Catheter Ablation of the Mitral Isthmus for Ventricular Tachycardia Associated With Inferior Infarction
Background Intraoperative mapping studies suggest that an isthmus of myocardium between the mitral valve annulus and the border of inferior myocardial infarction may play a role in the genesis of ventricular tachycardia. We examined the frequency with which a slow conduction zone within the mitral isthmus was critical to the maintenance of ventricular tachycardia associated with remote inferior infarction in patients undergoing catheter ablation.
Methods and Results In 4 of 12 patients, a critical zone of slow conduction was identified within the mitral isthmus. In each of these patients, two characteristic and morphologically distinct tachycardias were induced: a left bundle (rS in V1, R in V6), left superior axis morphology and a right bundle (R in V1, QS in V6), right superior axis morphology (cycle length, 610 to 320 ms). In each patient, a zone of slow conduction, shared by both morphologies, was characterized by diastolic potentials with electrogram-QRS intervals of 85 to 161 ms (21% to 47% of tachycardia cycle length) and entrainment with concealed fusion during pacing associated with stimulus-QRS intervals of 81 to 400 ms (20% to 91% of tachycardia cycle length). In each patient, a single radiofrequency energy application at the shared site of slow conduction eliminated inducibility of both morphologies. During follow-up of 1 to 11 months, no patient had recurrent tachycardia.
Conclusions The mitral isthmus contains a critical region of slow conduction in some patients with ventricular tachycardia after inferior myocardial infarction, providing a vulnerable and anatomically localized target for catheter ablation. Characteristic tachycardia morphologies may provide clinical markers for this underlying mechanism.
Catheter ablation of ventricular tachycardia (VT) associated with previous myocardial infarction has become increasingly successful as methods to localize vulnerable components of the reentrant circuit are refined.1 2 3 4 Global activation data in canine models5 6 7 and intraoperative mapping in humans8 9 10 11 indicate that many such circuits contain a narrow isthmus of variable length, isolated from adjacent myocardium by functional and/or anatomic barriers, through which conduction proceeds slowly during early diastole and middiastole. Ablation of sites within this narrow isthmus of slow conduction is more effective in abolishing VT than lesions delivered within a broader fan of exit sites activating later in diastole.5 12 13 14 15
Identification of critical slow conduction zones remains difficult since middiastolic activation may occur in regions of slow conduction not participating in the reentrant circuit.6 16 Pacing during tachycardia that results in entrainment without change in QRS morphology and with a long stimulus-QRS delay (entrainment with concealed fusion) was initially proposed as a criterion for confirming location of the paced site within the reentrant circuit.13 17 18 19 20 However, ablation at such sites does not always eliminate tachycardia.2 20 Subsequent refinements in pacing criteria resulted in more specific identification of critical slow conduction zones. These include the absolute or relative degree of stimulus-QRS delay during entrainment with concealed fusion,2 comparison of the stimulus-QRS interval during entrainment with concealed fusion to the electrogram-QRS interval during tachycardia,19 and analysis of the postpacing interval.2
Potential slow conduction zones may arise anywhere within or around the borders of the infarction and may be partially or totally functional.7 21 When anatomic barriers do form the borders of slow conduction zones, they often consist of strands of infarcted muscle interdigitating with viable myocardium.21 22 However, macroscopic anatomic features, such as a valve annulus or the orifice of major blood vessels, provide additional potential barriers. In VT associated with remote inferior myocardial infarction, successful surgical ablation often required placement of cryolesions within an isthmus of surviving myocardium between the mitral valve annulus and the infarct border.23 The mitral isthmus may thus constitute or contain a critical zone of slow conduction for some of these tachycardias.
The purpose of this study was to determine the frequency with which a slow conduction zone within the mitral isthmus is critical to the maintenance of VT associated with inferior infarction. We also sought to determine whether VTs resulting from this mechanism had unique or characteristic electrocardiographic features.
The study population consisted of 12 consecutive patients with recurrent sustained monomorphic VT and isolated remote inferior myocardial infarction who underwent mapping and catheter ablation (Table 1⇓). Each patient had at least one spontaneous episode of VT documented by 12-lead ECG. There were 11 men and 1 woman. The mean age was 61±11 years, and the mean left ventricular ejection fraction was 37±5%. Patients had between 2 and >40 episodes of sustained VT documented clinically. Each patient had recurrent VT or unacceptable side effects during one to three previous antiarrhythmic drug trials, including at least 3 months of amiodarone in 5 patients. All patients gave written informed consent for the procedure.
Electrophysiological studies were performed in the fasting state and in the absence of antiarrhythmic therapy except for patients receiving amiodarone. Quadripolar catheters with 2-mm spacing (Bard-USCI) were inserted into the femoral vein and positioned at the right ventricular apex and in the right ventricular outflow tract. A deflectable quadripolar catheter with 2-mm interelectrode spacing and either a 4-mm (Webster Laboratories) or 8-mm (EP Technologies) distal tip electrode was introduced into the left ventricle via a retrograde transaortic approach for mapping and ablation. Pacing was performed with a programmable stimulator (Bloom Associates Ltd). Pacing stimuli were delivered using constant current with a 2-ms pulse duration at twice diastolic threshold. An initial bolus of heparin (3000 U) was administered followed by 1000 U/h until completion of the procedure. Patients were deeply sedated with midazolam and fentanyl. Femoral arterial pressure and peripheral oxygen saturation were monitored continuously.
Twelve standard ECG leads, along with bipolar intracardiac electrograms, were continuously acquired, digitized (1000 samples per second), and displayed on a high-resolution video monitor at 200 mm/s for inspection (Arrhythmia Research Technologies). Data were stored on optical disk for retrieval and off-line analysis. Intracardiac electrograms were filtered at 30 to 500 Hz.
Mapping and pacing were performed during VT in all patients. Pacing and recording during sinus rhythm were not performed routinely. The position of the mapping catheter was assessed by biplane fluoroscopy. Attention was initially focused on the region of the mitral isthmus, and a minimum of three to four sites in the inferobasal left free wall adjacent to the mitral valve annulus were examined. Subsequently, the catheter was repositioned within or near regions of akinesis and dyskinesia previously identified by ventriculography. Potential target sites were identified as those having either presystolic activation (>60 ms) or middiastolic potentials. At these sites, pacing from the distal bipole of the mapping catheter was performed during tachycardia at cycle lengths 30 to 100 ms shorter than the tachycardia cycle length for 10 to 20 beats. Left ventricular pacing was performed at 5 to 10 ms and a pulse width of 2 ms. Occasionally, pulse duration was increased up to 9 mA if required to permit ventricular capture.
The output of a radiofrequency generator (Radionics) was delivered to the distal pole of the mapping catheter and a posteriorly positioned cutaneous patch (R-2 Corporation). An initial power of 20 to 30 W was applied during continuous impedance monitoring. Power was progressively increased to a maximum of 50 W over 10 to 20 seconds. If VT terminated during this time (without antecedent ectopic beats), energy application was continued for 90 to 120 seconds. Applications producing an impedance rise were immediately terminated. Potential target sites were initially selected on the basis of presystolic activation >60 ms or the presence of a middiastolic potential. While demonstration of entrainment with concealed fusion during pacing from the target site was considered optimal, its absence did not necessarily preclude delivery of radiofrequency current at selected sites.
If tachycardia terminated during radiofrequency application, programmed stimulation was repeated. Stimulation was continued until VT was induced or the entire protocol, including introduction of single, double, and triple extrastimuli at both the right ventricular apex and outflow tract, was completed.
VT was considered to be sustained if it lasted more than 30 seconds or required intervention for termination. Two tachycardias were considered to be morphologically distinct if they differed in the direction of the major deflection in any of the 12 surface ECG leads. For descriptive purposes, VTs with a predominantly positive deflection in lead V1 were considered right bundle tachycardias, and VTs with a predominantly negative deflection in lead V1 were considered left bundle tachycardias. We also used the method of Miller et al24 to more precisely characterize VT morphology.
The duration of presystolic activation was defined as the interval between electrogram onset in the mapping catheter and the onset of the QRS complex (EG-QRS interval). Middiastolic potentials were considered to be present if discrete low-amplitude signals were present after the completion of the QRS complex and before the onset of the next QRS complex. These potentials bore a fixed relationship to the following QRS complex and were separated from subsequent electrograms by an isoelectric interval.
Entrainment with concealed fusion was considered to be present when pacing stimuli delivered during VT advanced the following QRS complex to the paced cycle length without alteration in the QRS morphology of all 12 surface leads and with a delay between the pacing stimulus and the following QRS complex (S-QRS interval).
An ablation site was considered to be located within a critical slow conduction zone for a specific tachycardia if the following criteria were met: (1) During VT, presystolic activation of >60 ms or an isolated middiastolic potential was present. (2) Pacing at the same site resulted in entrainment with concealed fusion. (3) The S-QRS interval during entrainment with concealed fusion was >60 ms.2 (4) The S-QRS interval during entrainment with concealed fusion was similar (within 20 ms) to the EG-QRS interval during tachycardia.2 19 (5) VT terminated soon after onset of radiofrequency energy application.
Characteristics of Mitral Isthmus–Related Tachycardias
In 4 of the 12 patients (patients 1 through 4), a critical slow conduction zone was identified in the inferobasal free wall of the left ventricle immediately adjacent to the mitral valve annulus. In each of the 4 patients, two morphologically distinct tachycardias were induced (Table 2⇓): one with a left bundle (LB), left superior axis and one with a right bundle (RB), right superior axis QRS morphology. In each of the 4 patients, the critical slow conduction zone for both tachycardias was at the same or closely related (<1-cm separation) site.
The QRS configurations of each tachycardia were closely similar between the 4 patients. The right bundle tachycardias had monophasic R waves in lead V1 and QS or Rs configurations in V6 (Fig 1⇓). The precordial transition zone was in lead V3 or V4. The limb leads were characterized by right superior axis with tall R waves in lead AVR, and qr complexes in lead III. The left bundle tachycardias had an Rs configuration in lead V1 and a monophasic R wave in V6, with a somewhat variable precordial transition zone (Fig 2⇓). The limb leads were characterized by a left superior axis, with monophasic R waves in leads I and aVL. These distinct QRS morphologies were not observed in patients with inferior infarction in whom a critical slow conduction zone could not be identified within the mitral isthmus (Table 3⇓).
Three of the 4 patients with mitral isthmus tachycardia were treated previously with amiodarone and had 2 to 40 episodes of spontaneous left or right bundle VT with identical QRS configurations during the previous month. Two of the patients had defibrillators implanted during a prior hospitalization.
Results of Mapping and Ablation
Fig 3⇓ illustrates the results of activation mapping and pacing in patient 1. The left panel demonstrates a right bundle tachycardia with a cycle length of 440 ms. The mapping catheter recorded an isolated middiastolic potential with a fixed relationship 155 ms before the next QRS onset. The arrowheads indicate dissociated left atrial electrograms and emphasize the close proximity of the catheter tip to the mitral valve annulus. In the right panel, pacing at this site resulted in acceleration of the tachycardia to the paced cycle length without change in the QRS morphology, consistent with entrainment with concealed fusion. In this instance, the S-QRS is considerably longer than the EG-QRS interval during tachycardia. This latter finding is consistent with a location either within the slowly conducting portion of the circuit or an adjacent bystander slow conduction zone (vide infra). Upon termination of the right bundle tachycardia, no diastolic potentials were recorded.
With the mapping catheter at the same site, a left bundle tachycardia was induced that had a similar cycle length (Fig 4⇓, left). The middiastolic potential was no longer clearly visible, but presystolic activation of 90 ms was identified. Pacing from this site (Fig 4⇓, right) resulted in acceleration of the tachycardia to the paced cycle without change in QRS morphology, again consistent with entrainment with concealed fusion. The S-QRS interval of 93 ms during pacing was similar to the EG-QRS interval during tachycardia, compatible with a location with the critical slow conduction zone for this tachycardia.
With the catheter remaining in the same position, the right bundle tachycardia was reinduced. Radiofrequency energy was applied at a maximum power of 50 W, and the tachycardia terminated after 12 complexes. After completion of this application, neither the left nor the right bundle tachycardias could be reinduced. This patient had three previous unsuccessful radiofrequency applications during right bundle tachycardia, delivered at sites >1 cm laterally along the mitral isthmus, all of which showed presystolic activation. Entrainment with concealed fusion was demonstrated during right bundle tachycardias at one of these sites, but with an S-QRS interval of <60 ms. None of these previous applications were associated with termination of the tachycardia, and both morphologies remained inducible before mapping and ablation at the final site.
Fig 5⇓ illustrates the results of mapping and ablation in patient 3. With the catheter positioned under the mitral valve leaflet, a site was identified during right bundle tachycardia with an EG-QRS interval of 85 ms. As shown in the right panel, pacing from this site resulted in entrainment with concealed fusion and an S-QRS interval of similar duration, consistent with a location within the critical slow conduction zone for this tachycardia. The catheter was repositioned a few millimeters along the mitral annulus toward the septum. Diastolic potentials were not observed at this site during sinus rhythm. A slower left bundle tachycardia was induced (Fig 6⇓, left). A fractionated middiastolic potential with onset 155 ms before the QRS onset was identified. The arrowheads again demonstrate dissociated left atrial activation. In the right panel, pacing at this site produced entrainment with concealed fusion and an S-QRS interval of 155 ms, similar to the EG-QRS interval during tachycardia. Radiofrequency energy application at this site immediately terminated the tachycardia (Fig 7⇓). After completion of this application, neither the left nor the right bundle tachycardia could be reinduced. A single previous radiofrequency energy application delivered during right bundle tachycardia at a site 2 cm laterally had failed to terminate the tachycardia or alter the inducibility of either morphology.
The results of mapping and pacing at the successful ablation site in each of the four patients with mitral isthmus tachycardia are summarized in Table 2⇑. In each patient, data during both left bundle and right bundle tachycardias were examined at the same or nearly identical site, and a single radiofrequency application delivered during one of the two tachycardias rendered both morphologies noninducible. For all tachycardias, the EG-QRS interval was >60 ms and ranged from 21% to 47% of the tachycardia cycle length. Expressed as a function of the diastolic interval (offset of QRS to onset of next QRS14 ), activation at the ablation site ranged from 25% to 62% of the diastolic interval. For all tachycardias, entrainment with concealed fusion was demonstrated. In 7 of 8 tachycardias, the S-QRS interval was within 20 ms of the EG-QRS interval, strongly suggesting a location within the critical slow conduction zone.
During right bundle tachycardia in patient 1, pacing at the same site produced a much longer S-QRS interval than EG-QRS interval. It is possible that the mapping catheter was positioned at a slowly conducting bystander site rather than within the reentrant circuit. However, this bystander site would have been located very near the critical slow conduction zone, since the tachycardia was permanently ablated with a single radiofrequency application. Alternatively, the catheter was truly positioned within the critical slow conduction zone, but the faster pacing rate produced decremental conduction.20 25
Fig 8⇓ is a schematic illustration of the location of successful ablation sites in the 4 patients. Since our goal was to identify the slow conduction zone, we did not attempt to map global activation patterns. However, activation was recorded from several sites along the annulus during each tachycardia. As expected from the resulting QRS morphologies, activation along the isthmus proceeded away from the slow conduction zone toward the septum (eg, progressively shorter EG-QRS intervals) during left bundle tachycardia and toward the lateral free wall during right bundle tachycardia.
In the remaining 8 patients (patients 5 through 12, Table 3⇑), 14 morphologically distinct tachycardias were induced, none of which had QRS characteristics similar to those of isthmus-related tachycardias. Mapping and pacing at multiple sites within the mitral isthmus during each of these tachycardias failed to identify a critical slow conduction zone as previously defined. In 11 of 14 of these tachycardias (Table 3⇑), a site was identified remote from the region of the mitral isthmus where radiofrequency energy application terminated the tachycardia and eliminated its reinduction by programmed stimulation (median, 3 applications; range, 1 to 8). Middiastolic potentials were present at 10 of 11 successful sites, and all criteria for a critical slow conduction zone were fulfilled at 8 of 11 successful sites. Catheter ablation was unsuccessful in 3 tachycardias. Despite extensive mapping and pacing during each of these tachycardias, middiastolic potentials were not identified, and criteria for a critical slow conduction zone were not met at any site either within or remote from the isthmus. However, earliest presystolic activation for each of these tachycardias was recorded outside the isthmus region. In one of these patients (No. 6), two “blind” radiofrequency applications were given in the midportion of the mitral isthmus, which had no effect on the tachycardia. Collectively, these observations suggest that the mitral isthmus was not a critical participant in any of these tachycardias.
There were no immediate or late complications of the ablation procedure. No patient had clinical or echocardiographic evidence of new or worsened mitral regurgitation. In patients 1 and 2, no VT could be induced during completion of the postablation protocol. Both of these patients had previously implanted defibrillators. In patient 3, both isthmus-related tachycardias were no longer inducible, but a third morphologically distinct tachycardia (LB [QSV1,QrV6]–left superior axis; cycle length, 250 ms) was induced that slowed minimally with procainamide and was too unstable to map. This patient received an implantable defibrillator. Amiodarone was discontinued in each of these patients 3 months after the procedure. Patient 4 had no VT induced at the end of the procedure and was discharged on no antiarrhythmic therapy. During follow-ups of 11, 10, 7, and 2 months, respectively, no patient has had spontaneous tachycardia or defibrillator therapy.
In patients with nonisthmus-related tachycardia, 4 of 5 patients in whom all inducible VTs were eliminated remained free of recurrent VT without antiarrhythmic therapy during follow-up of 1 to 11 months. Patient 7, who had a previously implanted defibrillator, had multiple episodes of rapid irregular VT (cycle length <250 ms by stored electrograms) 4 months after the ablation procedure, resulting in multiple shocks. This patient was treated with amiodarone. Patient 11, in whom one (nonclinical morphology) of three tachycardias remained inducible at the end of the ablation procedure, underwent implantation of a defibrillator and has had no recurrent VT during 2 months of follow-up. The remaining 2 patients in whom ablation was not successful were treated with amiodarone and have remained free of recurrent ventricular tachycardia during 7 and 9 months of follow-up, respectively.
This study demonstrates that in one third of patients with recurrent VT and inferior myocardial infarction who underwent catheter ablation, an area of slow conduction critical to the maintenance of the tachycardia was located within the mitral isthmus. This critical zone of slow conduction was activated parallel to the mitral annulus in either direction, resulting in two distinct but characteristic QRS configurations not seen in tachycardias arising from other sites. Pacing maneuvers during both right bundle and left bundle tachycardias confirmed that the shared zone of slow conduction directly participated in the reentrant circuit. A single radiofrequency energy application within the shared slow conduction zone permanently eliminated both tachycardia configurations; this observation provides the strongest evidence that the slow conduction zone identified within the mitral isthmus played a critical role in the genesis and maintenance of these tachycardias.
The potential importance of the mitral isthmus as a critical component of the reentrant circuit in some patients with inferior myocardial infarction was suggested previously. In 1986, Hargrove et al23 reported their experience with surgical ablation of VT associated with inferior infarction. These investigators reported that standard localized endocardial excision at sites of presystolic activation resulted in elimination of inducible VT in only 56% of survivors. In contrast, inducible VT was eliminated in 93% of survivors in whom focal cryoablation of the residual isthmus between the infarction and the mitral valve annulus was performed in addition to the standard resection.
Role of Slow Conduction in Isthmus-Related Tachycardia
While the complete endocardial activation sequence of isthmus-related tachycardia was not defined in this study, the tachycardias appear similar to some of those reported by Hargrove et al.23 These investigators described a macroreentrant “continuous loop” circuit spanning the cardiac cycle with activation proceeding around the endocardial border of inferior infarction and incorporating the mitral isthmus. Activation within the isthmus occurred during early and middiastole. The presence or significance of slow conduction through this region during tachycardia was not defined. It is possible that the isthmus served merely as a passive conduit for relatively normal conduction, since the circumference of the infarction may be sufficiently large to permit reentry with only moderately depressed conduction velocities in other areas of the circuit.26 The isthmus between the infarction and the mitral valve annulus, by virtue of its narrow dimensions, may have been simply the most vulnerable point to interrupt this circumferential activation.
Our data provide strong confirmation that maintenance of isthmus-related VTs in patients with inferior infarction requires the participation of a slow conduction zone. Similar to the tachycardias described above during intraoperative mapping, we observed activation of the isthmus in early to middiastole (25% to 62% of diastolic interval). Pacing data during tachycardia from the ablation sites were consistent with the presence of a slow conduction zone that was an integral part of the circuit. Elimination of the tachycardias with a single focal radiofrequency lesion at these sites but not elsewhere confirmed the critical importance of these sites. “Continuous loop” macroreentrant VT around a dense scar has been described by Miller et al27 and Littman et al13 in patients with anteroapical infarction undergoing surgical mapping and ablation. Both investigators confirmed the requirement of a discrete slow conduction zone in maintaining these tachycardias.
Activation of the slow conduction zone in the isthmus could proceed either toward or away from the septum, producing different electrogram characteristics at the ablation site, opposite directions of presystolic breakthrough, and different but characteristic tachycardia morphologies. Fitzgerald et al28 have previously described reversal in the direction of activation as one mechanism by which multiple morphologically distinct tachycardias may arise from a single common zone of slow conduction. The general ECG features associated with both the left and right bundle morphologies are among the patterns described by Miller and coworkers24 for tachycardias with “sites of origin” on the septal and lateral aspects, respectively, of the inferobasal left ventricle. However, the specific features of both morphologies appear to distinguish isthmus-related tachycardias from others having adjacent “sites of origin” but arising through different mechanisms.
Mechanisms of VT in Inferior Infarction
While slow diastolic conduction through a narrow isolated endocardial isthmus may often provide the basis for reentry in postinfarction VT, available evidence suggests that a broad spectrum of mechanisms may be operative. Critical zones of slow conduction have been identified on the epicardial surface during intraoperative mapping in up to 15% of postinfarction VTs.11 13 29 Epicardial location of the reentrant circuit may be more common in inferior infarction.29 Even with dense epicardial and endocardial mapping, activation spanning all portions of the cardiac cycle cannot be recorded in a substantial portion of patients, and activation appears to spread radially from a single focus. Such patterns may reflect an intramural location of some or all components of the reentrant circuit.11 30 31 Such intramural pathways may not be limited to narrow isolated strands of surviving myocardium but may consist of relatively broad sheets spanning a large area.32 These complexities provide a potential explanation for the failure to identify critical slow conduction zones in some tachycardias associated with inferior infarction as well as the inability to ablate some of these tachycardias with an endocardially based approach.
The study population represents a small number of highly selected patients with recurrent hemodynamically stable VT associated with inferior infarction. The significance of slow conduction in the mitral isthmus may differ in patients presenting with less frequent or more unstable tachycardias. Further experience in a larger group of patients will be necessary to confirm the uniqueness of the specific right and left bundle configurations identified in this study.
We used bipolar pacing through catheters with large distal electrodes for mapping in this study. This method may diminish the precision of activation mapping and result in stimulation of a relatively large area of myocardium, potentially including tissue outside the zone of slow conduction.2
Postpacing intervals were not analyzed in this study since we were unable to obtain reliable electrogram recordings from the pacing electrodes immediately after termination of pacing; the validity of using intervals derived from more remote electrodes is uncertain. We therefore used similarity of EG-QRS intervals during tachycardia and S-QRS intervals during entrainment with concealed fusion, as suggested by Fontaine et al,19 to confirm location of target sites within the reentrant circuit and to exclude bystander areas of slow conduction. Stevenson et al2 presented cogent arguments that the similarity between the postpacing interval and the tachycardia cycle length may provide a better criterion for establishing the location of the paced site within the reentrant circuit. However, in their analysis, similarity of the EG-QRS interval during tachycardia and S-QRS intervals during entrainment with concealed fusion was actually a more stringent criterion for location within the circuit, though potentially less sensitive than the postpacing interval.
Catheter ablation of postinfarction VT remains problematic because of the presence of multiple potential reentrant circuits, imprecision of localization and mapping criteria, variable electrode tip-tissue contact, and the presence of highly resistive endocardial scar. However, in a subset of patients with inferior myocardial infarction, an isthmus of surviving tissue between the infarct border and the mitral valve annulus appears to constitute a critical region of slow conduction. The isthmus provides a particularly vulnerable and anatomically localized target for catheter ablation. Characteristic tachycardia morphologies may provide clinical markers for the presence of this underlying mechanism and may identify a subgroup of patients in whom postinfarction VT can be effectively eliminated by percutaneous techniques.
- Received April 20, 1995.
- Revision received June 26, 1995.
- Accepted August 3, 1995.
- Copyright © 1995 by American Heart Association
Morady F, Harvey M, Kalbfleisch SJ, El-Atassi R, Calkins H, Langberg JJ. Radiofrequency catheter ablation of ventricular tachycardia in patients with coronary artery disease. Circulation. 1993;87:363-372.
Stevenson WG, Khan H, Sager P, Saxon LA, Middlekauff HR, Natterson PD, Wiener I. Identification of reentry circuit sites during catheter mapping and radiofrequency ablation of VT late after myocardial infarction. Circulation. 1993;88:1647-1670.
Kim YH, Sosa-Suarez G, Trouton TG, O’Nunain S, Osswald S, McGovern BA, Ruskin JN, Garan H. Treatment of ventricular tachycardia by transcatheter radiofrequency ablation in patients with ischemic heart disease. Circulation. 1994;89:1094-1102.
El-Sherif N, Mehra R, Gough WB, Zeiler RH. Reentrant ventricular arrhythmias in the late myocardial infarction period: interruption of reentrant circuits by cryothermal techniques. Circulation. 1983;68:644-656.
Garan H, Ruskin JN. Localized reentry: mechanism of induced sustained monomorphic ventricular tachycardia in canine model of recent myocardial infarction. J Clin Invest. 1984;74:377-392.
Dillon SM, Allessie MA, Ursell PC, Witt AL. Influence of anisotropic tissue structure on reentrant circuits in the epicardial border zone of subacute canine infarcts. Circ Res.. 1988;63:182-206.
De Bakker JMT, van Capelle FJL, Janse MJ, Wilde AAM, Coronel R, Becker AE, Dingemans KP, van Hemel NM, Hauer RNW. Reentry as a cause of ventricular tachycardia in patients with chronic ischemic heart disease: electrophysiologic and anatomic correlation. Circulation. 1988;77:589-606.
Kaltenbrunner W, Cardinal R, Dubuc M, Shenasa M, Nadeau R, Tremblay G, Vermeulen M, Savard P, Pagé PL. Epicardial and endocardial mapping of ventricular tachycardia in patients with myocardial infarction. Circulation. 1991;84:1058-1071.
Gessman LJ, Agarwal JB, Endo T, Helfant RH. Localization and mechanisms of ventricular tachycardia by ice mapping 1 week after the onset of myocardial infarction in dogs. Circulation. 1983;68:647-666.
Littmann L, Svenson RH, Gallagher JJ, Selle JG, Zimmern SH, Fedor JM, Colavita PG. Functional role of the epicardium in postinfarction ventricular tachycardia: observations derived from computerized epicardial activation mapping, entrainment, and epicardial laser photoablation. Circulation. 1991;83:1577-1591.
Svenson RH, Littmann L, Colavita PG, Zimmern SH, Gallagher JJ, Fedor JM, Selle JG. Laser photoablation of ventricular tachycardia: correlation of diastolic activation times and photoablation effects on cycle length and termination: observations supporting a macroreentrant mechanism. J Am Coll Cardiol. 1992;19:607-613.
Gallagher JD, Del Rossi AJ, Fernandez J. Cryothermal mapping of recurrent ventricular tachycardia in man. Circulation. 1985;71:733-739.
Saltman AE, Dillon SM, Coromilas J, Witt AL. Influence of anisotropic structure of the infarct epicardial border zone on conduction. Fed Proc. 1987;46:1438. Abstract.
Miller JM, Marchlinski FE, Buxton AE, Josephson ME. Relationship between the 12-lead electrocardiogram during ventricular tachycardia and endocardial site of origin in patients with coronary artery disease. Circulation. 1988;77:759-766.
De Bakker JMT, van Capelle FJL, Janse MJ, Tasseron S, Vermeulen JT, de Jonge N, Lahpor JR. Slow conduction in the infarcted human heart: ‘zigzag’ course of activation. Circulation. 1993;88:915-926.
Fitzgerald DM, Friday KJ, Yeung Lai Wah JA, Bowman AJ, Lazzara R, Jackman WM. Myocardial regions of slow conduction participating in the reentrant circuit of multiple ventricular tachycardias: report on ten patients. J Cardiovasc Electrophysiol. 1991;2:193-206.
Svenson RH, Littmann L, Gallagher JJ, Selle JG, Zimmern SH, Fedor JM, Colavita PG. Termination of ventricular tachycardia with epicardial laser photocoagulation: a clinical comparison with patients undergoing successful endocardial photocoagulation alone. J Am Coll Cardiol. 1990;15:163-170.
Pogwizd SM, Hoyt RH, Saffitz JE. Reentrant and focal mechanisms underlying ventricular tachycardia in the human heart. Circulation. 1992;86:1872-1887.
Garan H, Fallon JT, Rosenthal S, Ruskin JN. Endocardial, intramural, and epicardial activation patterns during sustained monomorphic ventricular tachycardia in late canine myocardial infarction. Circ Res. 1987;60:879-896.
Downar E, Kimber S, Harris L, Mickleborough L, Sevaptsidis E, Masse S, Chen TCK, Genga A. Endocardial mapping of ventricular tachycardia in the intact human heart, II: evidence for multiuse reentry in a functional sheet of surviving myocardium. J Am Coll Cardiol. 1992;20:869-878.