Functional approach to site-by-site catheter mapping of ventricular reentry circuits in chronic infarctions

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Journal of Electrocardiology Vol. 27 Supplement

bright. Because the lights are dimmed to some extent in many laboratories, bright signals on a black background seem much easier on eye than dark signals on a white background. Colors must be selected so that they work well together and allow information to be read from various points in the room. Heart rate and blood pressure displays must be large, for good visibility at a distance. Signals must be displayed with a pixel thickness that makes them highly visible from across the room.

Conclusion If we keep in mind our goals of designing and implementing systems that provide flexibility, useability, and expandability, we can build systems that will not become obsolete for a long period of time. The systems will be able to grow as EP grows and will provide a foundation on which we may build to meet the challenges of this rapidly changing field.

Functional Approach to Site-by-Site Catheter Mapping of Ventricular Reentry Circuits in Chronic Infarctions

William G. Stevenson, MD

Ventricular tachycardia that occurs late after myocardial infarction is most commonly due to reentry in the chronic infarct scar. ~ Localization of these reentry circuits is crucial for successful ablation. Surgical ablation is often effective, even without precise localization, because a relatively large section of tissue is removed. Current catheter ablation techniques produce small lesions that must be precisely positioned in a critical segment of the reentry circuit to interrupt reentry. Mapping must be precise. The standard approach has been activation sequence mapping. The timing of electrical activation at multiple sites is used to trace the reentry circuit path. Activation sequence mapping is most accurate when many sites can be sampled simultaneously throughout the ventricles. For reasons that are discussed below, it is difficult to apply to catheter mapping of reentry circuits in infarct scars. An alternative approach is to interrogate a single site at a time, assessing the relation of the site to a reentry circuit from the effects of a perturbation such as heating, cooling, or electrical stimuli applied to the sitef1-6 Interruption of tachycardia by heating or cooling the site suggests that the site is in the reentry circuit (Fig. 1). Depolarizing electrical stimuli may reset the tachycardia in a characteristic manner. Many of these techniques are applicable to catheter mapping but are limited to those patients who have a hemodynamically tolerated, sustained, and stable tachycardia. From the Cardiovascular Division, Department of Medicine, Harvard Medical School Brigham and Women's Hospital Boston, Massachusetts.

Reprint requests: William G. Stevenson, MD, Cardiovascular Division, Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115.

Reentry Circuits in Infarct Scars Intraoperative activation sequence mapping has shown that reentry circuits in chronic infarct scars vary greatly in size and geometric configuration.7-~3 In many cases, the reentry path is complex and may traverse subepicardial, subendocardial, and intramural regions in the chronic infarct. Many circuits contain regions where conduction velocity is slowed, probably by decreased cell-to-cell coupling that accompanies surrounding fibrosis, ln4 Propagation through myocytes in the chronic infarct scar does not generate electrical activity detectable in the standard body surface electrocardiogram (ECG). The QRS complex in the standard ECG is inscribed by wave fronts that emerge from the scar to propagate across the ventricles. In some cases, the reentry circuit may be contained entirely within the chronic infarction, and the wave fronts exiting from the scar are not participating in the reentry circuit. In other cases, the wave fronts that exit the chronic infarction propagate along the border of the infarct and reenter it, returning to the regions of slow conduction in the scar. The region of slow conduction may extend over several centimeters or be confined to a relatively small area. Regions of slow conduction are desirable targets for ablation. They are critical for reentry, are an electrically abnormal, relatively small amount of tissue, and are unlikely to contribute important contractile function. Electrograms recorded from such areas typically have a low amplitude and multiple rapid components (fractionation) due to asynchronous activation of myocyte bundles (Fig. 1). Fractionated electrograms are a useful guide to the regions of

Site-by-Site Catheter Mapping in Chronic Infarctions A

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Fig. 1. Pacing during ventricular tachycardia (A) and termination of ventricular tachycardia by application of radiofrequency current (RF) at the mapping site (B). From the top of each tracing are 50 ms time lines, surface ECG leads I, aVF, Vl, and Vs, and a bipolar intracardiac recording filtered at 3 0 - 5 0 0 Hz from the distal electrode pair of the mapping catheter at left ventricular (LV) site! 10. (B) Recordings from the proximal electrode pair (p). The electrogram recorded at the mapping site is fractionated, with multiple rapid components, and has a duration longer than 150 ms. (A) Sustained monomorphic ventricular tachycardia with a cycle length of 530 ms is present. The last three beats of a stimulus train with a cycle length of 460 ms is shown. The stimuli accelerate tachycardia to the pacing rate without altering the QRS morphology, consistent with entrainment with concealed fusion. Pacing introduces noise in the bipolar recording, which decays after the last stimulus. The postpacing interval, indicated by the dashed line from the last stimulus, matches the tachycardia cycle length of 530 ms, consistent with pacing at a reentry circuit site. The S-QRS interval is 70 ms and matches the electrogram-toQRS interval as indicated by the dashed line from the last QRS onset to the bipolar electrogram. This relatively short SQRS interwal is consistent with pacing near the exit from the chronic infarction slow conduction zone. (B) Radiofrequency current applied to site 10 terminates ventricular tachycardia after four beats, followed by sinus rhythm. All times are in milliseconds. SMVT, sustained monomorphic ventricular tachycardia. From Stevenson et al. 6 With permission.

abnormal electrical activation. Fractionated electrograms may also arise from abnormal "bystander" regions that are not actually in the reentry circuit. 3.6a5-17 Fractionated broad electrograms, often > I00 ms in duration, also make precise assessment of activation time difficult, and can be obscured by depolarization of ,adjacent large masses of tissue in the infarct border zone. 9 Assessment of propagation through the chronic infarct scar can be difficult. Even intraoperative mapping with multiple simultaneous electrode recordings often fails to delineate an entire reentry circuit. With catheter mapping, the ability to assess only a few sites further complicates the interpretation of activation times. When the QRS complex is due to propagation of excitation wave fronts away from the infarct scar, sites in the chronic infarct proximal to the exit from the scar should be depolarized before QRS onset. Identification of "presystolic" electrical activity may indicate a reentry circuit site or a bystander region. We found that electrogram timing did not predict termination of ventricular tachycardia by application of radiofrequency (RF) current during catheter mapping. 6 Isolated mid-diastolic potentials were associated with tachycardia termination and may be due to depolarization of narrow isthmuses of tissue in the chronic infarct z o n e . 6,9A8

Application of Radiofrequency Current to Identify Reentry Circuit Sites During intraoperative mapping, impairment of conduction produced by digital pressure, focal cooling, and laser photoablation have been used to identify reentry circuit sites. 2-5 Termination of tachycardia suggests that the site

is in the reentry circuit, Application of RF current to heat the tissue at the electrode site can be used similarly during catheter mapping 6 (Fig. 1). There is extensive experience with RF ablation in patients with accessory atrioventricular connections (Wolff-Parkinson-White syndrome). Radiofrequency current application to the site of an accessory pathway produces conduction block when the temperature exceeds 48°C without causing propagated depolarizations. 19 We applied RF current to 248 sites during 31 sustained monomorphic ventricular tachycardias in 15 patients with chronic myocardial infarctions. 6 Radiofrequency application terminated ventricular tachycardia at 24 (10%) sites after an average of 13 seconds (range, 1-46 seconds). This suggests that tachycardia termination by RF application is relatively specific. There are several limitations to this approach, however. Lesions produced by RF catheter ablation are relatively small. Tachycardia termination probably indicates that a relatively narrow portion of the reentry circuit has been identified or that the circuit is small. If tachycardia fails to terminate, this does not exclude participation of the site in the reentry circuit. The mapping site may be in a relatively broad portion of the circuit where the RF lesion is too small to interrupt propagation. Temperature monitoring will be useful to ensure that heating actually occurs. 19

Programmed Electrical Stimulation at Mapping Sites Most hemodynamically stable ventricular tachycardias that occur in regions of chronic infarction can be entrained by pacing stimuliP °'21 This is consistent with the presence

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Journal of Electrocardiology Vol. 27 Supplement

of an excitable gap at all points in the reentry circuit after excitability has been restored, before arrival of the next circulating depolarization wave front. A premature stimulus during the excitable gap may reset or terminate the tachycardia. This allows programmed electrical stimulation to be used to assess the position of a mapping site relative to the reentry circuit, as is discussed below. For this purpose, we have performed unipolar stimulation, w i t h the exploring tip electrode of the mapping catheter serving as the cathode and an electrode in the inferior vena cava serving as a remote anode. This precludes the possibility of stimulation at the anode that can occur during bipolar pacing. 22

Functional Components of Reentry Circuits For studying the effects of programmed stimulation, we have developed a simple reentry circuit model 6'23 (Fig. 2). A circulating excitation wave front propagates through a slow conduction zone (SCZ) in the scar to the exit from

Outer Loop

the scar. The wave front then propagates through one or both of two different loops to return to the SCZ. An outer loop consists of the myocardium along the border of the scar. This is a broad path, and the excitation wave front also propagates away from the scar, generating electrical activity that contributes to the QRS complex, as it propagates through this loop. A second inner loop is contained within the chronic infarct, and depolarization of tissue in the inner loop is not detectable in the surface ECG. Depolarization of tissue in the SCZ also does not generate electrical activity detectable in the surface ECG. The SCZ has an entrance (site 10 in Fig. 2) and an exit where the excitation wave front leaves the SCZ (site 1 in Fig. 2). The SCZ exit may coincide with the exit from the scar where the wave front begins propagating through the myocardium away from the chronic infarct generating QRS onset. Alternatively, the SCZ exit may be located some distance within the scar. Using this simple scheme, a variety of potential reentry circuit types can be studied. A circuit may contain a single loop, multiple loops, and multiple SCZs. This scheme also allows for bystander regions that are adjacent to the reentry circuit but do not participate in the circuit. These may take the form of dead-end pathways (containing sites C, H, and E in Fig. 2). When a circuit has multiple loops, the loop with the shortest conduction time is the dominant loop that sets the tachycardia cycle length, and the other loops behave as bystanders.

Entrainment With Concealed Fusion

:r Loop ECG _~

Fig, 2. The functional components of a reentry circuit. The gray stippled area is the inexcitable scar. The path of excitation wave fronts are shown as black arrows. Selected sites are designated by numbers or letters. The reentry circuit consists of a slow conduction zone (SCZ) from site 10 to site 15 and then to site 1. The reentrant wave front propagates from the entrance to the SCZ near site 10, then through the SCZ to its exit at site 1. The reentry wave fronts then propagate through two loops. An inner loop from site 3 to site 6 and then to the SCZ entrance is contained within the chronic infarct scar. Depolarization of tissue in the inner loop is not detectable in the surface ECG. An outer loop from site 21 to site 25 and then site 30 courses along the border of the infarct scar. Wave fronts that depolarize the outer loop also propagate away from the scar, contributing to the QRS in the surface ECG. QRS onset occurs after the excitation wave front exits the SCZ and reaches site 38 at the edge of the infarct zone. Bystander pathways, containing sites E, C, and H are attached to the reentry circuit. Modified from Stevenson. 34 With permission.

When a train of stimuli at a rate slightly faster th.an that of the tachycardia captures a portion of the reentry circuit, each stimulus will reset the tachycardia. Continuous resetting of a reentry circuit is entrainment,x°'xl As classical entrainment was initially described, the pacing site was distant from th.e reentry circuit. Pacing stimuli produce excitation wave fronts that propagate over to the reentry circuit, altering the sequence of ventricular activation remote from the chronic infarct. The QRS complexes in the surface ECG are altered, reflecting fusion between the stimulated wave fronts and the excitation wave fronts emerging from the reentry circuit. Pacing stimuli at reentry circuit sites and some bystander sites can reset tachycardia without altering the QRS complex 6'1x'2x-25 (Figs. 1, 3). This has been called entrainment with concealed fusion (ECF), 6 exact entrainment, ix and a form of concealed entrainment. x5 The mechanism is illustrated in Figure 4. Stimulation at a site in the reentry circuit SCZ in the chronic infarct produces an orthodromic wave front that propagates to the exit and then across the ventricles, producing a QRS complex that has the same morphology as that of the tachycardia. The stimulated antidromic wave fronts that propagate from the stimulus site toward the entrance of the SCZ are contained in or near the infarct scar by collision with a returning orthodrornic wave front. Fusion QRS complexes, a halhnark of classical entrainment, are absent, but wave front collision generating fusion electrograms is

Site-by-Site Catheter Mapping in Chronic Infarctions

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Fig. 3. Two examples of entrainment with concealed fusion. From the top of each panel are surface ECG leads I, aVF, V~, and Vs, and[ a bipolar electrogram filtered at 30-500 Hz recorded ~rom an inferobasal left ventricular site (LV-6). In each panel, sustained monomorphic ventricular tachycardia having a cycle length of 480 ms is shown. The last three stimuli (S) of a stimulus train are shown. (A) The stimulus train has a cycle length of 440 ms. (B) The stimulus train has a slightly shorter cycle length of 420 ms. In botE panels, tachycardia is accelerated to the pacing cycle length, with no change in the QRS morphology, consistent with entrainment with concealed fusion. (A) The stimulus to QRS (S-QRS) measured from the last stimulus to the last QRS that is accelerated to the pacing cycle length is 330 ms. The S-QRS interval is slightly longer than the electrogram-to-QRS interval as indicated by the dashed line from t]be last QRS on the right. The postpacing interval is slightly longer than the ventricular tachycardia cycle length as indicated by the dashed line from the last stimulus. (B) Pacing at a ,,;lightly faster cycle length entrains tachycardia with concealed fusion. As compared to A, the S-QRS interval increases by 50 ms to 380 ms, and the postpacing interval increases by 80 ms, from 500 to 580 ms. These findings are consistent with further conduction slowing in the reentry circuit as the pacing rate is increased. From Stevenson. 3~ With permission.

occurring within the scar. Hence the term ECF. The same findings can be seen with single extrastimuli that reset the tachycardia. 6,26 Entrainment with concealed fusion indicates that the pacing stimuli are able to reset the circuit without altering the sequence of ventricular activation distant from the reentry circuit. It is likely that the pacing site is in or adjacent to the reentry circuit. This is supported by our findings during catheter mapping and RF ablation in patients. 6 Entrainment with concealed fusion was observed at 86 of 241 sites during mapping of 31 monomorphic ventricular tachycardJias. Radiofrequency application terminated ventricular tachycardia at 17% of ECF sites as compared with 6% of sites where entrainment with QRS fusion was observed (odds ratio of 3.4, with a 95% confidence interval of 1.4-8.3). Entrainment with concealed fusion can also

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Fig. 4. Data generated from a computer simulation of pacing in a slow conduction zone in a chronic infarct region. A reentry circuit schematic is at the top. The reentry circuit is similar to that in Figure 2 with a slow conduction zone from site 10 to site 1. Pacing is performed at site 15 within the slow conduction zone. In this and subsequent schematics, tachycardia excitation wave fronts are solid black arrows, stimulated orthodromic wave fronts are open arrows, and stimulated antidromic wave fronts are hatched arrows. A schematic ECG and representation of the activation time from the pacing site (site 15) are shown in the schematic at the bottom. A pacing stimulus (S) is represented by the vertical black line. A capturing stimulus during the excitable gap at site 15 produces orthodromic (open arrows) and antidromic (hatched arrows) wave fronts. The stimulated antidromic wave front travels toward site 10 where it is extinguished by collision with a returning tachycardia wave front (solid arrow). The stimulated orthodromic wave front travels from site 15 to site 1 and then out of the scar, producing an early QRS, and continues through the circuit, resetting the tachycardia. As shown in the ECG schematic, the advanced beat has the same QRS morphology as that of the tachycardia because the stimulated antidromic wave front is contained within the scar, and the stimulated orthodromic wave front exits the scar from the same site as the tachycardia wave fronts. The stimulated orthodromic wave front returns to the pacing site after one full revolution through the circuit. Hence, the interval from the stimulus to the next depolarization at the pacing site (postpacing interval) equals the tachycardia cycle length (391 ms). The S-QRS interval reflects the conduction time from the pacing site to the QRS onset site (248 ms). This equals the electrogram-to-QRS interval measured during tachycardia as indicated by the arrow from the first electrogram to QRS onset. All times are in milliseconds. Modified from Stevenson et al. 6 With permission.

134

Journal of Electrocardiology Vol. 27 Supplement

B

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interval 62O Fig. 5. Entrainment with concealed fusion during pacing at a bystander site in (A) a patient and (B) a computer simulation. From the top are 50 ms time lines, surface ECG leads I, aVF, Vl, and Vs, and a bipolar intracardiac recording from the distal electrodes of a left ventricular mapping catheter (LV-7/8). Sustained monomorphic ventricular tachycardia with a cycle length of 540-530 ms is present. The last three beats of a stimulus (S) train at a cycle length of 440 ms are shown. The QRS complexes are accelerated to the pacing rate. The S-QRS interval measured to the last entrained QRS complex (which occurs at the pacing cycle length) is 540 ms. The interval one tachycardia cycle length after the last stimulus is indicated by the dashed line. There is no evidence of electrical activity at that time in the bipolar recording. The dashed line from the last QRS indicates the point preceding the QRS onset by the S-QRS interval of 540 ms during pacing. There is no electrical activity inscribed at that point. Both of these findings are consistent with a bystander site. Radiofrequency application at this site failed to terminate ventricular tachycardia (now shown). (B) Data from a computer simulation. The tachycardia cycle length is 391 ms. A single stimulus (S) at bystander site C produces an excitation wave front that propagates to the reentry circuit and enters the slow, conduction zone at site 15. The wave front then splits into an orthodromic wave front (open arrow) traveling toward site 1 and an antidromic wave front (hatched arrow) traveling toward site 10. The antidromic wave front is extinguished within the infarct scar by collision with a returning tachycardia wave front (solid arrows). Antidromic wave fronts do not change the ventricular activation sequence outside the scar. The orthodromic wave front exits the slow conduction zone from the same site as the tachycardia wave fronts, and continues through the circuit, resetting the tachycardia. The QRS morphology of the advanced beat is similar to that of the tachycardia. Tachycardia is entrained with concealed fusion. The orthodromic wave front propagates through the circuit loops and arrives back at the stimulation site after propagating from the stimulus site to the circuit, through the circuit, and then back to the stimulus site. The postpacing interval (497 ms) equals the revolution time through the circuit plus the conduction time into and out of the circuit, and therefore exceeds the tachycardia cycle length. The S-QRS interval (299 ms) equals the conduction time from the stimulus site to the reentry circuit and then to the QRS onset site. The electrogram-QRS interval during tachycardia (193 ms) does not equal the S-QRS interval because as a tachycardia wave front travels from the slow conduction zone to the bystander site, a wave front is traveling through the distal portion of the slow conduction zone to the QRS onset site. All times are in milliseconds. Modified from Stevenson et al. 6 With permission.

occur at some bystander sites6'23 (Fig. 5). Analysis of the postpacing interval suggested that 25% of sites with ECF were bystanders in our series. Another potential source of error is failure to recognize subtle QRS morphology changes that indicate QRS fusion in the standard surface ECG. The faster the pacing rate, the further the antidromic wave front propagates before colliding with an orthodromic wave frontfl 7 If the pacing site is close to an entrance to the SCZ, for example, the antidromic wave front may propagate out away from the infarct region and depolarize myocardium distant from the scar, producing QRS fusion. 23 In this case, a stimulus train slightly faster than the tachycardia entrains tachycardia with concealed fusion and a faster train entrains tachycardia with QRS fusion.

Identifying Bystander Sites From the Postpacing Interval Analysis of electrograms at the pacing site during entrainment can help distinguish bystanders from reentry circuit sites. 6 During pacing at reentry circuit sites, the last stimulus produces an antidromic wave front that collides with the previous orthodromic wave front (Fig. 4). The pacing site is next depolarized by the stimulated orthodromic wave front after it has made one complete revolution through the reentry circuit. The interval from the last stimulus to the next depolarization at the pacing site, designated the postpacing interval, equals the time for one revo-

S i t e - b y - S i t e C a t h e t e r M a p p i n g in Chronic infarctions

lution through the reemry circuit, which is the tachycardia cycle length (Figs. i, 4). In contrast, during entrainment by pacing from a bystander site (Fig. 5), the excitation wave front from the last stimulus must propagate to the reentry circuit, through the circuit, and then back to the pacing site. The postpacing interval then exceeds the tachycardia cycle length. Because the postpacing interval reflects the conduction time to and from the circuit plus the conduction time through the circuit, it progressively increases as the conduction time between the pacing site and reentry circuit increases. Furthermore, if pacing at the reentry circuit site entrains tachycardia with QRS fusion, the postpacing interval still indicates conduction time through the circuit and cart be used to identify outer loop sites (see below). Limitations of the postpacing interval to identify reentry circuit sites have been studied in computer simulations and humans. 6 Because the postpacing interval reflects conduction time through the reentry circuit, any change in conduction during entrainment, such as conduction slowing at the faster rate, will be reflected in the postpacing interval. Conduction slowing is to be expected when the pacing rate substantially exceeds the tachycardia cycle length and in the presence of antiarrhythmic medications. In these cases, the postpacing interval can exceed the tachycardia cycle length during entrainment from a reentry circuit site (Fig. 3). It is likely that portions of the reentry path are defined by areas of functional block or collision of wave fronts. During entrainment, the location or extent of block may change, increasing the length of the reentry path, prolonging conduction times, and increasing the postpacing interval. 2s'29 To avoid altering conduction and the reentry path, pacing should be performed at the slowest cycle length that entrains tachycardia. For assessment of scanning single stimuli, the postpacing J[nterval should be determined from the latest stimulus that captures and resets the tachycardia. Analysis should be restricted to stimuli that are followed by resumption of the same tachycardia, because a change in QRS morphology or cycle length may indicate a change in the reentry circuit, although not always. 3° Analysis of the postpacing imerval requires identification of depolarization at the pacing site from the recorded electrogram. 6"3J We there~bre record electrograms from the mapping catheter electrode(s) used for stimulation. Pacing introduces electrical noJise that obscures these electrograms in some cases. Electrograms recorded from regions of slow conduction often have multiple rapid components and a long duration, and preciise determination of local activation is not always possible. In some cases, electrograms are generated by distant tissue. 9'32 After defining the postpacing interval in computer simulations, we evaluated it during entrainment of ventricular tachycardia at 152 endocardial sites. 6 In the bipolar recording from the distal electrodes, the point at an interval equal to the tachycardia cycle length after the last stimulus was identified (Figs. 3, 5). The minimum difference between the tachycardia cycle length and the postpacing interval was defined[ as the time from this point to the nearest electrogram. This difference versus the likelihood that RF current application would terminate ventricular tachycardia

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Fig. 6. The difference between the postpacing interval (PPI) following entrainment and ventricular tachycardia cycle length (VTCL) on the x axis versus the percent of sites where radiofreqnency current application terminated VT on the y axis. Data are from 152 sites where pacing entrained VT and a postpacing interval was measurable from the distal bipolar electrode pair of the pacing catheter. The number of sites (n) for each PPI-VTCL interval is shown below each column. Ventricular tachycardia was terminated at 20% of the sites where the PPI-VTCL difference was -<30 ms, and at 4% of the sites where the PPI-VTCL > 30 ms. Modified from Stevenson et al. 6 With permission. is shown in Fig. 6. Radiofrequency current terminated tachycardia at 20% of sites when the difference between the postpacing interval and ventricular tachycardia cycle length was 30 ms or less as compared with 4% for sites with longer differences.

Stimulus-QRS Interval During Entrainment With Concealed Fusion During pacing at a site in the reentry circuit, the stimulated orthodromic wave fronts are probably following the same course as the orthodromic tachycardia wave fronts. 6'12,33 During ECF, the stimulus to QRS interval (SQRS) reflects the conduction time from the pacing site to the site at which QRS onset occurs (the exit from the chronic infarct). At reentry circuit sites, the S-QRS interval should equal the electrogram to QRS interval during tachycardia, assuming that the electrogram reflects depolarization at the pacing site 37 (see Fig. 4). During pacing at a bystander site that entrains tachycardia with concealed fusion, the S-QRS interval indicates the conduction time from the pacing site to the circuit, then orthodromically through the circuit to the QRS onset site (Fig. 5). The SQRS interval usually will exceed the electrogram to QRS interval, although exceptions can occur. 6 The limitations of

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Journal of Electrocardiology Vol. 27 Supplement

T a b l e 1. Functional Classification of M a p p i n g Sites Based o n Entrainment

Entrainment with concealed fusion Reentry circuit sites: PPI-VTCL <30 ms or S-QRS-EG-QRS <20 ms Relation to circuit slow conduction zone(s) Exit S-QRS < 30% of VTCL Central S-QRS31-50% of VTCL Proximal S-QRS 51-70% of VTCL Loop S-QRS>70% of VTCL Bystander: PPI > VTCL Entrainment with QRS fusion Reentry Circuit Outer Loop: PPI-VTCL <30 ms Reentry Circuit Bystander: PPI-VTCL>30 ms EG-QRS, electrogram-to-QRS onset interval measured during tachycardia; PPI, postpacing interval; VTCL,ventricular tachycardia cycle length. From Ste'/enson.34 With permission.

this analysis are similar to those of the postpacing interval discussed above. The conduction times and reentry paths during entrainment must remain the same as during tachycardia, and the recorded electrogram must indicate depolarization of the pacing site. This analysis has been studied only during ECF. In our initial experience with humans, the S-QRS interval versus electrogram-QRS interval during ECF did not reliably predict tachycardia termination by RF application. 6 An S-QRS that matched the electrogram-QRS inter-

val within 20 ms was associated with a short difference between the postpacing interval and ventricular tachycardia cycle length in 93% of cases and was likely the cause of tachycardia termination by application of RF. An S-QRS interval that did not match the electrogram-QRS interval did not reliably predict the postpacing interval, however. The reasons for this discrepancy are not clear. It is possible that in some cases, the stimulated wave front exited from the chronic infarct over a slightly different path than the tachycardia wave fronts. This produced entrainment with subtle QRS fusion that was not detected in the five-lead surface ECGs used in this study. The S-QRS then does not indicate the conduction time from the pacing site to the exit used during tachycardia, but the postpacing interval still indicates the revolution time through the circuit.

Applying a Functional Reentry Circuit Site Classification The effects of programmed electrical stimulation can be used to relate an individual mapping site to its position in the reentry circuit relative to regions of slow conduction (Table 1). Reentry circuit sites at which pacing entrains tachycardia with concealed fusion are likely to be in the chronic infarct zone. The S-QRS indicates the conduction time from the pacing site to the exit from the infarct. A

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Fig. 7. Resetting with QRS fusion by pacing at a reentry circuit outer loop site in (A) a patient and (B) a computer simulation. Starting from the top of A are 50 ms time lines, surface ECG leads I, aVF, V1, and Vs, and a bipolar recording filtered at 30-500 Hz from a left ventricular mapping catheter (LV-6/8). Sustained monomorphic ventricular tachycardia at a cycle length of 470 ms is present. A single stimulus (S) at the mapping site alters the Q RS morphology of the following beat, consistent with rapid propagation of a stimulated wave front away from the scar. Tachycardia is reset. The postpacing interval (dashed line from stimulus) equals the tachycardia cycle length, consistent with a site in the reentry circuit. (B) Figure-of-eight reentry circuit similar to that in Figure 4 and a schematic ECG and intracardiac electrogram from the pacing site. The tachycardia cycle length is 463 ms. A single stimulus (S) in the outer loop (site L) produces orthodromic wave fronts (open arrows) and antidromic wave fronts (hatched arrows). The antidromic wave fronts propagate away from the stimulus site into the myocardium distant from the scar, altering the QRS morphology. The antidromic wave fronts also collide with the tachycardia wave fronts (solid arrows). The orthodromic wave front propagates to the common pathway entrance into the slow conduction zone, resetting the tachycardia. The stimulated orthodromic wave front returns to the pacing site after one revolution through the circuit, and the postpacing interval approximate the tachycardia cycle length. Modified from Stevenson et al. 6 With permission.

Site-by-Site Catheter Mapping in Chronic Infarctions

Ent QRS Fus Outer Loop Bystander Indeterminant 0

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137

Future Directions

RF Effect On VT ECF Sites SCZ Exit SCZ Central SCZ Proxirnall Loop Bystander

1 0 0 8 0 60 40 20

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40

Number of Sites % VT Termination Fig, 8. DalLa from 309 mapping sites in 18 patients with 47 different morphologies of sustained monomorphic ventricular tachycardia. Sites are classified according to their functional relation to the reentry circuit as shown in Table 1. The type of site is shown on the left. The number of sites is shown as the horizontal bars extending to the left of the 0 line. The likelihood that an application of radiofrequency current would terminate ventricular tachycardia is represented as the horizontal bar extending to the right of the 0 line. ECF, entrainment with concealed fusion; Ent QRS Fus, ,entrainment with QRS fusion; SCZ, slow conduction zone; VT, ventricular tachycardia. From Stevenson. 34 With permission.

short S-QRS indicates a position near the exit. The S-QRS becomes progressively longer as the pacing site is moved to more proximal sites in the circuit. Sites with very long S-QRS intervals are likely to be in an inner loop (Fig. 3). At outer loop sites, the stimulated excitation wave fronts can propagate away from the scar, altering the QRS configuration and entraining tachycardia with QRS fusion. These sites can be identified as within a reentry circuit from the postpacing interval, which approximates the tachycardia cycle length (Fig. 7). Pacing at bystanders may produce ECF but long postpadng intervals or entrainment with QRS fusion and long postpacing intervals. If pacing entrains tacbycardia with QRS fusion but the postpacing interval cannot be determined, the site is currently classified as indeterminant. The relation between the predicted mapping site location and termination by application of RF current is shown in Figure 8 for 309 sites in 18 consecutive patients. 34 The greatest likelihood of RF termination was observed at sites near or just proximal to the SCZ exit. This suggests that regions approaching the exit from the scar are often relatively narrow. Termination of ventricular tachycardia is u n c o m m o n at sites with very long S-QRS intervals (exceeding 70% of the tachycardia cycle length), consistent with inner loop sites in circuits with multiple loops or relatively wide loops. The likelihood of tachycardia termination by RF application is also low at outer loop sites and bystanders.

Programmed electrical stimulation at reentry circuit sites can be used to interrogate an individual site, determine if it is in the reentry circuit, and assess its position relative to regions of slow conduction in the circuit. This approach is immediately applicable to current catheter techniques. Our initial data are promising but must be extended to larger series of patients, especially given the heterogeneity of reentry circuit configurations in the postmyocardial infarction population. We hope that further characterization and understanding of h u m a n ventricular reentry circuits will be achieved by these investigations, allowing rapid targeting of sites for catheter ablation of this difficult arrhythmia.

References 1. Weiss JN, Nademanee K, Stevenson WG, Singh B: Ventricular arrhythmias in ischemic heart disease. Ann Intern Med 114:784, 1991 2. Carom J, Ward DE, Spurell RAJ, Rees GM: Cryothermal mapping and cryoablation in the treatment of refractory cardiac arrhythmias. Circulation 62:67, 1980 3. Gessman LJ, Endo T, Egan J e t al: Dissociation of the site of origin from the site of cryo-termination of ventricular tachycardia. PACE 6: I293, 1983 4. Svenson RH, Littmann L, Gallagher JJ et al: Termination of ventricular tachycardia with epicardial laser photocoagulation: a clinical comparison with patients undergoing successful endocardial photocoagulation alone. J Am Coll Cardiol 15:163, i990 5. Gallagher JD, Del Rossi AJ, Fernandez J et al: Cryothermal mapping of recurrent ventricular tachycardia in man. Circulation 71:733, 1985 6. Stevenson WG, Khan H, Sager P e t al: Identification of reentry circuit sites during catheter mapping and radiofrequency ablation of ventricular tachycardia late after myocardial infarction. Circulation 88:1647, 1993 7. de Bakker JMT, van Capelle FJL, Janse MJ et al: Macroreentry in the infarcted h u m a n heart: mechanism of ventricular tachycardias with a focal activation pattern. J Am Coll Cardiol 18:I005, I991 8. de Bakker JMT, van Capelle FJL, Janse MJ et al: Reentry as a cause of ventricular tachycardia in patients with chronic ischemic heart disease: electrophysiologic and anatomic correlation. Circulation 77:589, 1988 9. Downar E, Kimber S, Harris L et al: Endocardial mapping of ventricular tachycardia in the intact h u m a n heart. II. Evidence for multiuse reentry in a function sheet of surviving myocardium. J Am Coil Cardiol 20: 869, 1992 10. Kaltenbrunner W, Cardinal R, Dubuc M e t al: Epicardial and endocardial mapping of ventricular tachycardia in patients with myocardial infarction: is the origin

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11.

12.

13.

14.

15.

16.

17.

18.

19.

20.

21.

22.

of the tachycardia always subendocardially localized? Circulation 84:1058, 1991 Downar E, Harris L, Mickleborough LL et ah Endocardial mapping of ventricular tachycardia in the intact human ventricle: evidence of reentrant mechanisms. J Am Coll Cardiol 11:783, 1988 Littman L, Svenson RH, Gallagher JJ et al: Functional role of the epicardium in post-infarction ventricular tachycardia: observations derived from computerized epicardial activation mapping, entrainment, and epicardial laser photoablation. Circulation 83: 1577, 1991 Pogwizd SM, Hoyt RH, Saffitz JE et ah Reentrant and focal mechanisms underlying ventricular tachycardia in the human heart. Circulation 86:1872, 1992 de Bakker JMT, van Capelle FJL, Janse MJ et ah Slow conduction in the infarcted h u m a n heart: "zigzag" course of activation. Circulation 88:915, 1993 Brugada P, Abdollah H, Wellens HJJ: Continuous electrical activity during sustained monomorphic ventricular tachycardia: observations on its dynamic behavior during the arrhythmia. Am J Cardiol 55:402, 1985 Miller JM, Vassallo JA, Hargrove WC, Josephson ME: Intermittent failure of local conduction during VT. Circulation 72:1286, 1985 Littman L, Svenson RH, Gallagher J J, Selle JG: High grade entrance and exit block in an area of healed myocardial infarction associated with ventricular tachycardia with successful laser photo ablation of,the anatomic substrate. Am J Cardiol 64:122, 1989 Fitzgerald DM, Friday KJ, Wah JAYL et al: Electrogram patterns predicting successful catheter ablation of ventricular tachycardia. Circulation 77:806, 1988 Langberg J J, Calkins H, E1-Atassi R et al: Temperature monitoring during radiofrequency catheter ablation of accessory pathways. Circulation 86:1469, 1992 Okumura K, Olshansky B, Henthorn RW et ah Demonstration of the presence of slow conduction during sustained ventricular tachycardia in man: use of transient entrainment of the tachycardia. Circulation 75: 369, 1987 Henthorn RW, Okumura K, Olshansky B et ah A fourth criteria for transient entrainment: the electrogram equivalent of progressive fusion. Circulation 77:1003, 1988 Stevenson WG, Wiener I, Weiss JN: Contribution of the anode to ventricular excitation during bipolar programmed electrical stimulation. Am J Cardiol 57:582, 1986

23. Stevenson WG, Nademanee K, Weiss JN et ah Programmed electrical stimulation at potential ventricular reentry circuit sites: a comparison of observations in humans with predictions from computer simulations. Circulation 80:793, 1989 24. Morady F, Kadish A, Rosenheck S e t al: Concealed entrainment as a guide for catheter ablation of ventricular tachycardia in patients with prior myocardial infarction. J Am Coll Cardiol 17:678, 1991 25. Morady F, Frank R, Kou W H e t ah Identification and catheter ablation of a zone of slow conduction in the reentrant circuit of ventricular tachycardia in humans. J Am Coil Cardiol 11:775, 1988 26. Stevenson WG, Weiss JN, Weiner I et ah Resetting of VT: implications for localizing the area of slow conduction. J Am Coil Cardio 11:522, 1988 27. Stevenson WG, Woo MA: Determinants of antidromic wave front propagation during entrainment of reentrant arrhythmias. J Cardiovasc Electrophysiol 2:215, 1991 28. E1-SherifN, Gough WB, Restivo M: Reentrant ventricular arrhythmias in the late myocardial infaraction period. Part 14. Mechanisms of resetting, entrainment, acceleration, or termination of reentrant tachycardia by programming simulation. PACE 10:341, 1987 29. Schoels W, Restivo M, Caref EB et ah Circus movement atrial flutter in canine sterile pericarditis model: activation patterns during entrainment and termination of single-loop reentry in vivo. Circulation 83: 1716, 1991 30. Kimber SK, Downar E, Harris L e t ah Mechanisms of spontaneous shift of surface electrocardiographic configuration during ventricular tachycardia. J Am Coil Cardiol 20:1397, 1992 3 l. Khan HH, Stevenson WG: Activation times in and adjacent to reentry circuits during entrainment: implications for mapping ventricular tachycardia. Am Heart J 127:833, 1994 32. Damiano RJ, Blanchard SM, Asano T et ah Effects of distant potentials on unipolar electrograms in an animal model utilizing the right ventricular isolation procedure. J Am Coll Cardiol 11:1100, 1988 33. Fontaine G, Frank R, Tonet J, Grosgogeat Y: Identification of a zone of slow conduction appropriate for ventricular tachycardia ablation: theoretical considerations. PACE 12:262, 1989 34. Stevenson WG: Catheter mapping of ventricular tachycardia. In Zipes DP, Jalife J (eds): Cardiac electrophysiology: from cell to bedside. WB Saunders, Philadelphia, 1994 (in press)