in patients with isolated left atrial disease (e.g., mitral stenosis, left ventricular dysfunction), premature beats may be more likely to arise from the septal limb of the isthmus.
The mechanism by which unidirectional block occurs in the isthmus between the eustachian ridge and inferior vena cava and tricuspid annulus was not specifically addressed in this study. Anisotropy is one possible explanation for the site specificity of the unidirectional block ([17–19]). This nonuniform conduction allows propagation to occur faster in some directions and areas, which may result in an impulse reaching refractory tissue. Propagation in other areas proceeds slower, allowing adequate recovery in front of the wavefront. Disparate refractory periods may also play a significant role in producing unidirectional block in the flutter isthmus. As has been reported () for atria susceptible to atrial fibrillation, the dispersion of refractoriness might also be increased in patients with atrial flutter, allowing unidirectional block to occur at sites of relatively higher refractory periods than the rest of the circuit (). Both anisotropy as well as nonuniform refractoriness may be important in determining the site of unidirectional block during flutter initiation.
The six episodes of flutter that resulted from a Wenckebach-type block in the isthmus are intriguing. Conduction slowing may have played a role in these episodes. These episodes all occurred with rapid burst pacing (cycle length ≤210 ms), and there was evidence of delay from the stimulus to all the annular sites. This delay was most likely due to the fast pacing rate being near the functional refractory period of the atrium. An alternative explanation is that an atypical flutter was induced that converted to a typical flutter just as pacing was terminated. Because of the limited number of episodes, no definitive mechanism for this type of induction could be elucidated; however, it occurred in the minority of cases.
3.3 Clinical implications.
These findings imply that clockwise atrial flutter induced in the electrophysiology laboratory is clinically significant, even in patients with clinically documented counterclockwise flutter, and the induction of clockwise flutter is merely a function of the site of initiation. If the goal is to ablate the substrate for atrial flutter, then the induction of either direction of rotation implies that the substrate for flutter is present (or still present if ablation has been attempted).
These findings also demonstrate that the induction of atrial flutter in a patient with clinical flutter is extremely difficult, even before ablation, which implies that reinduction of flutter after ablation may not be an appropriate end point for determining immediate success. The inability to induce flutter in this situation may simply be a statistical phenomenon rather than a true demonstration of cure. Perhaps a better end point is the demonstration of bidirectional block at the ablation site with pacing, as recently described by several groups ([21–24]). In addition, the difficulty in inducing flutter does not prohibit ablation because this technique allows ablation of the flutter isthmus in sinus rhythm once typical (counterclockwise or clockwise) flutter has been demonstrated ([22–24]).
3.4 Limitations of the study.
Programmed stimulation was performed at only one cycle length and with up to only two extrastimuli. It is possible that longer (or shorter) cycle lengths or that more than two extrastimuli may have been more effective at producing flutter. In addition, no long–short protocols were performed. Whether such varied pacing protocols would result in an increased sensitivity and specificity of flutter induction cannot be answered by the present study.
The site of unidirectional block during initiation was determined by two methods: 1) a qualitative method in which the activation sequence of the halo and CS catheters were analyzed, and 2) a quantitative method in which differences in stimulation times were analyzed. Although the halo catheter recorded much of the flutter circuit, there were points along the septum that were not recorded. Clearly, higher density mapping would be preferred but is currently impractical in patients in the clinical electrophysiology laboratory. Epicardial mapping is limited by its inability to record from the intraatrial septum and the region of the low right atrium between the CS os and inferior vena cava. The quantitative method of analyzing differences in stimulation times used in this study assumes that the sites proximal and distal to (in the orthodromic direction of flutter: counterclockwise for smooth right atrium and clockwise for trabeculated right atrium) the unidirectional block were both activated antidromically (as related to each particular type of flutter) before the beat of flutter initiation. This was the case in every induction, as confirmed by analysis of the activation sequences. In addition, a change in Stim Time may result from decremental conduction rather than unidirectional block causing altered path and direction of activation. However, the analysis of the multipolar recordings showed reversal of activation sequence, confirming an altered direction of activation during initiation (Fig. 3and Fig. 4).
Even in patients with previously documented atrial flutter, this arrhythmia is difficult to induce with programmed stimulation. The type of flutter induced is dependent on the site of induction, with counterclockwise flutter induced from the smooth right atrium and clockwise flutter induced from the trabeculated right atrium. This site specificity of induction is a result of unidirectional block during initiation occurring in the isthmus in the low right atrium between the inferior vena cava, tricuspid annulus and the CS os.
↵2 Present address: Krannert Institute of Cardiology, Indiana University School of Medicine, Indianapolis, Indiana 46202.
☆ Dr. Olgin was supported by the American Heart Association, California Affiliate, Burlingame, California and is the recipient of a California Heart Association postdoctoral fellowship. Dr. Kalman was supported by the Ralph Reader Overseas Research Fellowship of the National Heart Foundation of Australia and the Telectronics Traveling Fellowship of the Royal Australian College of Physicians.
↵1 All editorial decisions for this article, including selection of referees, were made by a Guest Editor. This policy applies to all articles with authors from the University of California San Francisco.
- analysis of variance
- coronary sinus
- direct current
- electrocardiogram, electrocardiographic
- low lateral right atrium
- ΔStim Time
- activation time from stimulus to each electrogram
- Received April 5, 1996.
- Revision received September 23, 1996.
- Accepted October 25, 1996.
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