Catheter Mapping and Radiofrequency

Transcription

1 1647 Identification of Reentry Circuit Sites During Catheter Mapping and Radiofrequency Ablation of Ventricular Tachycardia Late After Myocardial Infarction William G. Stevenson, MD; Hafiza Khan, MD; Philip Sager, MD; Leslie A. Saxon, MD; Holly R. Middlekauff, MD; Paul D. Natterson, MD; Isaac Wiener, MD Downloaded from by guest on August 30, 2016 Background. Ventricular tachycardia reentry circuits in chronic infarct scars can contain slow conduction zones, which are difficult to distinguish from bystander areas adjacent to the circuit during catheter mapping. This study developed criteria for identifying reentry circuit sites using computer simulations. These criteria then were tested during catheter mapping in humans to predict sites at which radiofequency current application terminated ventricular tachycardia. Methods and Results. In computer simulations, effects of single stimuli and stimulus trains at sites in and adjacent to reentry circuits were analyzed. Entrainment with concealed fusion, defined as ventricular tachycardia entrainment with no change in QRS morphology, could occur during stimulation in reentry circuit common pathways and adjacent bystander sites. Pacing at reentry circuit common pathway sites, the stimulus to QRS (S-QRS) interval equals the electrogram to QRS interval (EG-QRS) during tachycardia. The postpacing interval from the last stimulus to the following electrogram equals the tachycardia cycle length. Pacing at bystander sites the S-QRS exceeds the EG-QRS interval when the conduction time from the bystander site to the circuit is short but may be less than or equal to the EG-QRS interval when the conduction time to the circuit is long. The postpacing interval, however, always exceeds the tachycardia cycle length. When conduction in the circuit slows during pacing, the S-QRS and postpacing intervals increase and the slowest stimulus train most closely reflects conduction times during tachycardia. Endocardial catheter mapping and radiofrquency ablation were performed during 31 monomorphic ventricular tachycardias in 15 patients with drug refractory ventricular tachycardia late after myocardial infarction. During ventricular tachycardia, trains of electrical stimuli or scanning single stimuli were evaluated before application of radiofrequency current at the same site. Radiofrequency current terminated ventricular tachycardia at 24 of 241 sites (10%') in 12 of 15 patients (80%o). Ventricular tachycardia termination occurred more requently at sites with entrainment with concealed fusion (odds ratio,3.4; 95% confidence interval [CI], 1.4 to 8.3), a postpacing interval approximating the ventricular tachycardia cycle length (odds ratio, 4.6; 95% CI, 1.6 to 12.9) and an S-QRS interval during entrainment of more than 60 milliseconds and less than 70%,o of the ventricular tachycardia cycle length (odds ratio, 4.9; 95% CI, 1.4 to 17.1). Ventricular tachycardia termination was also predicted by the presence of isolated diastolic potentials or continuous electrical activity (odds ratio, 5.2; 95% CI, 1.8 to 15.5), but these electrograms were infrequent (8% of all sites). Combinations of entrainment with concealed fusion, postpacing interval, S-QRS intervals, and isolated diastolic potentials or continuous electrical activity predicted a more than 35% incidence of ventricular tachycardia termination during radiofrequency current application versus a4% incidence when none suggested that the site was in the reentry circuit. Analysis of the postpacing interval and S-QRS interval suggested that 25% of the sites with entrainment with concealed fusion were in bystander areas not within the reentry circuit. At restudy 5 to 7 days later, 6 patients had no monomorphic ventricular tachycardia inducible, and inducible ventricular tachycardias were modified in 4 patients. None of these 10 patients have suffered arrhythmia recurrences during a follow-up of 316±199 days, although 4 continue to receive previously ineffective medications. Conclusions. Regions giving rise to reentry after myocardial infarction are complex and can include bystander areas, slow conduction zones, and isthmuses for impulse propagation at which radiofequency current lesions can interrupt reentry. (Circulation. 1993;88[part1]: ) * KEY WORDs ventricular tachycardia radiofrequency* myocardial infarction * reentry * ablation * death, sudden * mapping

2 1648 Circulation Vol 88, No 4, Part 1 October 1993 Jn patients with ventricular tachycardia late after a myocardial infarction, areas of slow conduction in infarct scars serve as the substrate for reentry and are desirable targets for surgical and catheter ablation.1-9 This slowly conducting tissue may be identified during endocardial catheter mapping by fractionated electrograms,9-12 mid-diastolic electrograms,13 and long delays between a capturing stimulus and the QRS complex resulting from the stimulus.1' Not all such areas participate, however, in reentry circuits. To further determine if a mapping site is actually within a reentry circuit, programmed electrical stimulation at the site has been suggested."1'4-21 At some sites, pacing entrains or resets the ventricular tachycardia with a stimulus to QRS (S-QRS) delay and without a change in QRS morphology This has been called by various authors entrainment with concealed fusion, concealed entrainment, and exact entrainment. Computer simulations and intraoperative mapping have shown that entrainment with concealed fusion can be due to depolarization of the pacing site within the reentry circuit with propagation of the stimulated orthodromic wave fronts along a path similar to that of the tachycardia wave fronts, whereas stimulated antidromic wave fronts collide in or near the circuit with orthodromic wave fronts and therefore do not depolarize surrounding myocardium to alter the QRS.1'5"7 Entrainment with concealed fusion is consistent with pacing at a site in the reentry circuit but also may occur at some "bystander" sites that are adjacent to the reentry circuit but are not participating in the circuit itself.'7,22-26 Fontaine et a12' suggested that during entrainment with concealed fusion produced by pacing within the circuit, the S-QRS interval should match the electrogram to QRS (EG-QRS) interval recorded during the tachycardia, whereas stimulation at bystander sites should produce an S-QRS interval longer than the EG-QRS interval. The effects of programmed stimulation on activation times is difficult to study in humans and animal models of ventricular tachycardia because it is difficult to repeatedly stimulate and record from a variety of sites in the same reentry circuit. In the first part of this study, computer simulations are used to develop and refine criteria for differentiating reentry circuit sites from bystander sites adjacent to the circuit. The second part of the study evaluates these criteria during catheter mapping in humans. To determine whether a site is likely to be in the reentry circuit, radiofrequency current is applied to the site during ventricular tachycardia to assess whether heating terminates the tachycardia. This approach is analogous to the "ice-mapping" used by Gallagher et a127 and Gessman28 and laser photocoagulation used by Littman et al'5 and Svenson et a129 during intraoperative ventricular tachycardia mapping. As radiofrequency lesions are relatively small, ventricular tachycardia termination probably indicates that the site not only participates in the reentry circuit but also is in a relatively narrow isthmus for the Received January 19, 1993; revision accepted June 15, From the Divisions of Cardiology, UCLA School of Medicine, UCLA Medical Center and Wadsworth VA Medical Center, Los Angeles, Calif. Correspondence to William G. Stevenson, MD, Cardiovascular Division, Brigham and Women's Hospital, 75 Francis St, Boston, MA B ECG A ECG FIG 1. Schematics of two figure-eight reentry circuits. Gray stipled regions are not excitable during tachycardia. Arrows indicate propagation of excitation wave fronts through the circuit. Specific sites in the circuits are indicated by numbers, and sites in bystanderpathways are indicated by letters. Sites 1 through 10 are in the inner loop, and sites 21 through 30 are in the outer loop. Sites 10 through 20 are in the common pathway (CP), with site 10 being at the entrance and site 1 being at the exit. The CP and the inner loop were designated as being inside the scar. The QRS onset occurs when the wave front exits from the scar as indicated by the vertical arrows to the schematic ECG tracing shown below each circuit. In the circuit shown in A, the QRS onset coincides with exitfrom the CP at site 1. A bystanderpathway containing site C is attached to the CP. In the circuit shown in B, there is a path through the scar from the CP exit at site 1 to the exit from the scar at site 38. The QRS onset does not occur until the excitation wave front exits from the CP and reaches site 38. Bystander pathway E is attached to this path between the CP exit and the QRS onset site. A bystander pathway containing site C is attached to the CP, and a bystanderpathway containing site H is attached to the inner loop. circulating wave front. Absence of ventricular tachycardia termination during tissue heating could indicate that the site is in a broad path within the circuit or outside the circuit. Therefore, a large number of sites in a variety of monomorphic ventricular tachycardias and patients were investigated. Methods Computer Simulations Figure-eight reentry model Computer simulations of figure-eight ventricular tachycardia reentry circuits were performed using a previously described program.17'30 In the figure-eight circuit (Fig 1), two wave fronts propagate around two arcs of conduction block sharing a common central pathway Each circuit

3 consists of anatomically fixed reentrant paths with an inner loop (from site 1 to site 10 in Fig 1) and an outer loop (from site 21 to site 30 in Fig 1). The common central pathway and the inner loop are designated to be within the scar and therefore would generate only low-amplitude electrical activity not detectable on the surface ECG. The QRS onset occurs when the excitation wave front exits the scar.10,15,29 The exit from the scar either coincides with the common pathway exit at site 1 (Fig 1A) or is distant from the common pathway exit (Fig lb).10 In the latter case, the excitation wave front propagates from site 1 in the circuit through a path in the scar to exit from the scar (from site 1 to site 38 in Fig 1B). Bystander pathways (eg, the path from site 15 to site C in Fig 1A and 1B) can be attached to any point in the circuit. For simplicity, results are reported for circuits of the same size with an inner loop radius of 2 cm. For each of the 32 to 50 segments specified in these circuits, the basal conduction velocities and refractory periods are specified. The iterative program then calculates activation times and the direction of wave front propagation for each site in the circuit.17 Based on existing data, conduction velocities of 0.5 to 0.8 m/s were used for inner and outer loops, decreasing to 0.1 to 0.2 m/s in the central common pathway.5'9 Basal refractory periods (150 to 200 milliseconds) generally were specified to create excitable gaps with sufficient duration to allow a range of premature stimuli to capture. Changes in refractory periods were modeled as an exponential function of the diastolic interval after the formula of Elharrar et al.36'37 Programmed stimulation. At selected sites in the circuit and bystander pathways, the effects of premature depolarizing stimuli were simulated. Single stimuli scanning the cardiac cycle in 10- to 30-millisecond decrements and 10-beat trains of stimuli were investigated. After each scanning stimulus or stimulus train, the tachycardia was returned to the basal state by restarting the simulation. Decremental conduction. During resetting or entrainment, the conduction time through circuit segments may remain constant or may lengthen Conduction velocity slowing in response to premature excitation (decremental conduction) was simulated as a monoexponential function of the diastolic interval.17'30 Definitions used in computer simulations. Common pathway exit is the site at which orthodromic wave fronts exit from the common pathway (site 1 in Fig 1). Common pathway entrance is the site at which the orthodromic wave fronts enter the common pathway (site 10 in Fig 1). QRS onset site is the site at which orthodromic wave fronts first reach the edge of the scar after leaving the common pathway exit (site 1 in Fig 1A; site 38 in Fig 1B). Dominant loop is the circuit loop outside the common pathway that has the shortest conduction time and thus establishes the tachycardia cycle length when conduction times are not identical in the inner and outer loops. EG-QRS interval is the interval from the activation during ventricular tachycardia to the following QRS onset (Fig 2A). For analysing stimulation sequences that reset or entrained the reentry circuits, we used the following definitions: S-QRS interval is, for single stimuli during tachycardia, the interval from the stimulus to the first advanced QRS (Fig 2A). For trains of stimuli, it is the interval from the B Stevenson et al Ablation of Reentry Circuits 1649 A Site ECG ECG S EG-QR 48 S-RS Site V post-pacing Interval post-pacing Interval FiG 2. Schematics of a figure-eight circuit and tracings of the surface ECG and electrogram timing recorded from stimulation site 15 in the common pathway. In this and Fig 3 through 13, solid arrows indicate nonstimulated tachycardia excitation wave fronts. Open arrows indicate excitation wave fronts traveling in an orthodromic direction produced by capturing stimuli. Stimulated antidromic wave fronts are shown as hatched arrows. All times are given in milliseconds. Stimulus capture at site 15 produces an orthodromic wave front that travels from site 15 to the common pathway exit at site 1 and then to the QRS onset near site 33. A stimulated antidromic wavefront travelsfrom site 15 toward the common pathway entrance at site 10 but collides with the returning nonstimulated orthodromic wave front from the previous tachycardia beat and is extinguished within the common pathway. The stimulated orthodromic wave front advances the tachycardia without change in QRS morphology and then continues through the circuit to reset the tachycardia (entrainment with concealed fusion). The cycle length of this tachycardia circuit is 391 milliseconds. In A below the reentry circuit schematic, the ECG effect ofa single stimulus at site 15 is illustrated. In this and all subsequent tracings, the stimulus artifact is the thick vertical line designated S. The intervalfrom the local electrogram (activation time) during tachycardia at site 15 to the following QRS on the surface ECG is 248 milliseconds (EG-QRS). The interval from the stimulus at site 15 to the advanced QRS (S-QRS interval) is 248 milliseconds. The postpacing interval from the stimulus to the succeeding electrogram is 391 milliseconds, which is equal to the tachycardia cycle length. In B, the effect ofa train ofstimuli at site 15 is illustrated. The pacing cycle length of the train is 350 milliseconds. The EG-QRS interval during tachycardia is 248 milliseconds and is equal to the intervalfrom the last stimulus in the train to the last QRS advanced to the pacing cycle length (S-QRS). The postpacing interval is the interval from the last stimulus to the following electrogram and is equal to the tachycardia cycle length of 391 milliseconds. last stimulus to the last QRS that was entrained to the pacing cycle length (Fig 2B). Postpacing interval is the interval from the stimulus to the succeeding activation

4 1650 Circulation Vol 88, No 4, Part 1 October 1993 Downloaded from by guest on August 30, 2016 TABLE 1. CharacterIstics of Patients With Drug Refractory Ventricular Tachycardia Left Radio- Ventricular Ventricular Ventricular Map- frequency Age, Myocardial Eectlon Tachycardia Tachycardias ping Term* Patient y Infarction Fraction Morphologies Drug Included Sites Sites 1 45 Inferior Inferior Sotalol+bretylium Inferior Amiodarone+procainamide Anterior Amiodarone Inferior Amiodarone Inferior Amiodarone Anterior+inferior Amiodarone Inferior Sotalol+procainamide Inferior Amiodarone+procainamide Anterior+inferior Amiodarone Lateral Amiodarone Anterior Amiodarone Anterior+inferior Amiodarone Inferior Amiodarone Anterior+inferior Amiodarone Mean±SD 66± ± ±1 16 ± ±1.6 *Ventricular tachycardia termination by radiofrequency application. at the stimulus site. For stimulus trains, the last stimulus is used. Activation of sites in the common pathway and inner loops that were designated as within the scar was assumed not to alter activation distant from the scar and hence would not alter the QRS complex. Antidromic wave front propagation out from the scar via the outer loop was assumed to alter ventricular activation distant from the scar, before colliding with an orthodromic wave front. In this case, an index of QRS fusion was calculated as the fraction of the outer loop outside the scar that was activated by the antidromic wave front. Studies of Human Ventricular Tachycardia Endocardial catheter mapping and radiofrequency ablation were performed in 15 consecutive patients referred between January 1990 and November 1992 for therapy of recurrent ventricular tachycardia despite antiarrhythmic therapy. All patients were men who had spontaneous and inducible sustained monomorphic ventricular tachycardia due to prior myocardial infarction (Table 1). Ventricular tachycardia was incessant in 4 patients (patients 2, 4, 13, and 14). At the time of study, 12 patients were receiving amiodarone. Amiodarone had been discontinued 6 weeks before the procedure in patient 12. Sotalol had been discontinued 3 days before the procedure in patient 1. In 3 patients, procainamide was administered intravenously during the study to attempt to slow ventricular tachycardia and improve hemodynamic tolerance. The mean left ventricular ejection fraction was During electrophysiological testing, more than one morphology of monomorphic ventricular tachycardia was observed in all patients (mean, 3.3±+1.7 morphologies). After informed consent was obtained, mapping and radiofrequency catheter ablation were performed according to the protocol approved by the institutional human subjects protection committees. Following local anesthesia with 2% lidocaine, electrode catheters were inserted percutaneously into the femoral veins and positioned in the right ventricular apex, His bundle position, and inferior vena cava. Left ventricular mapping was performed with 6F or 7F steerable catheters (EP Technologies, Mountain View, Calif, or Webster Laboratories, Baldwin Park, Calif). These catheters had a 4-mm distal tip electrode and 2 to 2.5 mm between the distal two electrodes. Access to the left ventricle was achieved via the femoral artery and retrograde across the aortic valve. Left ventricular mapping was performed via transatrial septal puncture for the second procedure in patient 12. Patients were kept heavily sedated with intermittent doses of midazolam and meperidine. Femoral arterial pressure and peripheral oxygen saturation were monitored continuously. Mapping Surface ECG leads (I, avf, V,, and V5) were recorded simultaneously with intracardiac electrograms at paper speeds of 100 mm/s for mapping and at 50 mm/s during radiofrequency current application (PPG Medical Systems, Pleasantville, NY). Bipolar intracardiac electrograms recorded from the distal and proximal electrode pair of the mapping catheter were filtered at 30 to 500 Hz. We also attempted to record filtered and unfiltered (0.05 to 500 Hz) unipolar electrograms from the distal electrode, although this was frequently limited by noise and baseline drift. To avoid potentially confounding effects of depolarization alternately at the cathode and anode during bipolar pacing, all left ventricular stimulation was unipolar with the distal electrode of the mapping catheter serving as the cathode

5 Sustained ventricular tachycardia is tachycardia requiring an intervention for termination. Radiofrequency termination site is a mapping site at which ventricular tachycardia terminated during the application of radiofrequency current without antecedent ec- Downloaded from by guest on August 30, 2016 and the inferior vena cava electrode serving as an anode.41 Catheter position was assessed by fluoroscopy in two planes and in 6 patients also by transesophageal echocardiography.42 Sites were distinguished from each other by catheter position on fluoroscopy and/or transesophageal echocardiography, and differences were supported by differences in electrogram morphology. Attention was initially focused on areas of akinesis or dyskinesis on echocardiography or previous ventriculography. If ventricular tachycardia was not incessant, areas of fractionated electrograms were sought during sinus rhythm, and a standard 12-lead ECG was recorded at these sites during ventricular pacing at a cycle length of 550 to 400 milliseconds.11'40'43 When a site with evidence of slow conduction was identified from fractionated electrograms and/or an S-QRS interval of more than 40 milliseconds during pace-mapping,11 the mapping catheter was maintained at this site, and ventricular tachycardia was initiated by programmed stimulation from the right ventricular apex. The mapping catheter was then used for programmed electrical stimulation during tachycardia. Once stable, ventricular tachycardia was initiated, or if ventricular tachycardia was incessant, fractionated electrograms were sought during ventricular tachycardia, and programmed electrical stimulation was performed at these sites. If ventricular tachycardia was hemodynamically well tolerated, programmed stimulation consisted of single stimuli having an amplitude of 10 ma and a pulse width of 2 milliseconds scanning the entire cardiac cycle, followed by 8- to 15-beat stimulus trains usually starting at cycle lengths 20 to 40 milliseconds shorter than the ventricular tachycardia cycle length and decreasing by 20 milliseconds until entrainment with QRS fusion occurred or ventricular tachycardia terminated. If ventricular tachycardia was not well tolerated, only trains of stimuli were assessed. In the last 8 patients, trains of stimuli routinely were used first, and single scanning stimuli were reserved for further definition of sites suspected of participating in the reentry circuit based on the effects of the stimulus trains. If stimuli failed to capture and tissue contact appeared adequate on echocardiography or fluoroscopy, the stimulus pulse width was increased to 9 milliseconds, and pacing attempts were repeated. Stable tachycardias were not routinely terminated to allow pace mapping. The paced QRS morphology during sinus rhythm was not used to select or exclude sites for further evaluation. Radiofrequency Current Application Radiofrequency current was applied to a site during ventricular tachycardia if stimuli entrained the ventricular tachycardia and the site appeared to be in an area of scar as assessed from the presence of fractionated electrograms and/or a delay of more than 40 milliseconds between the stimulus and the ensuing QRS complex. A complete map of the ventricle was not required before selecting a site for radiofrequency current application. Radiofrequency current at 500 KHz was applied to the large-tip electrode of the mapping catheter and two cutaneous electrode patches (R-2 Corp, Niles, Ill) on the posterior thorax, which had a combined surface area of 190 cm2. In the first patient, low-power (12 to 20 W) applications for 30 to 60 seconds were used. However, as radiofrequency application was well tolerated Stevenson et al Ablation of Reentry Circuits 1651 and studies of supraventricular tachycardia demonstrated that greater powers often were required, applications of 20 to 35 W for 15 to 30 seconds were used in subsequent patients. If ventricular tachycardia terminated during the application, radiofrequency current was continued for a total of 45 to 60 seconds. Radiofrequency application was immediately terminated if current fell, indicating an impedance rise, or evidence of boiling at the electrode tip was observed on transesophageal echocardiographic imaging.42 If radiofrequency current failed to terminate ventricular tachycardia, the catheter was moved to a new site, and the procedure was repeated. If radiofrequency current terminated ventricular tachycardia, we attempted to enlarge the lesion by moving the catheter tip to four sites within 5 mm (as assessed by comparison with the electrode tip length) of the initial lesion and applying radiofrequency current for 45 to 60 seconds at each site during sinus rhythm. Programmed stimulation from the right ventricle was then repeated to attempt to reinitiate tachycardia. If any sustained monomorphic ventricular tachycardia with a cycle length of more than 250 milliseconds was initiated, the mapping procedure was repeated until the entire endocardial circumference of the infarct scar had been evaluated. When tachycardias were poorly tolerated despite administration of procainamide to slow the arrhythmia, volume repletion, and low-dose dopamine infusion, as in patients 3, 8, and 9, the number of sites evaluated with both programmed stimulation and radiofrequency application was more limited. Radiofrequency current was then applied to areas of slow conduction identified from fractionated electrograms and stimulus to QRS delays during pace mapping."1 Programmed electrical stimulation followed immediately by radiofrequency current application was performed at 248 sites during 31 monomorphic ventricular tachycardias. Seven applications were excluded from analysis because ventricular tachycardia terminated and then spontaneously reinitiated as current application continued (one application), ventricular tachycardia changed morphology during current application (four applications), or ventricular tachycardia termination was preceded by ventricular premature beats (two applications). In the 241 remaining applications, ventricular tachycardia either terminated without antecedent ectopy or persisted throughout the current applications. Stimulus trains were analyzed for 196 sites, and single stimuli were analyzed for 45 sites. Five to seven days after the procedure, right ventricular programmed stimulation was repeated. Stimulation included single, double, and triple extrastimuli during pacing from the right ventricular apex and outflow tract at two drive cycle lengths (usually 400 and 600 milliseconds). Seven patients (patients 2, 3, 4, 5, 12, 14, and 15) underwent two procedures due to persistently inducible or recurrent tachycardia. Definitions for Ventricular Tachycardia Studies in Humans

6 1652 Circulation Vol 88, No 4, Part 1 October 1993 topy or a change in ventricular tachycardia morphology. Continuous electrical activity is low-amplitude fractionated electrical activity bridging the cardiac cycle in the bipolar recordings from the distal electrodes. Isolated diastolic potential is a low-amplitude, short-duration (typically less than 40 milliseconds) potential occurring after the end of the QRS complex and before the onset of the following QRS complex.13 No attempt was made to dissociate the potential from the tachycardia by pacing distant from the recording site, but only potentials that were consistent in presence and relation to the QRS complexes were included. The following features were assessed from programmed electrical stimulation during tachycardia (Figs 4, 5, and 8). Entrainment with fusion is continuous resetting of ventricular tachycardia with constant QRS fusion.44"45 Entrainment with concealed fusion is continuous resetting of ventricular tachycardia by stimuli that do not alter the QRS morphology and with a delay between the stimulus and the QRS onset.' For the purposes of this analysis, we will not distinguish between resetting by single stimuli and continuous resetting by stimulus trains, and both are designated entrainment for brevity.45 Postpacing interval is the interval from the last stimulated beat that entrained the tachycardia to the next bipolar electrogram recorded from the pacing site. PPI-VTCL difference is the difference between the postpacing interval and the ventricular tachycardia cycle length. S-QRS interval is the interval from the stimulus that entrained the ventricular tachycardia to the onset of the following QRS. EG-QRS interval is the interval from the electrogram onset to the following QRS onset. S-QRS-EG-QRS difference is the difference between the S-QRS interval and the EG- QRS interval measured to the portion of the electrogram that produces the minimum difference. To minimize effects of possible conduction slowing during programmed stimulation, which prolongs the postpacing interval and S-QRS intervals as the stimulation rate increases, the slowest stimulus trains and latest capturing stimuli that reliably entrained ventricular tachycardia were analyzed (see below). As shown in Figs 4, 5, and 8, electrograms recorded from areas of slow conduction are usually fractionated, and precise assessment of activation time is difficult.llz 12,46It is likely that local activation occurs at some time during the electrogram inscription. Therefore, if any portion of the electrogram preceded the QRS by an interval equal to the S-QRS interval, the S-QRS was considered to match the EG-QRS (Fig 4A and Figs SA and SB). Otherwise, the minimum distance between the S-QRS and EG-QRS intervals was measured. Similarly, if electrograms were present at an interval equal to the ventricular tachycardia cycle length following a stimulus that entrained the tachycardia, the postpacing interval was considered to match the ventricular tachycardia cycle length (Fig 4A). Therefore, if continuous electrical activity was recorded from a site with entrainment (seven sites), the postpacing interval matched the ventricular tachycardia cycle length and the S-QRS matched the EG-QRS. At 10 of the 241 sites, electrical stimuli captured, but electrograms were of insufficient amplitude to be defined, and EG-QRS and postpacing interval were not obtainable. We attempted to record standard 12-lead ECGs of each ventricular tachycardia morphology induced. However, this was not always possible. In the absence of a 12-lead ECG, leads I, avf, V,, and V5 were compared, and any ventricular tachycardia that differed from all other ventricular tachycardias in the direction of the major deflection recorded in any of these leads was designated as a distinct ventricular tachycardia morphology. Statistical Analysis Continuous data are expressed as mean± 1 SD. Groups were compared with Student's t test and x2 tests. Fisher's exact test was used for dichotomous variables when less than five discrete variables were present in any cell. To assess independent predictors of ventricular tachycardia termination by radiofrequency current, a logistic regression model was used (PROGRAM LR, BMDP Statistical Software, University of California, 1988). In the multivariate model, parameters measurable only during entrainment (postpacing interval and S-QRS) were designated as absent if pacing did not entrain the ventricular tachycardia. The goodness-of-fit X2was used to test fit of the model to the data. Results Computer Simulations Sites in the reentry circuit common pathway. The effect of stimulation at sites in the common pathway is illustrated in Fig 2. In this and subsequent figures, nonstimulated excitation wave fronts are shown as solid arrows. Excitation wave fronts produced by capturing stimuli that travel in the orthodromic direction in the circuit are shown as open arrows, and those traveling in the antidromic direction away from the stimulus site are shown as hatched arrows. Stimulus capture at common pathway site 15 produces an orthodromic wave front traveling from the stimulus site toward the common pathway exit (site 1) and an antidromic wave front traveling from the stimulus site toward the common pathway entrance (site 10). The antidromic wave front collides with the returning orthodromic wave front (solid arrows) from the previous tachycardia beat. When the site of collision is within the scar, as in this case, the antidromic wave front is confined in or near the circuit and does not alter the sequence of activation distant from the circuit.'7,30 The orthodromic wave front propagates out from the common pathway at site 1, to the exit from the scar (near site 33), advancing the tachycardia without changing the QRS morphology of the advanced beat, as shown schematically in Figs 2A and 2B. The stimulated orthodromic wave front also continues through the circuit, reentering the common pathway and resetting the tachycardia. An electrogram recorded from the region of antidromic and orthodromic wave front collision would have an altered appearance due to "fusion" of activation fronts. However, this fusion is concealed within the circuit. This response subsequently will be referred to as entrainment with concealed fusion. The EG-QRS interval during tachycardia measured from local activation at site 15 to the QRS onset indicates the conduction time from this site to the QRS onset site. Similarly, the S-QRS interval during entrainment indicates the conduction time from

7 A B ECG /248 i/2~~53 Shte S~te 15 v/ v post-pacing Interval ECG S te V post-pacing Interval FIG 3. ECG and electrogram schematics are shown from a circuit with the same configuration and conduction velocities as in Fig 2. In contrast to the circuit in Fig 2, conduction velocity slows in response to premature stimuli. The cycle length of the tachycardia circuit is 391 milliseconds, and the electrogram-to-qrs (EG-QRS) interval at site 15 is 248 milliseconds. In A, a stimulus 370 milliseconds after activation at the site resets the tachycardia, but the stimulus-to-qrs (S-QRS) interval increases to 253 milliseconds and exceeds the EG-QRS interval by 5 milliseconds. The postpacing interval is 398 milliseconds and exceeds the tachycardia cycle length. In B, a more premature stimulus 260 milliseconds after activation at the site further slows conduction velocity. The S-QRS increases to 274 milliseconds, and the postpacing interval increases to 430 milliseconds. All times are given in milliseconds. site 15 to the QRS onset site. Thus, the S-QRS equals the EG-QRS interval (248 milliseconds in Fig 2) unless conduction in the circuit slows with the premature stimulus (see below). At sites near the common pathway exit (site 1), the S-QRS and EG-QRS intervals are relatively short since the conduction time to the site of QRS onset is short. Both intervals become progressively longer as the stimulation site moves further from the common pathway exit toward the common pathway entrance (from site 1 toward site 10). Also, the closer the stimulus site is to the common pathway entrance at site 10, the more likely it is that the stimulated antidromic wave front from sufficiently premature stimuli or rapid trains will propagate out from the scar (from site 10 to site 30 in Fig 2), changing the morphology of the QRS complex even though the pacing site is in the common pathway.7 Less premature stimuli or slower trains at these sites will, however, still entrain tachycardia with concealed fusion. The postpacing interval at the stimulus site reflects the conduction time from the stimulus site to the common pathway exit at site 1, through the dominant loop to the common pathway entrance at site 10, and finally back to the stimulus site. The postpacing interval is, therefore, the time for one revolution time through the circuit and is equal to the tachycardia cycle length unless velocity in the circuit diminishes with premature stimuli (see below). If conduction velocities in the circuit slow with premature depolarizations, the conduction time from the Stevenson et al Ablation of Reentry Circuits 1653 A SMVT-3 '1 11 == AW~~~~~~~~~~~~~72 LV-101 J ri B RF ON - 37 volts, 440 ma AVIF V1, 1.J. d..j.. ~- LV-10 dup m E'1 'lil IT r ' ' I n _ NW m l. 11 Il2 742a FIG 4. A and B show tracings of ventricular tachycardia from patient 5. The findings during programmed electrical stimulation in A are consistent with pacing at a reentry circuit site near an "exit"from the infarct scar. From the top of each tracing are 50-millisecond time lines; surface ECG leads I, avf, V,, and V5; and bipolar intracardiac recordings from the distal electrode pair of the mapping catheter at left ventricular site 10. The proximal electrodes (p) are also shown in B. In A, sustained monomorphic ventricular tachycardia with a cycle length of 530 milliseconds is present. The last three beats of a train of stimuli at a cycle length of 460 milliseconds is shown. The ventricular tachycardia is continually reset without an alteration in the QRS morphology consistent with entrainment with concealed fusion. The stimulus-to-qrs (S-QRS) interval is 70 milliseconds. As shown in the last beat of the tracing, the electrogram onset at the recording site occurs 70 milliseconds before the QRS onset. Thus, the S-QRS matches the electrogram-to-qrs (EG- QRS) interval. Unipolar pacing at left ventricular site 10 markedly increases the noise at the site, but following the last stimulus, the electrogram is again visible, occurring slightly less than 530 milliseconds after the last stimulus. Thus, the postpacing interval matches the ventricular tachycardia cycle length of 530 milliseconds. In B, radiofrequency current is applied to site 10 during ventricular tachycardia. Tachycardia terminates after four beats, with restoration of sinus rhythm. (See text for discussion.) stimulus site to the QRS onset site increases as stimuli become more premature or the pacing rate of stimulus trains is increased. As illustrated in Fig 3, the S-QRS interval increases, exceeding the EG-QRS interval. Similarly, the time required for the stimulated wave front to propagate through the circuit increases, prolonging the postpacing interval, which then exceeds the tachycardia cycle length. The latest capturing stimuli and slowest trains that still entrain the tachycardia produce the least alteration in conduction times so the S-QRS most closely approximates the EG-QRS and the postpacing interval approximates the tachycardia cycle length. Examples of pacing at possible common pathway sites in two patients are shown in Figs 4 and 5. In Fig 4, sustained ventricular tachycardia with a cycle length of 530 milliseconds is present. A train of stimuli at a cycle

8 1654 Circulation Vol 88, No 4, Part 1 October 1993 A 'I'l li 1 I I'lll. T AVV1 vi, V5 LV7-1 Bi3-4 r_ B AVF,t, V5\ LV7-1 Bi 1- Bi3_ unt 1 AVF5Z Bi 1-2- LV7-10 1,Ii1lh V5= _ Uni 1 RF ON - 35v 490ma "11!Piiiii L 450 L 'WE FIG 5. A through C show tracings of ventricular tachycardia from patient 10. The findings in B are consistent with pacing at a site in the reentry circuit. From the top of each tracing are 100-milliseconds time lines; surface ECG leads I, avf, V,, and V5; and bipolar intracardiac recordings from the distal electrode pair (Bi 1-2), proximal electrode pair (Bi 3-4), and unipolar recordings from the distal (Uni-1) and second (Uni-2) electrodes of the mapping catheter at left ventricular site Sustained monomorphic ventricular tachycardia has a cycle length ranging from 420 to 450 milliseconds. In A, a vertical line indicates the QRS onset. Fractionated electrical activity is recorded from the mapping catheter (Bi 1-2) with a smallpotential \ immediately preceding the QRS onset ~Ny' and potentials extend 210 milliseconds <-""r after the QRS onset. In B, the last three beats of a train of stimuli at a cycle ~'\ length of 400 milliseconds is shown. The ventricular tachycardia is continually reset without an alteration in the QRS morphology consistent with en- L trainment with concealed fusion. The S-QRS interval is 230 milliseconds. An electrogram could not be recorded 655 from the distal electrode pair during pacing, and the postpacing interval therefore is not obtainable. As shown in A, low-amplitude fractionated activity is present 230 milliseconds preceding the QRS onset in the bipolar electrogram (Bi 1-2). The S-QRS was classified as matching the EG-QRS interval. In C, radiofrequency current is applied to site 10 during ventricular tachycardia. Tachycardia terminates after two beats, with restoration ofsinus rhythm. (See text for discussion.) length of 460 milliseconds entrains the tachycardia without altering the QRS morphology compared with the ventricular tachycardia beats. The S-QRS interval is 70 milliseconds and matches the EG-QRS interval. The postpacing interval is 530 milliseconds, which matches the ventricular tachycardia cycle length. These two features suggest that the pacing site is in the reentry circuit. The relatively short S-QRS interval suggests that the site is located near the exit from the scar to the surrounding myocardium. Application of radiofrequency current to the mapping catheter at this site (Fig 4B) terminated ventricular tachycardia after four beats. In Fig 5, sustained monomorphic ventricular tachycardia with a cycle length of 420 milliseconds is present. During pacing at a cycle length of 400 milliseconds, the tachycardia is entrained with concealed fusion (Fig SB). The S-QRS interval is 230 milliseconds. The bipolar electrogram recorded from the site in the absence of pacing (Bil-2 in Fig SA) is long and fractionated. Low-amplitude potentials are present 230 milliseconds before the QRS onset. During pacing, the signal from the distal electrode pair could not be recorded and therefore the postpacing interval is not available. The S-QRS during entrainment with concealed fusion matches the EG-QRS consistent with a site in the reentry circuit. The S-QRS interval of 230 milliseconds suggests that the site is some distance proximal to the exit site of a common pathway. Application of radiofrequency current to the mapping catheter terminated ventricular tachycardia after two beats (Fig SC). Bystander pathways attached to the common pathway. Results from a computer simulation showing effects of stimulation in a bystander pathway attached to the common pathway are shown in Fig 6. During tachycar-

9 ECG S Site C ECG post-pacing interval dia, site C in the bystander is depolarized by an orthodromic wave front from site 15 (as in Fig 1). Wave fronts from relatively late stimuli at bystander site C collide with the tachycardia excitation wave front traveling from site 15 toward site C and are extinguished in the bystander pathway without resetting the tachycardia circuit (Fig 6). Thus, the bystander site can be dissociated from the tachycardia. Excitation waves from earlier stimuli, or trains of sufficiently rapid stimuli, exit the bystander pathway and enter the common pathway at site 15, producing an orthodromic wave front that travels from site 15 toward the common pathway exit at site 1 (Fig 6B). An antidromic wave front is also produced that propagates from site 15 toward site 10. As during stimulation at site 15, the antidromic wave front collides with a returning orthodromic wave front in or near the circuit, while the stimulated orthodromic wave front propagates through the circuit, resetting the tachycardia without altering the QRS (entrainment with concealed fusion). The S-QRS interval is the conduction time from site C in the bystander path to site 15 in Stevenson et al Ablation of Reentry Circuits 1655 FIG 6. Schematic and tracings of a single stimulus at site C in the bystanderpathway attached to the common pathway at site 15 are shown. The reentry circuit is the same as in Fig 2. Open arrows indicate orthodromic excitation wave fronts produced by capturing stimuli, hatched arrows are antidromic wave fronts from stimuli, and closed arrows are nonstimulated excitation wave fronts. The tachycardia cycle length is 391 milliseconds. In A, the wave front from a relatively late single stimulus at site C collides with the nonstimulated orthodromic wave front travelingfrom site 15 to site C and is extinguished within the bystander pathway without resetting the tachycardia. Despite stimulus capture, the tachycardia is not disturbed. B shows the effects ofan earlier stimulus, which produces an excitation wave front that is sufficiently premature to exit the bystander pathway and enter the common pathway at site 15. This produces an orthodromic wave front that travels from site 15 to the common pathway exit at site 1 and then to the QRS onset site near site 33. A stimulated antidromic wave front travels from site 15 toward the common pathway entrance at site 10 and collides with a returning nonstimulated orthodromic wave front near site 10. The stimulated orthodromic wave front continues through the circuit resetting the tachycardia without changing the QRS morphology (entrainment with concealed fusion). The electrogram at site C precedes the QRS onset because the conduction time from site 15 to site C (53 milliseconds) is shorter than the conduction time from site 15 to site 33 (246 milliseconds). The electrogram to QRS interval during tachycardia at site C is equal to the difference between these two conduction times or =193 milliseconds. The stimulus to QRS interval is the conduction time from site C to site 15 in the common pathway plus the conduction time from site 15 to the QRS onset near site 33, which is a total of 299 milliseconds. The postpacing interval is the time the stimulated excitation wave front takes to travel from site C to site 15, then make one revolution through the circuit, before propagating backfrom site 15 to site C, which is a total of 497 milliseconds. Thus, pacing at this bystander site, the stimulus to QRS interval exceeds the electrogram to QRS interval, and the postpacing interval exceeds the tachycardia cycle length. the common pathway plus the conduction time from site 15 to the QRS onset site (299 milliseconds in Fig 6B). The S-QRS interval does not match the EG-QRS interval because during tachycardia, as an excitation wave from the orthodromic wave front propagates from site 15 in the common pathway to site C in the bystander pathway, the orthodromic wave front continues toward the common pathway exit at site 1 and then to the exit from the scar, producing the QRS onset. If the conduction time from common pathway site 15 to bystander site C is less than the conduction time from site 15 to the QRS onset site, the electrogram at site C will precede the QRS onset by an interval equal to the difference between these two conduction times (193 milliseconds in Fig 6B). The S-QRS interval will then exceed the EG-QRS interval. Possible variations in the relation of the EG-QRS and S-QRS intervals for sites in bystander paths attached to the common pathway are illustrated in Fig 7. For bystander site A, the EG-QRS is shorter than the S-QRS (as in Fig 6A) because the conduction time from

10 1656 Circulation Vol 88, No 4, Part 1 October 1993 Downloaded from by guest on August 30, 2016 ECG A -v B-AV-277 C r ~ Pa QRS onset site. The electrogram at site B then follows the QRS onset produced by the orthodromic wave front /... that depolarized site B. The EG-QRS interval is then measured to the following QRS (377 milliseconds) and exceeds the S-QRS interval of 322 milliseconds. It also is theoretically possible for the S-QRS interval to approximate the EG-QRS interval at bystander sites. This is illustrated for site C in Fig 7 and occurs when the conduction time from the bystander site to the common pathway is equal to half of the tachycardia cycle length. icing at Conduction In summary, the S-QRS progressively lengthens as E SiteS timep the conduction time increases from the bystander pac- 2-5RS to 98 ing site to the common pathway. The EG-QRS interval recorded from a bystander site during tachycardia de pends on the conduction time from the common path way to the bystander site relative to the conduction 154 from the time circuit site at the bystander path entrance to 18 =A 154 the QRS onset site. Thus, the EG-QRS may be shorter FIG 7. Schematic ofa figure-eight circuit with a relatively long than, longer than, or equal to the S-QRS obtained from bystander pathway attached to site 18 in th e common pathway. pacing at the bystander site. The latter two situations, Schematic tracings ofthe ECG and recordin, gsfrom site 18 in the however, occur when the conduction time from the common pathway and sites A through C in the bystander common pathway to the bystander site is relatively long. pathway are shown below the circuit. A thick line indicates the This long conduction time tends to prevent all except QRS onset of the second beat. For each situ e, the electrogram to relatively early single stimuli or rapid stimulus trains QRS interval during tachycardia is shown tuo the left of the QRS from prematurely depolarizing the common pathway onset line. To the right ofeach electrogram tiracingis the stimulus because, as shown in Fig 6A, the excitation wave front to QRS interval obtained by pacing at the srite (not shown) and from late stimuli will collide in the bystander pathway the conduction time from each bystand4!er site to common with a wave front from the tachycardia circuit and will pathway site 18. Conduction in this circbwit does not behave not reset the tachycardia. Thus, if stimulation at a decrementally. At site 18 in the common ppathway, the electro- bystander site entrains tachycardia with late single gram to QRS interval during tachycardia e?quals the S-QRS of stimuli or stimulus trains slightly faster than the tachylectrogram precedes cardia cycle length, the S-QRS most likely will exceed 154 milliseconds. Recording at site A, the e the QRS onset because the conduction time; from site 18 to sitea the EG-QRS interval. of 98 milliseconds is shorter than the cond& iction time from site When pacing and recording from the bystander 18 to the QRS onset site (site 32). The edlectrogram to QRS pathway, the postpacing interval is always longer than interval is =56 milliseconds. Pacinggat bystander sitea the tachycardia cycle length (Fig 6B). This is because the stimulus to QRS interval is the conduction time from site A the stimulated excitation wave front must travel from to site 18 (98 milliseconds) plus the time fr om site 18 to site 32 the stimulus site through the bystander pathway, enter (154 milliseconds) and is 252 milliseconds, exceeding the elec- the circuit (at site 15 in Fig 6), and then make one trogram to QRS interval during tachycar dia. exceedia. The postpacing the etcig revolution through the circuit, before propagating back up the bystander pathway to activate the pacing interval at site A is the tachycardia cycle lei nbgth of 391 millisec- site again. The postpacing interval is equal to the onds plus 2(98) =587 milliseconds. At site R the electrogram tachycardia cycle length plus the conduction time from occurs after the QRS onset because the cond~uction time from site the bystander site to the circuit and the conduction 18 to bystander siteb of168 milliseconds ecxceeds the conduction time from the circuit to the bystander site. The postelectrogram to QRS pacing interval therefore increases as the distance timefrom site 18 to the QRS onset site. The interval is measured to the following QRS and is 377 millisec- between the circuit and the bystander site increases. onds, which exceeds the stimulus to QIRS interval of 322 When pacing from bystander pathways attached near milliseconds ( ). The postpacing initerval during stimu- the circuit entrance at site 10, the antidromic wave front lation at site B is 391+2(168) =587 milliseconds. The conduc- from very early stimuli or rapid trains may propagate tion time from site 18 to bystander site C of 196 milliseconds out from the common pathway entrance into adjacent exceeds the conduction tine from site R8 to site 32 and is myocardium before colliding with the tachycardia approxuamtely half of the tachycardia cycle length of 391 milli- orthodromic wave front. This may alter the QRS morluring tachycardia is phology, as noted above. seconds. The electrogram to QRS interval 349 milliseconds and is almost equal to the S-QRS of 350 Stimulation at a bystander site in a patient is shown in milliseconds ( ). The postpacing jinterval at site C is Fig 8. Sustained monomorphic ventricular tachycardia 391+2(196)=783 milliseconds, markedly texceeding the tachy- with a cycle length of 540 milliseconds is present. A cardia cycle length. CP indicates reentry ci rcuit common path- train of stimuli at a cycle length of 440 milliseconds way; S-QRS, stimulus to QRS interval entrains tachycardia with minimal or no change in QRS morphology, consistent with entrainment with con- site A is less cealed fusion (Fig 8A). The S-QRS interval is 540 the common pathway at site 18 to bystaander than the conduction time from site 18 to the QRS onset milliseconds and exceeds the EG-QRS interval. The at site 32. In contrast, the conduction time from site 18 postpacing interval exceeds the ventricular tachycardia to site B exceeds the conduction time ifrom site 18 to the cycle length of 530 milliseconds. Application of radio-

11 B RF OFF - After 50v 540 ma for 45 sec FIG 8. A and B show tracings of ventricular tachycardia from patient 2 The findings in A are consistent with pacing at a bystander site adjacent to the reentry circuit. From the top of each tracing are 50-millisecond time lines; surface ECG leads I, avf, V,, and V5; and bipolar intracardiac recordings from the distal electrode pair of the mapping catheter at left ventricular site 7-8. In B, recordings from the proximal electrode pair (Bi 3-4); a filtered, unipolar tracing from the distal electrode of the mapping catheter; and a bipolar recording from the right ventricular apex (RVA) also are shown. In A, sustained monomorphic ventricular tachycardia with a cycle length of 520 to 540 milliseconds is present. The last three beats of a train of stimuli at a cycle length of 440 milliseconds at left ventricular site 7/8 is shown. The ventricular tachycardia is continually reset with minimal or no alteration in the QRS morphology, consistent with entrainment with concealed fusion. The stimulus to QRS interval from the last stimulus to the last entrained beat is 540 milliseconds. As shown in the last beat of the tracing, 540 milliseconds before the QRS onset, there is no electrical activity recorded, and the stimulus to QRS interval does not match the electrogram to QRS interval. After the final stimulus at site 7/8, the next electrogram occurs after 680 milliseconds. Thus, the postpacing interval markedly exceeds the ventricular tachycardia cycle length of 540 milliseconds. In B, the last 2 seconds ofa 45-second radiofrequency current application to site 10 during ventricular tachycardia is shown. Radiofrequency application has no effect on the tachycardia. (See text for discussion.) frequency current to the mapping catheter failed to terminate ventricular tachycardia (Fig 8B). Stimulation in a Dominant Inner Loop. The inner loop in this computer model is within the scar and would not generate electrical potentials detectable in the surface ECG. A variety of responses can be seen with stimulation at sites in a reentry circuit dominant inner loop, as illustrated in Fig 9. Minimally premature stimuli entrain the tachycardia with concealed fusion and with a long S-QRS interval reflecting the conduction time from the stimulus site to the common pathway and then through Stevenson et al Ablation of Reentry Circuits 1657 the common pathway to the QRS onset (Fig 9B). If conduction velocities in the circuit do not change, the S-QRS interval equals the EG-QRS interval, and the postpacing interval equals the tachycardia cycle length. Earlier premature stimuli may entrain tachycardia with QRS fusion when the stimulated orthodromic wave front depolarizes site 10 at the junction of the outer loop, inner loop, and common pathway and is sufficiently premature to propagate antidromically to site 30 and then out of the scar (Fig 9B). This tends to occur when the inner loop pacing site is close to the common pathway entrance. The S-QRS interval measured to the advanced, unchanged QRS still equals the EG-QRS interval, and the postpacing interval equals the tachycardia cycle length. A third type of response is seen when the common pathway exit is captured antidromically (Fig 9C). Pacing at a site in the inner loop produces an orthodromic wave front that propagates from the stimulus site (site 3 in Fig 9C) toward the entrance of the common pathway (site 10). The stimulated antidromic wave front propagates toward site 1 and then out to the QRS onset site. When the stimulated antidromic wave front captures the QRS onset site, the QRS morphology is not changed, but the S-QRS is markedly shorter than the EG-QRS interval due to the shorter conduction time from the inner loop site (site 3) to the common pathway exit (site 1) in the antidromic direction, as opposed to the conduction time from the inner loop site (site 3) to the common pathway entrance (site 10), and then through the common pathway in the orthodromic directions If the stimulated orthodromic wave front does not encounter refractory tissue in the common pathway, in which case tachycardia terminates, it continues through the circuit, producing a second QRS complex from the same stimulus. As shown, the stimulus is then followed by two premature QRS complexes-one from the antidromic wave front and one from the orthodromic wave front. The postpacing interval still equals the tachycardia cycle length. A short distance between the inner loop site and QRS onset site increases the likelihood that the antidromic wave front from early stimuli or rapid trains will capture the QRS onset site. When there is a path from the common pathway exit (site 1) to the QRS onset site (site 38 in Fig 1B), the inner loop sites closest to the slow conduction exit are depolarized before the QRS onset during tachycardia. The EG-QRS interval at these sites then is much shorter than the S-QRS interval, as discussed below. Bystander loops. Bystander inner loops were simulated by specifying a shorter conduction time through the outer loop compared with the inner loop. The outer loop then depolarizes the common pathway and is the dominant loop. Effects of pacing in the "nondominant" inner loop are illustrated in Fig 10. Relatively late capturing stimuli at inner loop site 6 produce excitation wave fronts that collide within the inner loop with excitation wave fronts from the tachycardia circuit and have no effect on the tachycardia (Fig loa). Thus, the site can be dissociated from the tachycardia. As shown in Fig lob, the wave fronts from earlier stimuli reach the common pathway entrance before the orthodromic wave front from the dominant outer loop and reset or entrain the tachycardia circuit. In this case, the S-QRS interval is longer than the EG-QRS interval. The

12 1658 Circulation Vol 88, No 4, Part 1 October 1993 to capture the QRS onset site, resulting in a shorter S-QRS interval. Also, stimulated orthodromic wave fronts may exit the scar from the common pathway entrance, producing QRS fusion (as in Fig 9B). Whether these responses occur depends on the by- Downloaded from by guest on August 30, 2016 ECG A S ite post-pacing interval B 21; ECG Site post-pacing interval Site 3A post-pacing interval FIG 9. Schematics and tracings of the responses to single stimuli at sites in the dominant inner loop. Sites 1 through 10 are in the inner loop within the scar. The QRS onset occurs after the excitation wave front exits from the scar near site 33. Open arrows indicate excitation wave fronts produced by capturing stimuli, hatched arrows are antidromic waves from the stimuli, and closed arrows indicate nonstimulated excitation wave fronts. The cycle length this reentry circuit is 463 milliseconds. In A, a stimulus at site 6 resets the tachycardia with concealed fusion. A stimulated orthodromic wave front travels from the pacing site 6 to the common pathway entrance at site 10. The stimulated antidromic wave front travels from site 6 toward site 3, colliding with a tachycardia orthodromic wave front. The long stimulus to QRS of 412 milliseconds reflects the conduction time of the stimulated orthodromic wave front from site 6 to the common common pathway entrance at site 10, then through the common common pathway, andfinally to the QRS onset at site 33, and equals the electrogram to QRS interval during tachycardia of 412 milliseconds. The postpacing interval equals the time for one revolution through the circuit of 463 milliseconds. In B, the effects of an earlier stimulus at site 6, which resets the tachycardia with QRS fusion, is shown. The stimulated orthodromic wave front from pacing site 6 captures site 10 at the intersection ofthe inner loop, common pathway, and outer loop. This orthodromic wave front is sufficiently early to propagate antidromically to outer loop site 30 and then outside the scar, changing the QRS morphology. The QRS immediately following the stimulus is altered. The stimulus to QRS interval of the subsequent advanced, unchanged QRS produced by the stimulated orthodromic wave front as it exits from site 33 equals the electrogram to QRS interval during tachycardia of 412 milliseconds. The postpacing interval equals the tachycardia cycle length of 463 milliseconds. C shows the effect ofpacing at site 3 in the inner loop close to the common pathway exit. A stimulus at site 3 produces an orthodromic wave front that travels from site 3 to site 6 and then to the common pathway entrance at site 10. A stimulated antidromic wave front travels from pacing site 3 towards the common pathway exit. When the stimulated orthodromic wave front captures the QRS onset site, the situation illustrated in A, in which entrainment with concealed fusion and with a long stimulus to QRS delay results. However, if the stimulated antidromic wave front captures site 33, the morphology of the advanced QRS is unchanged, but the stimulus to QRS interval reflects the conduction time from pacing site 3 to site 1 and then to site 33 (101 milliseconds) in the antidromic direction. Meanwhile, the stimulated orthodromic wave front continues through the circuit, and if it does not encounter refractory tissue in the region of the common pathway where the stimulated antidromic wave front collided with a tachycardia wave front, propagates out ofthe common pathway to produce a second premature QRS complex. Thus, in this case, there is a double response to a single stimulus. The postpacing interval remains equal to the tachycardia cycle length. postpacing interval equals the revolution time through the slower nondominant loop and common pathway, which is longer than the tachycardia cycle length. Just as when pacing from a dominant inner loop (Fig 9C), it is possible for stimulated antidromic wave fronts

13 Stevenson et al Ablation of Reentry Circuits 1659 A K K ~~~~~~30 h ~~~~isr QRS onset Downloaded from by guest on August 30, 2016 ECG 44 = Site S post-pacing interval B 30 ~~~~ 1~~~~~ ECG vs~~ty 393 /412 Site Site post-pacing interval FIG 10. A and B show the effect of pacing at site 6 in a nondominant inner loop, which has a longer conduction time than the outer loop and therefore behaves as a bystander. In A, a minimally premature stimulus produces an orthodromic wave front (open arrows) traveling toward site 10 and an antidromic wave front (hatched arrows) traveling toward site 1. The stimulated antidromic and orthodromic wave fronts collide with the nonstimulated tachycardia wave fronts (solid arrows), and the tachycardia is not affected. In B, an earlier stimulus produces an orthodromic wave front (open arrows) that captures the common pathway entrance at site 10 before the nonstimulated tachycardia wave front (solid arrows). This stimulated orthodromic wave front then continues through the common pathway to reach the QRS onset site and reset the tachycardia without changing in QRS morphology. The stimulated antidromic wave front (hatched arrows) is contained within the inner loop by collision with a tachycardia wave front near site 3. During tachycardia, site 6 is activated shortly after the QRS onset; as a result, the interval from the electrogram to the following QRS (electrogram to QRS interval during tachycardia) is long (393 milliseconds). The S-QRS interval is the conduction time from site 6 to site 10 and then through the common pathway to site 33 (412 milliseconds), and it exceeds the electrogram to QRS interval. The postpacing interval at site 6 is the revolution time through the slower nondominant loop (463 milliseconds) and exceeds the tachycardia cycle length. stander site location, conduction times in the circuit, and stimulus timing, just as for stimulation at dominant inner loop sites. Sites between the common pathway and QRS onset site. At sites in the pathway between the common pathway ECG /70 ~ OS t Site post-pacing interval FIG 11. The response to a premature single stimulus at site 32 in the path between the common pathway exit at site 1 and the QRS onset is shown. Site 32 is close to the QRS onset site; therefore, the electrogram to QRS interval is relatively short (70 milliseconds). When pacing at site 32, a stimulated orthodromic wave front (open arrows) propagates to the QRS onset site, producing an early QRS without a change in morphology. The stimulated orthodromic wave front also travels through the nondominant outer loop. A stimulated antidromic wave front (hatched arrows) travels from pacing site 32 to the common pathway exit at site 1 and into the common pathway, where it collides with a nonstimulated tachycardia wave front (solid arrows) and is extinguished. The antidromic wave front also propagates into and through the dominant inner loop, resetting the tachycardia. The stimulus to QRS interval is the conduction time from site 32 to the QRS onset site and is the same as the electrogram to QRS interval tachycardia (70 milliseconds). The postpacing interval is the tachycardia cycle length plus twice the conduction time from site 32 to the common pathway at site 1 (488 milliseconds) and exceeds the tachycardia cycle length just as in the case of bystander pathways. exit and the QRS onset (Fig 11), the EG-QRS interval is shorter than at common pathway circuit sites due to the close proximity to the QRS onset site. Capturing stimuli produce an orthodromic wave front that propagates toward the edge of the scar and an antidromic wave front that propagates toward the common pathway exit (site 1). The orthodromic wave front exits the scar, producing an early QRS identical in morphology to the tachycardia QRS complex. The S-QRS interval is relatively short and equals the EG-QRS interval. In Fig 11, the stimulated orthodromic wave front also propagates through the nondominant outer loop. The antidromic wave front from relatively late stimuli may collide with a tachycardia wave front before reaching the circuit, failing to reset or entrain the tachycardia (not shown). In Fig 11, the antidromic wave front is sufficiently premature to propagate into the common pathway before it collides with a tachycardia orthodromic wave front. The antidromic wave front also propagates into the dominant inner loop, advancing the tachycardia. The postpacing interval exceeds the tachycardia cycle length because the stimulated excitation wave front must propagate from the stimulus site to the circuit at site 1, make a revolution through the circuit, and then propagate back from site 1 to the stimulus site. As the

14 1660 Circulation Vol 88, No 4, Part 1 October 1993 stimulus site moves closer to the common pathway exit at site 1, the postpacing interval approaches the tachycardia cycle length. A delay from the common pathway exit at site 1 to the site of QRS onset also importantly affects measurement of EG-QRS intervals at other sites in the circuit. At sites in the common pathway, the EG-QRS and S-QRS intervals are longer than those expected when the common pathway exit and QRS onset site are the same. The sites in the loops outside but closest to the common pathway exit are activated before QRS onset due to a shorter conduction time from the common pathway exit to the loop site than from the common pathway exit to the QRS onset site. The EG-QRS interval that is measured to the QRS immediately following the electrogram then is markedly shorter than the S-QRS interval, even though the site is in the circuit. Stimulation in a separate bystander pathway connected to the pathway between the common pathway exit and the QRS onset site, such as site E in Fig 1B, has effects similar to stimulation in a bystander pathway attached to the circuit. The S-QRS interval can be longer than, shorter than, or equal to the EG-QRS interval, but the postpacing interval is always more than the tachycardia cycle length. Stimulation in a dominant outer loop. The outer loop in this model propagates along the border of the scar. As shown in Fig 12, stimulation in the outer loop produces an excitation wave front that propagates rapidly away from the stimulus site to the surrounding myocardium. This alters the sequence of activation distant from the reentry circuit, altering the QRS complex. The antidromic stimulated wave front collides in the myocardium outside the scar with an orthodromic wave front from the tachycardia circuit. The QRS complex immediately following the stimulus reflects fusion between the stimulated and tachycardia excitation wave fronts. The stimulated orthodromic wave front continues through the circuit, resetting the tachycardia; this is classic entrainment.44"45 The S-QRS interval is short due to rapid propagation of the stimulated wave front away from the pacing site, and the QRS morphology of the premature beat is altered. The stimulus site is next activated after the stimulated orthodromic wave front has made one revolution through the circuit. The postpacing interval equals the tachycardia cycle length if pacing does not alter the conduction velocities in the circuit. If the outer loop is nondominant due to a shorter conduction time through the inner loop, the outer loop behaves as a bystander, and the postpacing interval exceeds the tachycardia cycle length (not shown). Catheter Mapping in Human Ventricular Tachycardia Effects of programmed stimulation. Radiofrequency current application terminated ventricular tachycardia at only 24 of 241 sites (10%). Examples are shown in Figs 4, 5, and 8. A radiofrequency termination site was identified for 16 of the 31 ventricular tachycardias in 12 of the 15 patients (80%). The responses to programmed stimulation are shown in Table 2. Ventricular tachycardia termination occurred at 15 of 86 sites (17%) with entrainment with concealed fusion compared with 9 of 155 sites (6%) with other responses to programmed stimulation (P=.005), including 7 of 129 sites (5%) with ECG S Site L post-pacing Interval FIG 12. The effects of a premature stimulus in a dominant outer loop are shown. The outer loop in this modelpropagates along the border ofthe scar. Thepacing site is distantfrom the exit ofthe common pathway and QRS onset site. A premature stimulus at site L in the outer loop produces antidromic wave fronts (hatched arrows) and orthodromic wave fronts (open arrows). The stimulated wave fronts propagate rapidly away from the site, altering the sequence of ventricular activation distant from the circuit. The antidromic wave fronts also collide with tachycardia orthodromic wave fronts (solid arrows). The stimulated orthodromic wave fronts propagate through the circuit, resetting the circuit and entraining the tachycardia with QRSfusion. The QRS following the stimulus is different from the tachycardia QRS complexes, and the stimulus to QRS interval is short due to rapid propagation awayfrom the stimulus site. The stimulus site is next activated by the returning orthodromic wave front after one revolution through the circuit and therefore is equal to the ventricular tachycardia cycle length (463 milliseconds). entrainment with QRS fusion (P=.01 versus entrainment with concealed fusion sites). Radiofrequency energy was similar for entrainment with concealed fusion sites (25 ±7 W) compared with all other sites (24+6 W, P=.6). The mean time to radiofrequency termination was 13±13 seconds (range, 1 to 46 seconds). The mean time for radiofrequency application at sites without ventricular tachycardia termination was 29±13 seconds. An impedance rise during radiofrequency application or bubbles on transesophageal echocardiography suggesting boiling at the catheter tip occurred at 11 of 24 sites TABLE 2. Programmed Stimulation During Ventricular Tachycardia Radlofrequency Terminate Ventricular Total Tachycardla % Entrained + concealed fusion 86 15* 17 Entrained + QRS fusion Capture not entrained Terminated/change ventricular tachycardia No capture Total *P=.01 vs entrained + QRS fusion sites.

15 TABLE 3. Postpacing Interval-Ventricular Tachycardia Cycle Length Difference PPI-VTCL, ms Total Radiofrequency Term % > Total PPI indicates postpacing interval; VTCL, ventricular tachycardia cycle length; and radiofrequency term, ventricular tachycardia termination by radiofrequency application. (46%) with radiofrequency termination compared with 70 of 217 sites (32%) without ventricular tachycardia termination (P=.2). At five sites, a stimulus that did not produce a propagated response terminated ventricular tachycardia.40a47-49 This has been hypothesized to indicate block of the stimulated wave front within the circuit or an effect of a subthreshold stimulus and therefore to indicate that the pacing site is in the reentry circuit. At two of the sites, other stimuli entrained the ventricular tachycardia with concealed fusion and radiofrequency current terminated ventricular tachycardia at both of these sites. Of the remaining three sites, other stimuli entrained ventricular tachycardia with QRS fusion at two sites and had no other effect at the third. Radiofrequency current failed to terminate ventricular tachycardia at these three sites. Postpacing interval. The postpacing interval after tachycardia entrainment was obtainable for 152 sites, and the differences between the postpacing interval and ventricular tachycardia cycle length are shown in Table 3. Tachycardia termination occurred at 13 of 64 sites (20%) with a postpacing interval that was within 30 milliseconds of the ventricular tachycardia cycle length (Figs 4 and 5) compared with 4 of 88 sites (4%) with a postpacing interval more than 30 milliseconds longer than the ventricular tachycardia cycle length (Fig 8) (P=.003). The postpacing interval was also strongly correlated with entrainment with concealed fusion. The postpacing interval was within 30 milliseconds of the ventricular tachycardia cycle length at 40 of 53 entrainment with concealed fusion sites (75%) but at only 24 of 99 entrainment with QRS fusion sites (24%) (P<.0001). Radiofrequency energy was similar at sites with a PPI-VTCL difference of less than 30 milliseconds (24±7 W) compared with sites with larger PPI-VTCL differences (24±6 W, P=.6). S-QRS interval. Comparison of the S-QRS interval during entrainment and the EG-QRS interval during ventricular tachycardia assumes that the stimulated wave fronts exit from the circuit along the same pathway as the ventricular tachycardia wave fronts. Analysis of the S-QRS-EG-QRS difference therefore is performed only for the 81 sites at which pacing entrained ventricular tachycardia with concealed fusion and for which Stevenson et al Ablation of Reentry Circuits 1661 TABLE 4. S-QRS-EG-QRS Difference for Entrainment With Concealed Fusion Sites Radlofrequency S-QRS-EG-QRS, me No. Termination % < > Total S indicates stimulus; and EG, electrogram. electrograms were discernible (Table 4). Radiofrequency current terminated ventricular tachycardia at 8 of 41 sites (20%) in which the S-QRS-EG-QRS difference was 20 milliseconds or less (Figs 4 and 5), but radiofrequency termination also occurred at 6 of 40 sites (15%) with larger S-QRS-EG-QRS differences (P=.45). The postpacing interval was available for 53 sites with entrainment with concealed fusion (Table 5). The PPI-VTCL and S-QRS-EG-QRS intervals were concordant, both suggesting that the site was either in or out of the circuit at 72% of sites (P=.001), and 27 of 29 sites (93%) that had a short S-QRS-EG-QRS also had a short PPI-VTCL. Radiofrequency current terminated ventricular tachycardia at 7 of 27 sites (26%) for which both the PPI-VTCL and S-QRS-EG-QRS differences were short. However, a long S-QRS-EG-QRS difference does not preclude radiofrequency termination of tachycardia if the PPI-VTCL difference is short. Radiofrequency current also terminated ventricular tachycardia at 3 of 13 such sites (23%). Radiofrequency current terminated ventricular tachycardia at only one of 11 sites (9%) at which both the PPI-VTCL and S-QRS- EG-QRS differences were long. At only two sites, the S-QRS-EG-QRS difference was less than 20 milliseconds, but the PPI-VTCL difference was more than 30 milliseconds, and radiofrequency current at these sites did not terminate ventricular tachycardia. For sites that are in the reentry circuit, activation time can be assessed from the S-QRS interval during entrainment with concealed fusion as well as from electrogram timing Table 6 summarizes S-QRS intervals during entrainment with concealed fusion for 54 sites likely to be in the reentry circuit as indicated by a PPI-VTCL difference of less than 30 milliseconds or an S-QRS-EG-QRS difference of less than 20 milliseconds. Only one site had an S-QRS interval of less than 60 milliseconds. Radiofrequency current terminated ventricular tachycardia at 10 of 31 sites (32%) with an S-QRS interval of less than 70% of the ventricular tachycardia cycle length but at only 2 of 23 sites (9%) with longer S-QRS intervals (P=.04). Considering all 215 sites at which pacing entrained ventricular tachycardia with or without concealed fusion, radiofrequency terminated ventricular tachycardia at 14% of the 132 sites with an S-QRS interval of less than 70% of the ventricular tachycardia cycle length and longer than 60 milliseconds but at only 4% of the 83 sites with S-QRS intervals outside this range (P=.008).

16 1662 Circulation Vol 88, No 4, Part 1 October 1993 TABLE 5. Postpacing Interval Versus S-QRS-EG-QRS Difference at Entrainment With Concealed Fusion Sites Radiofrequency PPI-VTCL, S-QRS-EG-QRS, <30 ms <20 ms No. Termination % Total S indicates stimulus; EG, electrogram; PPI, postpacing interval; and VTCL, ventricular tachycardia cycle length. Downloaded from by guest on August 30, 2016 Electrograms. Bipolar electrograms were definable at 231 sites (Table 7 and Fig 13). The long-duration, low-amplitude fractionated signals often recorded from areas of scar during endocardial catheter mapping, as illustrated in Figs 4, 5, and 8, make assessment of local activation difficult. The electrogram onset relative to the QRS (EG-QRS) is shown in Table 7. For comparison among ventricular tachycardias with various cycle lengths, this interval is also expressed as a fraction of the ventricular tachycardia cycle length. Radiofrequency termination occurred at sites with an electrogram onset occurring anywhere from the last 30% of the cardiac cycle (late diastole) to the first 30% of the cardiac cycle (early systole). There was no relation between electrogram duration and ventricular tachycardia termination by radiofrequency (Fig 13). Radiofrequency application terminated ventricular tachycardia at 6 of 19 sites (32%) that had either an isolated diastolic potential (4 of 12 sites) or continuous electrical activity (2 of 7 sites). Radiofrequency application terminated tachycardia at 8% of the 222 sites without these electrograms (P=.005). However, isolated diastolic potentials and continuous activity were observed at only 8% of sites and identified only 25% of radiofrequency termination sites. Isolated diastolic potentials were more common at sites with entrainment with concealed fusion (11%) than at sites without entrainment with concealed fusion (2%, P=.005) and tended to be more common at sites with a PPI-VTCL difference of less than 30 milliseconds during entrainment (11% versus TABLE 6. S-QRS During ECF At Probable Reentry Circuit Sites S-ORS, % VCL Total Radlofrequency Termination % < > Total ECF indicates entrainment with concealed fusion; S, stimulus; and VTCL, ventricular tachycardia cycle length. Sites had entrainment with concealed fusion with either PPI or S-QRS intervals, suggesting the site was within the reentry circuit. 5%), although this did not reach statistical significance (P=.2). Predictors of ventricular tachycardia termination by radiofrequency. Factors associated with radiofrequency termination sites and combinations of these factors with odds ratios obtained from univariate logistic regression are shown in Table 8. The combination of entrainment with concealed fusion, a PPI-VTCL difference of less than 30 milliseconds, and an S-QRS interval of more than 60 milliseconds and less than 70% of the ventricular tachycardia cycle length was associated with a 36% likelihood of radiofrequency termination. An isolated diastolic potential or continuous electrical activity plus TABLE 7. All Sites Electrogram Characteristics for Total Radiofrequency Term V % EG-ORS onset, ms < to to to to > CEA Isolated DP EG-QRS/VTCL, ms < > EG duration, ms < > CEA indicates continuous electrical activity; CL, cycle length; DP, diastolic potential; Term, terminate, VT, ventricular tachycardia; and EG, electrogram. n=231.

17 Stevenson et al Ablation of Reentry Circuits 1663 ECG l l l Downloaded from by guest on August 30, 2016 ECF ENT U^ Bystanders W 1 l I 1~~~~ +s I -~ 1 a +- I R l 4k I I I I A I l l a FIG 13. Schematic representation of electrogram onset and duration relative to the QRS onset is shown. Electrogram timing was normalized to the ventricular tachycardia cycle length. The QRS onset is indicated by a vertical reference line. At the top is a schematic of the ECG. Horizontal lines extendfrom the electrogram onset to its end. Electrograms are grouped from top to bottom: sites with entrainment with concealed fusion and a postpacing interval or stimulus to QRS interval that suggested that the site was in the reentry circuit (ECF), sites with entrainment with QRS fusion and a postpacing interval suggesting that the site was in the circuit (ENT), or bystander sites. Sites at which a radiofrequency application terminated tachycardia are indicated by arrows. (See text for discussion.) entrainment with concealed fusion or a favorable postpacing interval were associated with a high likelihood of ventricular tachycardia termination. In contrast, if all of these features were absent, the likelihood of ventricular tachycardia termination was only 4%. In a multivariate logistic regression model (Table 9) using 178 sites with complete data, the postpacing interval isolated diastolic potentials or continuous electrical activity, and an S-QRS interval of more than 60 milliseconds and less than 70% of the ventricular tachycardia cycle length were independent predictors of tachycardia termination. When the postpacing interval was removed from the model, entrainment with concealed fusion was also an independent predictor (P=.04; relative risk, 3.1) with isolated diastolic potentials or continuous electrical activity and an S-QRS interval of more than 60 milliseconds and less than 70% of the ventricular tachycardia cycle length. Follow-up. There were no complications related to the procedure. Follow-up electrophysiological testing was performed 5 to 7 days after the procedure. Of 12 patients in whom radiofrequency termination sites were identified, 6 were rendered free of any inducible monomorphic ventricular tachycardia, sustained monomorphic ventricular tachycardia of a new morphology and cycle length was inducible in 3 patients, and in the remaining 3 patients at least one morphology of a previously observed ventricular tachycardia remained inducible. Of the 3 patients without a radiofrequency termination site identified, monomorphic ventricular tachycardia was inducible in all, although of a new morphology in one patient. Antiarrhythmic medications were discontinued in 5 of the 6 patients without inducible ventricular tachycardia. The same previously ineffective medications were continued in 2 patients whose inducible ventricular tachycardia appeared to be modi-

18 1664 Circulation Vol 88, No 4, Part 1 October 1993 Downloaded from by guest on August 30, 2016 TABLE 8. Predictors of Radiofrequency Termination ECF Yes No PPI-VTCL <30 ms Yes No DP or CEA Yes No S-QRS <70% VTCL >60 ms Yes No ECF+PPI-VTCL <30 ms* Yes No ECF+PPI+S-QRS <70% >60 ma Yes No ECF+DP or CEA Yes No DP or CEA+PPI Yes No Any DP/CEA/PPI/ECF Yes No Radiofrequency Odds No. Termination % Ratio 95% Cl CEA indicates continuous electrical activity; Cl, confidence interval; DP, isolated diastolic potential; ECF, entrainment with concealed fusion; PPI, postpacing interval; VTCL, ventricular tachycardia cycle length; and S, stimulus. *PPI-V.CL <30 ms during ECF or entrainment with QRS fusion. fied, and the third received an implantable defibrillator without antiarrhythmic medications. During a mean follow-up of 316±199 days, the 10 patients without inducible ventricular tachycardia or with only a new Logistic Regression Analysis for TABLE 9. Predictors of Tachycardia Termination by Radiofrequency Application Coefficlent +SEM P Odds Rato 95% Cl PPI-VTCL <30 ms S-QRS >60 ms <70% VTCL DP or CEA 1.04± The goodness-of-fit x2 was 6.34, P=.71, indicating that the model fit the data. CEA indicates continuous electrical activity; DP, isolated diastolic potential; Cl, confidence interval; ECF, entrainment with concealed fusion; PPI, postpacing interval; and VTCL, ventricular tachycardia cycle length. ventricular tachycardia morphology inducible have remained free of ventricular tachycardia recurrences. Of the 5 patients with persistently inducible ventricular tachycardia, 2 died within the next 2 weeks due to incessant ventricular tachycardia and cardiogenic shock, 1 underwent cardiac transplantation, 1 is alive with recurrent episodes of ventricular tachycardia terminated by an automatic implantable defibrillator, and 1 who had incessant ventricular tachycardia prior to the procedure had no ventricular tachycardia recurrences but died of congestive heart failure 3 months after the procedure. Discussion Studies in canine models,3,7,10,32-35 intraoperative mapping in humans,6,8,9,15 as well as analysis of resetting and entrainment of ventricular tachycardia17-20,25,38,39,50 provide strong evidence that ventricular tachycardias that arise from chronic myocardial infarcts are due to reentry and contain areas of slow conduction that are

19 desirable targets for ablation. During catheter mapping, areas of slow conduction are identified by long, fractionated electrograms and long S-QRS delays during pacing. Not all areas from which abnormal electrograms are recorded participate, however, in ventricular tachycardia reentry circuits. The existence of bystander areas in human infarct scars was suggested by Brugada et a124 and others2223,26 who observed fractionated electrograms that appeared to arise from an area of slow conduction but could be dissociated from the reentry circuit. Fractionated electrograms and diastolic electrical activity recorded at some sites appear and disappear without a change in the tachycardia,23,24 and cooling at some of these sites during intraoperative "cryothermal mapping" fails to alter the ongoing tachycardia.22 These "bystander areas" may be adjacent to the reentry circuit but are not critical for the maintenance of the tachycardia. The purpose of our study was to define criteria that could be applied during catheter mapping for differentiating bystander sites from sites that are participating in reentry circuits. We chose to develop criteria in computer simulations of reentry circuits because it is difficult to evaluate a variety of circuits with repeated trials of stimulation at multiple points in a given circuit in animal models. Radiofrequency Mapping During ventricular tachycardia mapping in humans, we used radiofrequency termination of ventricular tachycardia as an indication that the site was in a reentry circuit. Radiofrequency current does not stimulate neuromuscular fibers, which is consistent with the absence of ventricular ectopy or tachycardia resetting observed during radiofrequency application.5' Occasionally, abrupt onset of radiofrequency current application produces an ectopic beat. This was avoided in our study by ramping up the energy over 1 to 2 seconds. We excluded from analysis the two radiofrequency applications during which ventricular tachycardia termination was preceded by possible ectopic beats. It is theoretically possible that mild pain that sometimes accompanies radiofrequency application could terminate ventricular tachycardia by eliciting a reflex sympathetic or parasympathetic response, but our patients were heavily sedated. The low incidence of ventricular tachycardia termination, occurring during only 10% of radiofrequency applications, also makes this explanation unlikely. Ventricular tachycardia termination during radiofrequency application appeared to be a site-specific response, consistent with heating a portion of the reentry circuit. The failure of radiofrequency application to terminate ventricular tachycardia does not absolutely indicate that the site is outside the reentry circuit. Extensive intraoperative mapping studies have shown that ventricular tachycardia circuits in patients involving infarct scars often are relatively large, involving broad loops of circulating wave fronts, which may even propagate through myocardium beyond the infarct scar itself.5,6,8,9,1529,46 Some circuits involve broad sheets of fibers with entrances and exits into narrower passages through scar tissue. A relatively small radiofrequency lesion is unlikely to interrupt propagation through a wide sheet of tissue. It is encouraging, however, that Stevenson et al Ablation of Reentry Circuits 1665 ventricular tachycardia termination sites could be identified in the majority of patients. Entrainment With Concealed Fusion During ventricular tachycardia, pacing at some abnormal sites entrains ventricular tachycardia in a manner strikingly different than that observed during pacing at sites distant from the tachycardia circuit.15,17-20,25,50 The ventricular tachycardia is entrained but with an S-QRS delay and without a change in morphology of the paced QRS complex compared with those of the tachycardia. This is consistent with stimulation at a site in the reentry circuit or in an adjacent bystander area and has been called "exact entrainment" or "concealed entrainment." The term "concealed entrainment" was initially coined by Okumura and coworkers52 from studies of circus movement atrioventricular reentry tachycardia. Pacing at sites distal to the area of slow conduction (the atrioventricular node), stimulus capture was evident, but the heart appeared to be captured by excitation wave fronts from the stimulus site rather than the reentry circuit, and criteria for entrainment could not be demonstrated. This contrasts with stimulation at some ventricular tachycardia reentry circuit sites, which entrains the circuit but with the QRS having the same morphology as the tachycardia, with no QRS fusion because collision of the stimulated wave front and the tachycardia circuit wave fronts occurs within the scar.'5,17-20 We have therefore referred to this phenomena as "entrainment with concealed fusion." In our computer simulations, entrainment with concealed fusion could occur during pacing at bystander sites adjacent to the reentry circuit. Morady et a125 found that entrainment with concealed fusion was a poor predictor of successful DC shock ablation for ventricular tachycardia, further supporting the possible importance of bystander areas of slow conduction. In the present study, entrainment with concealed fusion was strongly related to ventricular tachycardia termination by a radiofrequency application at the site. Although radiofrequency current terminated ventricular tachycardia at only 17% of entrainment with concealed fusion sites, ventricular tachycardia terminated at only 6% of other sites. Failure of radiofrequency current to terminate ventricular tachycardia may indicate that the site is a bystander or is within a portion of the circuit that is broader than the width of the radiofrequency lesion. Analysis of the postpacing interval provides further insight. The postpacing interval, available for 53 entrainment with concealed fusion sites, suggested that 40 of these sites (75%) were within the circuit and 25% were bystanders. This suggests that bystander areas are relatively common in post-myocardial infarction ventricular tachycardia. Postpacing Interval Our observations on the postpacing interval in computer simulations are consistent with recent studies of entrainment of atrial flutter and circus movement reentry tachycardia.53,54 The postpacing interval represents the conduction time from the pacing site to and through the reentry circuit and back to the pacing site. It is always greater than the tachycardia cycle length when pacing at sites outside the circuit such as in a bystander pathway, nondominant bystander loop, or in a path

20 1666 Circulation Vol 88, No 4, Part 1 October 1993 from the common pathway exit to the QRS onset site. For sites in the reentry circuit, the postpacing interval equals the tachycardia cycle length if pacing does not alter conduction velocity or the pathway for propagation in the circuit. When conduction velocity slows in response to premature stimuli or rapid stimulus trains, the postpacing interval is longer than the tachycardia cycle length, particularly with very premature stimuli or rapid stimulus trains. In patients, activation time at the pacing site is difficult to assess from areas with long, fractionated electrograms. We assumed that activation occurred at some time during inscription of the bipolar electrogram. It is possible that some of this signal represents far-field electrical activity.46'55 In some cases, depolarization of small bands of fibers may generate such a low-amplitude signal that it is not detectable with endocardial mapping catheters in the electrical environs of the catheterization laboratory.5'46 Recording and pacing from the same electrode are necessary, and in some cases the signal is obscured for a prolonged interval after stimulation, precluding measurement of the postpacing interval. Conduction velocity in areas of slow conduction can behave decrementally in response to premature stimuli, and this is of particular concern in the presence of antiarrhythmic drugs, as in our study.18'38,50'56 In addition, the pathways for propagation through the reentry circuits can be determined at least in part by areas of functional block, which could be altered by premature stimuli. To attempt to minimize these potential concerns, the postpacing interval was measured from the latest capturing stimuli or slowest stimulus trains that entrained the ventricular tachycardia. We obtained the postpacing interval at 152 sites. A postpacing interval within 30 milliseconds of the ventricular tachycardia cycle length was strongly predictive of ventricular tachycardia termination during radiofrequency current. Comparison of S-QRS Interval With EG-QRS Interval Fontaine et at21 suggested that both the EG-QRS interval and the S-QRS interval during entrainment with concealed fusion reflect the conduction time from the pacing site to the QRS onset site for sites in the reentry circuit but not for sites in bystander areas. Thus, at circuit sites, the S-QRS during entrainment with concealed fusion should match the EG-QRS during ventricular tachycardia. Our computer simulation results support this hypothesis for many sites, but important exceptions were identified that can be suspected from analysis of other features during stimulation. First, if conduction in the circuit slows with premature stimuli or stimulus trains, the S-QRS interval lengthens and exceeds the EG-QRS interval at circuit sites as well as at bystander sites. Progressive lengthening of conduction intervals with premature stimuli or rapid trains is not uncommon and can be detected by plotting S-QRS intervals or the postpacing interval versus stimulus timing.18'38'39'50'56 Changing conduction velocity should also be suspected if RR interval oscillations occur after pacing In such situations, the slowest pacing rate and latest capturing stimuli will provide the closest approximation of conduction times during tachycardia. Second, when the conduction time from the circuit common pathway to a bystander site is long, resulting in bystander depolarization by an excitation wave after that wave has produced the QRS onset, the S-QRS can be either less than or equal to the EG-QRS interval. The latter situation occurs when the conduction time through the bystander pathway is equal to half of the tachycardia cycle length. At these bystander sites with relatively long conduction times to the circuit, resetting or entrainment would be seen only with very early stimuli or relatively rapid, long-duration stimulus trains. Less premature stimuli would capture the bystander site but have no effect on the tachycardia, identifying it as a bystander site. Another exception occurs with sites in a pathway between the common pathway exit and the QRS onset site. At these sites, the S-QRS interval equals the EG-QRS interval despite the location outside the circuit. The postpacing interval exceeds the ventricular tachycardia cycle length, however, distinguishing such sites from those in the circuit. A change in the QRS morphology during pacing may indicate that a stimulated antidromic wave front has exited the circuit from a site other than that used by the tachycardia wave fronts. The S-QRS-EG-QRS difference therefore was evaluated only for sites at which pacing entrains ventricular tachycardia with concealed fusion. At 27 of 29 sites where the S-QRS during entrainment with concealed fusion approximated the EG-QRS interval, the postpacing interval approximated the ventricular tachycardia cycle length, suggesting that they were within the circuit. Radiofrequency current terminated ventricular tachycardia at 26% of these sites. However, at 49% of the entrainment with concealed fusion sites at which the S-QRS did not match the EG-QRS, the postpacing interval matched the ventricular tachycardia cycle length, and radiofrequency current termination also occurred at some of these sites. Thus, failure of the S-QRS to match the EG-QRS did not reliably indicate that the site was distant from the circuit. The reasons for this are not clear, although we can speculate. In some circuits, the exit from a common pathway or slow conduction zone may have a broad fan-shaped configuration.1s If the conduction time from the common pathway exit to the QRS onset site changes during pacing, as could occur during propagation through a broader fan-shaped region, without changing the reentry circuit path, the S-QRS will not match the EG-QRS, although the postpacing interval will continue to match the ventricular tachycardia cycle length. A slight shift in the exit from the scar may not alter the QRS morphology sufficiently to be detectable. It is also possible that at high stimulus strengths, portions of the circuit were captured that were adjacent to the area producing the local electrogram. It is theoretically possible that local activation at the site was due to depolarization of a narrow band of fibers, the activation of which was not discernible from the bipolar catheter recordings, and that far-field activity was responsible for the signals recorded.46'55 We would expect this similarly to affect the PPI-VTCL relationship, however. The S-QRS-EG- QRS difference was assessed only at sites having entrainment with concealed fusion, and the number of sites with radiofrequency termination is relatively small. Evaluation of a larger number of sites, perhaps with greater fidelity recordings, is necessary to further define the predictive value of the S-QRS-EG-QRS relation.

21 S-QRS Interval Analysis of the S-QRS interval during entrainment with concealed fusion provides a further clue to the location of narrow regions in the circuit potentially susceptible to catheter ablation. The S-QRS interval should approximate the conduction time from the stimulus site to the exit from the scar if conduction velocity and pathway do not substantially change during entrainment. For entrainment with concealed fusion sites, radiofrequency termination occurred at 33% of sites having a S-QRS interval of more than 60 milliseconds and less than 70% of the ventricular tachycardia cycle length. Radiofrequency current terminated ventricular tachycardia at only 2 of 18 sites (11%) that appeared to be within the circuit based on the postpacing interval but had S-QRS intervals longer than 70% of the ventricular tachycardia cycle length. These findings are consistent with a recent report by Svenson et a129 of laser irradiation to terminate ventricular tachycardia during intraoperative mapping. Successful termination sites had activation times preceding the QRS onset by as much as 120 milliseconds. This would correspond to activation prior to the QRS onset by an interval 40% of the ventricular tachycardia cycle length assuming a ventricular tachycardia cycle length of 300 milliseconds (the mean value in their report). Electrograms During Catheter Mapping Catheter mapping allows sampling from only a few sites at a time. Evaluating the timing of electrograms relative to the QRS onset is a common practice but has been disappointing as a guide for catheter ablation.61,62 We also found that the onset of the local electrogram was a poor indicator of tachycardia termination during radiofrequency application. Fitzgerald and coworkers13,63 and Josephson and coworkersm suggested that isolated diastolic potentials and continuous electrical activity may identify reentry circuit sites. In the present study, isolated diastolic potentials or continuous electrical activity were associated with entrainment with concealed fusion and with ventricular tachycardia termination by radiofrequency application, suggesting that these sites often were in the reentry circuit. However, isolated diastolic potentials and continuous electrical activity were uncommon findings, occurring at only 8% of the sites, and identified only 25% of radiofrequency termination sites. Study Limitation Our computer simulations used anatomically fixed figure-eight reentry circuits. For some in vivo reentry circuits, the path of reentry wave front propagation is determined by regions of functional block or collision of excitation wave fronts.33,34,65 Our criteria, which are based on activation times, are valid only when the reentry path through the circuit does not change during entrainment. This requirement is supported by the observations of Littmann and coworkers,15 who studied entrainment during intraoperative mapping of subepicardial reentry circuits in humans. During entrainment with concealed fusion (exact entrainment), there was no change in the global epicardial activation sequence. Our present findings in humans also support the applicability of this model. In a canine model, however, El-Sherif Stevenson et al Ablation of Reentry Circuits 1667 and coworkers65 demonstrated that pacing at sites distant from the common pathway of a reentry circuit could alter the path of wave front propagation through the circuit while apparently entraining the tachycardia. Altering the reentry wave front pathways also altered the ventricular tachycardia cycle length and/or ventricular activation sequence on cessation of pacing. When the ventricular tachycardia cycle length or morphology is altered after cessation of pacing, it is possible that the reentry circuit has changed, and our criteria may not apply. The immediate resumption of the morphologically identical tachycardia at the same cycle length after cessation of pacing is, however, very common,15-21,38,39"44 although it may not exclude subtle changes in the reentry circuit pathway during stimulation. Intraoperative mapping studies suggest that a variety of reentry circuit configurations are possible involving subepicardial, subendocardial, and intramural reentry pathways.5-9'15'46 Although we evaluated a large number of sites, our observations are from a relatively small number of patients representing the most severe end of the spectrum of ventricular tachycardia, with multiple ventricular tachycardia morphologies, depressed ventricular function, and failure to respond to antiarrhythmic medications. It is likely that our experience reflects a biased sample of the types of reentry circuits. It is possible that ventricular reentry circuits are smaller or more easily abolished in less severe cases. During the mapping procedure, all except one patient were receiving antiarrhythmic medications, which are likely to alter electrical properties of the reentry circuits. We targeted only areas having abnormal electrograms to avoid damaging normal myocardium and to limit the duration of the procedure. It is theoretically possible that narrow isthmuses of normal tissue could participate in a reentry circuit and would not have been identified in this study. The percentage of ventricular tachycardia termination sites does not necessarily reflect the size of reentry circuits relative to the ventricle as we did not systematically evaluate areas distant from infarct scars. Comparison of the S-QRS interval and postpacing interval with the electrograms recorded from a site is based on the assumption that local activation occurs during inscription of the electrograms at the site. The precise activation is difficult to assess from fractionated low-amplitude electrograms typical of slow conduction in regions of scar. We used a liberal definition for match of the S-QRS with EG-QRS and postpacing interval with ventricular tachycardia cycle length (anywhere within the electrogram) because we thought it preferable to optimize sensitivity for identifying reentry circuit sites and because it was not possible to know whether any or all of the multiple rapid deflections recorded (Figs 4 and 5) indicated depolarization at the pacing site. A postpacing interval within 10 milliseconds of the electrogram occurred at only 30% of sites during entrainment, and the S-QRS was within 10 milliseconds of the EG-QRS at only 44% of entrainment with concealed fusion sites. It is possible that recording from more closely spaced electrodes would improve the accuracy of these methods. Tissue heating during radiofrequency application depends on adequate contact between the electrode and myocardium Good electrode myocardial tissue con-

22 1668 Circulation Vol 88, No 4, Part 1 October 1993 TABLE 10. Programmed Stimulation During Ventricular Tachycardia Site ECF PPI=VTCL S-QRS=EG-QRS Common pathway Dominant inner loop + + +/- Dominant outer loop - + Bystanders Dead-end pathway +/- - Rare Loop +/- _ Path from CP exit to QRS-onset site *Effect of the latest stimulus or slowest stimulus train that entrains tachycardia without changing the reentry path or conduction velocities. CP indicates common pathway; EG, electrogram; PPI, postpacing interval; VTCL, ventricular tachycardia cycle length; S, stimulus; and ECF, entrainment with concealed fusion. tact was indicated by the ability to pace 227 of 241 sites, stability on fluoroscopy, and stability on transesophageal echocardiography for 71 sites in six of our patients. Radiofrequency application quickly impairs cardiac electrical function in a focal area as indicated by the almost immediate conduction block observed when radiofrequency energy is applied to the site of accessory atrioventricular pathways in the Wolff-Parkinson-White syndrome.67 When observed, ventricular tachycardia termination usually occurred within 15 seconds of initiating radiofrequency application. The mean duration of radiofrequency application was 29±13 seconds at sites without ventricular tachycardia termination. An impedance rise or evidence of boiling on echocardiography indicative of heating to temperatures substantially greater than needed for lesion formation was observed during one third of radiofrequency applications, providing further evidence that tissue heating was occurring.42'66 However, temperature monitoring was not available during this study, and we cannot exclude the possibility that the failure of radiofrequency current to terminate ventricular tachycardia at sites predicted to be within the circuit was due to absence of tissue heating in some cases. Implications These findings and recent intraoperative mapping studies suggest a complex picture of ventricular reentry circuits arising from chronic myocardial infarcts. Isthmuses for impulse propagation exist in regions of scar and may contain zones of slow conduction. Focal radiofrequency lesions at some of these sites are capable of terminating ventricular tachycardia. The entrances to these isthmuses appear to be broader, and although in the circuit, a focal radiofrequency lesion at the entrance may be less likely to interrupt reentry. The circuit may contain loops outside the slow conduction pathways, possibly along the border of the scar, through relatively normal myocardium. Pacing at these sites entrains the ventricular tachycardia with QRS fusion due to propagation of the stimulated wave front rapidly away from the scar, but the postpacing interval approximates the ventricular tachycardia cycle length. Radiofrequency ablation at these sites is rarely successful in terminating ventricular tachycardia. Bystander areas of slow conduction are relatively common and may be recognized by dissociation of electrograms from the tachycardia13 and the postpacing interval during entrainment at the site. Radiofrequency application at bystander sites rarely terminates ventricular tachycardia. The possibility of multiple entrances and exits from the slowly conducting tissue can theoretically allow a variety of reentry circuit configurations to form.46 It is possible for an area of slow conduction that is a bystander relative to one tachycardia circuit to participate in another circuit.63 Examination of the S-QRS interval, electrograms relative to the QRS, and the postpacing interval may allow refinement in the localization of mapping sites relative to the reentry circuit, as summarized in Table 10. Slow conduction areas within the reentry circuit are attractive sites for catheter ablation. The optimal lesion size required for success and the importance of bystander slow conduction areas remain to be determined. Acknowledgment Supported in part by grant-in-aid 940 GI-1 from the American Heart Association, Greater Los Angeles Affiliate. References 1. Stevenson W, Weiss JN, Wiener I, Nademanee K. Slow conduction in the infarct scar: relevance to the occurrence, detection and ablation of ventricular reentry circuits resulting from myocardial infarction. Am Heart J. 1989;117: Klein H, Karp RB, Kouchoukos NT, Zorn GL, James TN, Waldo AL. Intra-operative electrophysiologic mapping of the ventricle during sinus rhythm in patients with a previous myocardial infarction: identification of the electrophysiologic substrate of ventricular arrhythmias. Circulation. 1982;66: El-Sherif N, Scherlag BJ, Lazzara R, Hope RR. Reentrant ventricular arrhythmias in the late myocardial infarction period, 1. Conduction characteristics in the infarction zone. Circulation. 1977;55: Josephson ME, Horowitz LN, Farshidi A. Continuous local electrical activity: a mechanism of recurrent ventricular tachycardia. Circulation. 1978;57: de Bakker JMT, van Capelle FJL, Janse MJ, van Hemel NM, Hauer RNW, Defauw J, Vermeulen F, de Wekker P. 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24 1670 Circulation Vol 88, No 4, Part 1 October Kay GN, Epstein AE, Plumb VJ. Resetting of ventricular tachycardia by single extrastimuli: relation to slow conduction within the reentrant circuit. Circulation. 1990;81: Marchlinski FE. Characterization of oscillations in ventricular refractoriness in man after an abrupt increment in heart rate. Circulation. 1987;75: Watanabe M, Zipes DP, Gilmour RF. Oscillations of diastolic interval and refractory period following premature and postmature stimuli in canine cardiac purkine fibers. PACE. 1989;12: Frame LH, Simson MB. Oscillations of conduction, action potential duration, and refractoriness: a mechanism for spontaneous termination of reentrant tachycardia. Circulation. 1988;78: Ross DL, Dassen WRM, Vanagt EJ, Brugada P, Bar FWHM, Wellens HJJ. Cycle length alteration in circus movement tachycardia using an atrioventricular accessory pathway. Circulation. 1982;65: Morady F, Scheinman MM, Di Carlo L, Davis JC, Herre JM, Griffin JC, Winston SA, De Buitleir M, Hantler CB, Wahr JA, Kou WH, Nelson SD. Catheter ablation of ventricular tachycardia with intracardiac shocks: results in 33 patients. Circulation. 1987;75: Garan H, Kuchar D, Freeman C, Finkelstein D, Ruskin JN. Early assessment of the effect of map-guided transcatheter intracardiac electrical shock on sustained ventricular tachycardia secondary to coronary artery disease. Am J Cardiol. 1988;61: Fitzgerald D, Friday KJ, Yeung-Lai-Wah J, Bowman AJ, Lazzara R, Jackman WM. Myocardial regions of slow conduction participating in the reentrant circuit of multiple ventricular tachycardia: report on ten patients. J Cardiovasc Electrophysiol. 1991; 2: Josephson ME, Horowitz LN, Farshidi A. Continuous local electrical activity: a mechanism of recurrent ventricular tachycardia. Circulation. 1978;57: El-Sherif N, Gough WB, Restivo M. Reentrant ventricular arrhythmias in the late myocardial infarction period, 14. mechanisms of resetting, entrainment, acceleration, or termination of reentrant tachycardia by programmed stimulation. PACE. 1987;10: Haines DE, Verow AF. Observations on electrode-tissue interface temperature and effect on electrical impedance during radiofrequency ablation of ventricular myocardium. Circulation. 1990;82: Jackman WM, Wang X, Friday KJ, Roman CA, Moulton KP, Beckman IU, McClelland JH, Twidalean, Hazlitt HA, Prior MI, Margolis PD, Calme JD, Overholt ED, Lazarra R. Catheter ablation of accessory atrioventricular pathways (Wolff-Parkinson-White syndrome) by radiofrequency current. N EngI J Med. 1991;324:

25 Identification of reentry circuit sites during catheter mapping and radiofrequency ablation of ventricular tachycardia late after myocardial infarction. W G Stevenson, H Khan, P Sager, L A Saxon, H R Middlekauff, P D Natterson and I Wiener Downloaded from by guest on August 30, 2016 Circulation. 1993;88: doi: /01.CIR Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX Copyright 1993 American Heart Association, Inc. All rights reserved. Print ISSN: Online ISSN: The online version of this article, along with updated information and services, is located on the World Wide Web at: Permissions: Requests for permissions to reproduce figures, tables, or portions of articles originally published in Circulation can be obtained via RightsLink, a service of the Copyright Clearance Center, not the Editorial Office. Once the online version of the published article for which permission is being requested is located, click Request Permissions in the middle column of the Web page under Services. Further information about this process is available in the Permissions and Rights Question and Answer document. Reprints: Information about reprints can be found online at: Subscriptions: Information about subscribing to Circulation is online at: