ELECTROPHYSIOLOGY
Substrate mapping vs. tachycardia mapping using CARTO in patients with coronary artery disease and ventricular tachycardia: impact on outcome of catheter ablation
Department of Cardiology, St Georg Hospital, Hamburg, Germany
Manuscript submitted 22 June 2005. Accepted after revision 26 July 2006.
* Corresponding author: II. Med. Abteilung, Asklepios Klinik St Georg, Lohmühlenstrasse 5, 20099 Hamburg, Germany. Tel: +49 40 181885 2305; fax: +49 40 181885 4444. E-mail address: antz{at}uke.uni-hamburg.de
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Aims For ablation of ventricular tachycardia (VT) in patients after myocardial infarction, a three-dimensional mapping system is often used. We report on our overall success rate of VT ablation using CARTO in 47 patients, with a subgroup analysis comparing VT mapping with the results of mapping that had to be performed during sinus rhythm or pacing (substrate mapping).
Methods and results A CARTO map was performed and VT ablation attempted using two strategies: Patients in the VT-mapping group had incessant VT (four patients) or inducible stable VT (18 patients) such that the circuit of the clinical VT could be reconstructed using CARTO. During VT, the critical area of slow conduction was identified using diastolic potentials and conventional concealed entrainment pacing. In contrast, patients in the substrate-mapping group had initially inducible VT. However, a complete VT map was not possible because of catheter-induced mechanical block (six patients) or because haemodynamics deteriorated during the ongoing VT (19 patients). Therefore, pathological myocardium was identified by fragmented, late- and/or low-amplitude (<1.5 mV) bipolar potentials during sinus rhythm or pacing, and the ablation site was primarily determined by pace mapping inside or at the border of this pathological myocardium. Acute ablation success in all patients with regard to non-inducibility of the clinical VT or any slower VT was 79% after a single ablation procedure, but increased to 95% after a mean of 1.2 ablation procedures. However, chronic success was 75%, when it was defined as freedom from any ventricular tachyarrhythmia (VT or VF) during a follow-up of 25±13 months. In the subgroup analysis, patients in the VT-mapping group were not significantly different from patients in the substrate-mapping group with regard to age (65±7 vs. 65±9 years), ejection fraction (30±7 vs. 30±8%), VT cycle length (448±81 vs. 429±82 ms), number of radiofrequency applications (17±9 vs. 14±6 applications), use of an irrigated tip catheter (23 vs. 32%), and ablation results.
Conclusion When using a CARTO-guided approach for VT ablation in patients with coronary artery disease, the freedom from any ventricular arrhythmia is high (75%), but leaves the patient at a 23% risk of developing fast VT/VF during follow-up. Mapping during sinus rhythm or pacing is as successful as mapping during VT.
Key Words: Catheter ablation, Ventricular tachycardia, Electroanatomical mapping, Internal defibrillator
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Introduction |
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Catheter ablation in patients with ischaemic ventricular tachycardia (VT) based on conventional mapping techniques is associated with low success rates and is limited to patients with stable VT.1
However, even these patients can be difficult to treat by ablation if multiple morphologies are induced or if the target VT is mechanically blocked during mapping. Therefore, <10% of patients with VT and coronary artery disease are suitable for catheter ablation.2 However, the electroanatomical mapping system CARTO (Haifa, Israel) allows a three-dimensional anatomical reconstruction of the ventricles during sinus rhythm or pacing. This helps to identify the substrate for VT by differentiating scar tissue, anatomical and functional barriers, and areas of slow conduction.3
It has been shown that the application of linear lesions guided by CARTO can reduce VT episodes in patients with non-tolerated VT.3,4 Combined sinus rhythm mapping and limited mapping during VT demonstrated a significant reduction of internal cardioverter and defibrillator (ICD) interventions in patients in whom the critical isthmus could be identified.5 In many centres, VT ablation using CARTO is attempted by performing a complete CARTO map during VT in all patients. However, this is not possible in the majority of patients due to mechanical block of the VT by catheter manipulation or haemodynamic deterioration during long-lasting VT. We report on our overall success rate on VT ablation using CARTO in 47 patients, with a subgroup analysis comparing VT mapping with the results of mapping that had to be performed during sinus rhythm or pacing (substrate mapping).
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Patients
Over a period of 3 years, endocardial catheter mapping and radiofrequency (RF) current ablation were performed in 47 consecutive patients (four females; mean age 65±8 years) with clinically sustained, haemodynamically tolerated monomorphic VT remote from myocardial infarction (>3 months) by use of the electroanatomical mapping system CARTO (Figure 1). Haemodynamic tolerance was defined as preservation of consciousness and no resuscitation required during the clinical arrhythmia. However, 22 patients (47%) had previously undergone ICD implantation, resulting in fast arrhythmia termination by the device. The median number of VT episodes prior to ablation was 7 (range 1–930 episodes) within 6 months prior to ablation. The locations of previous myocardial infarctions were 22 inferior (10 aneurysms), 22 anterior (17 aneurysms), and three with both locations (Table 1).
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At the time of study inclusion, 43 of 47 patients were on antiarrhythmic drug therapy. They received amiodarone alone (28 patients) or in combination with other antiarrhythmic drugs (seven patients), and eight were treated with sotalol.
Coronary angiography, left ventriculography, and transthoracic echocardiography were performed in all patients prior to the ablation. Written informed consent was obtained at least 24 h before the procedure.
Electrophysiological study
A conventional computerized electrophysiological (EP) system (EP Laboratory, Quinton Electrophysiology Corporation, Ontario, Canada) and the electroanatomical mapping system CARTO were used. Patients were continuously monitored throughout the entire EP procedure by invasive systemic and pulmonary arterial pressure, non-invasive oxygen saturation, and urinary flow. The procedures were performed under deep sedation using continuous pump infusion of propofol. For systemic anticoagulation, repeat bolus injections of heparin based on ACT measurements were given (target value 250–300 s). The standard access to the left ventricle was retrograde across the aortic valve (35 patients). In six patients, an antegrade transseptal access was used because of severe atherosclerosis of the aorta or peripheral arteries, and in six further patients, the LV was mapped via combined access because anatomical variations did not permit mapping of the entire left ventricle by the retrograde approach alone.
Right ventricular stimulation
Programmed ventricular stimulation with up to three extrastimuli at two different sites (right ventricular apex and outflow tract) was performed in an attempt to induce the clinical VT and/or any other non-clinical VT. VT was considered clinical if either the 12-lead morphology matched the previously documented VT or if the cycle length was within a range of ±30 ms of the VT cycle length documented by the ICD. If the induced VT led to haemodynamic deterioration within 2 min in the sedated patient, the VT was considered unmappable (19 patients).
Mapping
Electroanatomical mapping
Mapping (and ablation) was performed using 7F steerable catheters with either a conventional 4 mm tip (NaviStarTM) or a 3.5 mm irrigated tip electrode (NaviStar ThermoCoolTM, Biosense-Webster Ltd, Diamond Bar, CA, USA). Spatial reference was obtained from a second sensor equipped catheter (RefStarTM, Biosense-Webster Ltd) placed on the patient's back. Local activation time was measured in relation to a time reference derived from an appropriate surface ECG lead. Mapping was performed in a bipolar recording mode with a filter setting of 30–400 Hz.
Initial CARTO map
An activation map and voltage map of the entire left ventricle were performed during sinus rhythm, atrial or right ventricular pacing in all patients except for those with incessant VT. Although the automatic annotation was set to maximum value, each electrogram was re-annotated to the beginning of the local bipolar potential (reproducible pre-systolic or diastolic potentials were considered as representing local activation, i.e. localized isolated channels). The voltage map was used in a bipolar mode for the identification of sites with abnormal signals. Voltages of <1.5 mV were considered abnormal. Scar tissue was considered at sites with no reproducible local bipolar potential and, if in doubt, failure of bipolar pacing capture with highest possible output (10 V, 2.9 ms pulse duration). The upper limit of the colour voltage display was set to 1.5 mV such that only normal tissue was coloured purple.3
Patients were divided into a VT-mapping group (patients with inducible or spontaneous VT, in whom the circuit of the clinical VT could be reconstructed using CARTO) and a substrate-mapping group (patients in whom a complete VT map was not possible because of catheter-induced mechanical block or because the induced VT was unmappable due to haemodynamic deterioration during VT).
VT-mapping group
A complete activation and propagation map during the clinical and/or any other slower VT was performed, and the setting of the annotation window was equal to the VT cycle length. The CARTO VT map was combined with conventional entrainment pacing at sites with diastolic potentials according to the methods for entrainment as previously described.6–9
Substrate-mapping group
Following the initial map during sinus rhythm or right ventricular pacing, pace mapping in the left ventricle was performed. Sites where pace mapping matched the spontaneous VT morphology and where the delay between the stimulus and the onset of the QRS-complex was at least 50 ms were classified as potential target sites within a protected isthmus. However, if the VT morphology was matched without a delay of the stimulus to QRS interval, the site was classified as an exit.9
In those patients in whom systematic VT mapping was not possible, because the clinical VT became haemodynamically unstable under sedation in the EP laboratory, the mapping catheter was placed at a potential target site during sinus rhythm or pacing. Then, the VT was induced, entrainment attempted, and RF current applied as soon as diastolic activity was recorded. If the VT terminated within 30 s, the RF current application was continued; if not, the RF current application was stopped and the VT was terminated by overdrive pacing or external DC cardioversion.
Ablation strategies
In both the VT-mapping group and the substrate-mapping group, patients were treated with focal ablation (treatment with point ablation in an attempt to ablate a critical channel) and/or linear ablation (lines placed inside the infarct or at its border, connecting electrical barriers, or arranged in a cross-like fashion through the infarct area).
Ablation settings
RF current (500 kHz) was applied between the distal electrode of the mapping catheter and a cutaneous patch electrode. Conventional RF applications were delivered using a temperature-controlled mode (maximum 60°C; maximum 180 s; 30–50 W; EP shuttle, Cordis-Stockert Ltd, Freiburg, Germany). For irrigated tip, RF applications 30–50 W were applied with a temperature limit of 45°C at a cooling rate of 30 mL/min. The continuous flow during mapping was 2 mL/min.
Endpoints and success of ablation
The endpoint of focal applications in the VT-mapping group was VT termination by RF and in the substrate-mapping group, the elimination of isolated potentials. The endpoint for linear ablation (lines or cross-lines) was the completion of the designed lines. Acute success was defined as non-inducibility of the clinical VT and any VT slower than the clinical VT, either at the end of the ablation procedure (VT-mapping group) or in a repeat EP stimulation study before hospital discharge (substrate-mapping group), but allowed induction of fast VT (cycle length >30 ms faster than the clinical VT) or VF. In both groups, chronic success during follow-up was divided into freedom from targeted VTs (defined as no recurrence of the clinical VT or any VT slower than the clinical VT) and freedom from any VT/VF (defined as no occurrence of sustained ventricular arrhythmia, including fast VT and ventricular fibrillation).
Management after ablation
Patients were monitored for at least 12 h in the intensive care unit. Continuous infusion of therapeutic heparin for 24 h was followed by 100 mg/d aspirin or by oral anticoagulation with phenprocoumon.
A repeat stimulation study was scheduled 2 days (median) after ablation in the substrate-mapping group.
If during the same hospitalization a patient had a VT recurrence after the first ablation procedure was performed with a conventional 4 mm tip electrode, a repeat ablation was immediately performed aiming at consolidating the initial ablation strategy using an irrigated tip electrode. Since only limited mapping was performed during these repeat procedures, they were not included into the procedure-related data analysis (Table 1).
Follow-up
Follow-up started after hospital discharge and was performed every 3 months in the ICD-outpatient clinic or by trans-telephonic evaluation of events provided by the patient and the referring physician.
Patients who underwent cardiac transplant or died non-arrhythmogenically were considered as having reached the end of follow-up, whereas patients who experienced an arrhythmogenic death were rated as an occurrence of VF. If patients died during the initial hospitalization, they were not part of the follow-up and therefore were not considered in the chronic success rates.
Statistical analysis
Data mean±standard deviation was used to describe continuous variables with normal distribution; otherwise median and range were used. For diagnostic parameters, the absolute and relative frequencies were counted. In all cases, the statistics were calculated using non-parametric tests (Mann–Whitney, 
2) and using Fisher's exact method because the data set was small. A two-tailed probability of <0.05 was regarded as significant. The P-values were individually interpreted as exploratory. Statistics were calculated with SPSS 11.5 (SPSS Inc., Chicago, IL, USA).
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Entire patient cohort
In the initial right ventricular stimulation (performed in the patients who did not have incessant VT), the clinical VT could be induced in all patients with additional 3±2 (range 1–10) non-clinical VT morphologies.
In the 47 patients, a total of 61 ablation procedures was performed (1.2±0.5; range one to four procedures). These include 14 repeat procedures due to VT recurrences, performed either during the same hospitalization (four procedures; in all of them, a conventional 4 mm tip electrode was used in the initial procedure) or during follow-up (10 procedures). An irrigated tip electrode was used in a total of 17 of 61 (28%) procedures (13 initial procedures (Table 1) and in all four repeat procedures performed during the same hospitalization).
All patients discharged from the hospital completed a follow-up period of at least 4 months. The mean follow-up period of the entire cohort was 25±13 months (range 4–48 months). Thirty-six patients (77%) finally had an ICD. Twenty-nine patients (62%) were treated with specific antiarrhythmic drugs: 25 patients (86%) amiodarone and four patients (14%) sotalol.
The acute ablation success in all patients with regard to non-inducibility of the clinical or any slower VT was 79% (34/43) after a single ablation procedure and was unknown in four patients in the substrate-mapping group who did not undergo repeat stimulation. A total of three patients died in hospital. During follow-up of the remaining 44 patients, chronic success regarding freedom from the clinical VT or any slower VT was 95% (42/44) after all (1.2±0.5) ablation procedures in both groups. However, 23% (10/44) of the patients had fast VT or ventricular fibrillation during follow-up, and one of them (VT-mapping group) underwent successful linear re-ablation. Therefore, chronic success regarding freedom from any sustained ventricular arrhythmia including fast VT and ventricular fibrillation was 75% (33/44) after all ablation procedures.
VT-mapping group
In the 22 patients of the VT-mapping group, a CARTO map of the LV in sinus rhythm or pacing (18 patients; 173±81 points, diastolic volume 249±87 mL) and during VT (22 patients; 139±77 points) was obtained (Table 1). A critical zone of slow conduction during VT was identified in 20 of the 22 patients by a combination of CARTO- and conventional mapping techniques, and the VT was terminated with a median of two RF pulses1–4 within this area (Figure 2). In 16 patients, a median of one additional line (maximum five lines) was applied to connect scar to scar and/or scar to the mitral annulus, and in three patients, a cross-line ablation was placed through the area with abnormal potentials (Figure 3). The mean length of all linear lesions was 50±35 mm (range 20–158 mm). The mean number of RF pulses in the VT-mapping group was 17±9 (range 5–31).
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Ablation was acutely successful after the initial procedure in 17 of 22 patients (77%) (Figure 4). Owing to early VT recurrence after the initial ablation with a conventional 4 mm tip electrode, re-ablation using an irrigated catheter was performed at the same sites during the same hospitalization in three patients, and this increased the acute success rate to 91% (20 of 22 patients). In two patients, the clinical VT remained inducible at the end of the procedure, and both were discharged with an ICD and antiarrhythmic drug treatment. In five patients, the previous antiarrhythmic drug treatment was discontinued and in five modified. Eight patients received a new ICD after ablation because of severely impaired LV function and induction of rapid VTs.
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During a total follow-up of 24±12 months after hospital discharge in the VT-mapping group (range 4–47 months), the two patients in whom the clinical VT remained inducible had recurrences of that arrhythmia. However, VT was frequent in only one of them requiring linear re-ablation 6 months later, resulting in no more VT during further follow-up of 27 months when he died of cancer. Two other patients had a slower VT (compared with the clinical VT) after hospital discharge and underwent successful linear re-ablation using CARTO at 1 month and at 18 months, with no more VT recurrences during further follow-up. A total of five patients had fast VT (>30 ms faster than the clinical VT) in hospital (one patient) or fast VT/VF during follow-up after hospital discharge (four patients). The fast VT/VF was controlled by the ICD in three patients, and two patients with a stable but different and faster VT (compared with the clinical VT) underwent a repeat CARTO-guided ablation procedure while still in hospital (after 7 days) or during outpatient follow-up (at 11 months).
In the VT-mapping group, there was a total of four deaths. Two patients died in the hospital 2 and 28 days after the procedure: one patient was referred for ablation of an incessant VT and septic shock following a massive anterior wall myocardial infarction, and the ablation procedure was performed as a measure of last resort. The VT was ablated successfully, but the patient died 2 days afterwards due to the sepsis. The second patient died in the hospital, 28 days after the initial procedure, of heart failure and sepsis without VT recurrence after the second ablation procedure using an irrigated tip catheter. In two patients, late death of non-cardiac cause occurred 26 and 27 months post-ablation.
Substrate-mapping group
In 25 patients, only a CARTO map during sinus rhythm or pacing was performed either because the sedated patient became haemodynamically unstable during the ongoing VT in the EP laboratory (19 patients) or a long-lasting mechanical block of the target VT occurred (six patients) (Figure 1). A mean of 217±87 points were acquired to reconstruct the LV (diastolic volume 257±117 mL). Ablation with 14±6 RF-applications was performed to block protected channels inside the infarct (<1.5 mV bipolar amplitude) or at its border, as well as to connect scar to scar and/or scar to the mitral annulus. A median of two lines (maximum of three lines) was performed, with a mean length of all lines of 64±36 mm (range 25–141 mm).
In a total of four patients in the substrate-mapping group, a non-clinical slow VT was reproducibly induced. In all of these patients, a CARTO-VT map was obtained and the VT was successfully ablated.
After the initial procedure, ablation was acutely successful in 17/21 patients (81%) who had a repeat EP study (three patients refused a second RV stimulation, and one patient had died due to periprocedural pericardial tamponade) (Figure 5). Owing to early VT recurrence after an initial ablation with a conventional 4 mm tip electrode, re-ablation using an irrigated tip catheter was performed at the same sites during the same hospitalization in one patient, and this increased the acute success rate to 18/21 patients (86%). In three patients, the clinical VT (two patients) or a slower VT (one patient) was inducible at control stimulation (Figure 5). Previous antiarrhythmic drug therapy was discontinued in nine patients and modified in two patients. Six patients received an ICD after ablation because of impaired LV function and induction of rapid VT.
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During a total follow-up after hospital discharge of 26±14 months (range 5–48 months) in the substrate-mapping group, one of the two patients with inducible clinical VT had no recurrence and the other had a single episode of VF, successfully terminated by his ICD. Including the latter patient, a total of six patients in the substrate-mapping group had fast VT (>30 ms faster than the clinical VT) or VF during follow-up. Of these patients, five were controlled with antiarrhythmic drugs and ICD, whereas one female patient died unwitnessed (probably suddenly). During follow-up, five other patients had recurrences of the clinical or slower VT: the patient with the slow VT inducible at repeat stimulation had recurrences of that VT (underwent three, finally successful re-ablations of that arrhythmia during follow-up). One of the patients who had refused repeat stimulation had recurrence of the clinical VT (underwent successful re-ablation during follow-up), and three of the acutely successful ablated patients developed a new slow VT that was different from the original clinical VT (two of these patients underwent successful re-ablation, whereas one patient did not, because the VTs were well managed by the antitachycardia pacing of his ICD, and he is listed for heart transplantation because of severe heart failure).
In the substrate-mapping group, one patient underwent heart transplantation 17 months after ablation without any VT recurrences, and a total of three patients died: one patient died in the hospital the night after the procedure from electromechanical dissociation after cardiac tamponade. Another patient died 17 months after ablation from pump failure after re-infarction without arrhythmias. The above mentioned female patient who died unwitnessed during sleep 8 months after the procedure was a patient with an anterior wall infarct, an ejection fraction of 40%, and a clinical VT cycle length of 410 ms, which was not re-inducible at the control EP study, who refused an ICD or antiarrhythmic drugs other than a beta-blocker (metoprolol).
VT-mapping group vs. substrate-mapping group
There were no statistical differences in the comparison of demographic data and procedure parameters of the two groups, except for a higher median number of applied ablation lines in the substrate-mapping group compared with the VT-mapping group (two lines vs. one line, respectively) (Table 1). During the ablation procedure, one patient of each group developed acute left heart failure, requiring catecholamines, furosemide, nitrates, and mechanical ventilation. Both procedures were continued after haemodynamic stabilization of the patient. There was no difference between the outcome between the VT-mapping group and the substrate-mapping group.
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Discussion |
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Different, electroanatomically guided, mapping and ablation strategies for ablation of stable,10
unstable,3,4 or both stable and unstable VT5 have been previously described. These studies used long linear lesions along the infarct border3 or ablated critical isthmuses within the infarct area identified during sinus rhythm, pacing, or VT.5,10 In fact, the outcome of those patients, in whom a critical isthmus of the VT could be identified, was significantly better compared with patients in whom an isthmus could not be characterized. In this setting, it has also been shown that ablation of a single channel can abolish more than one VT10–12 and detailed sinus rhythm mapping of an infarct area can identify such critical channels.13
In the present investigation, VT ablation was planned to be performed by a complete CARTO map during VT in all patients. However, in the majority of patients, this was not possible due to mechanical block of the VT by catheter manipulation or haemodynamic deterioration during long-lasting VT. The main finding of this study was that the outcome of the patients was the same, no matter whether complete VT mapping could be performed or only substrate mapping. This indicates that careful mapping of the infarct area during SR or pacing is as effective to identify critical channels as it is during VT mapping, the latter often being associated with a higher risk of jeopardizing the patient's health due to abnormal haemodynamics. The overall success of the present investigation compares well with data from patient cohorts in the literature.5 This is of particular interest because in the present study, only clinical and slower VT were targeted compared with targeting all inducible VT in other studies.14 The similar results may be due to the fact that in the present investigation VT ablation was followed by prophylactic connections of electrical barriers (i.e. scar to scar or scar to mitral annulus) in the majority of patients.
Although the mean length of the ablation lines is the same in both groups, there is statistically a higher median number of applied ablation lines in the substrate-mapping group compared with the VT-mapping group (two lines vs. one line, respectively). One explanation may be that in the substrate-mapping group, more prophylactic lines were applied because the critical isthmus was harder to identify and ablation success was harder to assess, especially in the 20% of patients in whom the VT was mechanically blocked.
Of note was that the acute ablation success in all patients with regard to non-inducibility of the clinical VT or any slower VT was 79% after a single ablation procedure, but increased to 95% after all ablation procedures during follow-up. This indicates that the substrate of VT in ischaemic coronary artery disease often is complex and that a mean of 1.2 procedures per patient was necessary to eliminate the clinical or slower VT using non-irrigation technology in the majority of procedures (72%). In addition, the risk of clinical occurrence of faster VT remained in 23% of our patients after hospital discharge such that additional ICD implantation may be necessary. This conclusion has also been suggested by Zado et al.15 who found that the risk for spontaneous rapid VT after successful ablation of stable ischaemic VT by use of conventional ablation technology was 10% in a series of 50 patients.
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The index arrhythmia was considered a stable VT if the patient remained conscious and needed no resuscitation during the clinical arrhythmia. However, 22 patients (47%) had previously undergone ICD implantation, resulting in fast arrhythmia termination by the device. As a result, our patient cohort may also include some ICD patients with unstable VT, who were terminated by their ICD before they could have led to unconsciousness.
The present study was not a randomized investigation comparing prospectively VT-mapping and substrate mapping. In most of the patients of both groups, prophylactic linear RF ablations were applied for connection of electrical barriers, or ablation targeted diastolic potentials during sinus rhythm or pacing, suggesting areas of slow conduction. The identical outcome of both groups may be related to these additional prophylactic lines.
Another limitation may be that irrigated tip ablation was used in only 28% of procedures, however, to the same extent in both groups. A higher success rate may be expected if irrigated technology was used in more patients because this would result in deeper and larger lesions and therefore a more effective substrate modification and channel elimination.16,17 In the four patients with an early recurrence during the same hospital stay, all the initial ablations had been performed using a conventional 4 mm tip electrode. The use of the irrigated tip catheter during the re-ablation procedure at the same sites consolidated the previously produced lesions, which were most likely smaller and shallower. If the irrigated catheter had been used in the initial ablation, it is very likely that this would have prevented early VT recurrence. It, therefore, seems justified to combine both the conventional and the irrigated ablation procedures and rate them as acute success.
Our hospital policy to ablate only the clinical or slower VT, but not faster VT, may have led to a lower success rate compared with centres which target all induced VT morphologies. The rationale for not targeting the faster VT was that they must have a shorter zone of slow conduction than the clinical VT and that the ICD could be easily programmed for their effective termination.
Since it is sometimes difficult to differentiate between a focal ablation, an enlarged focal ablation, and a linear ablation, we refrained from differentiating between these approaches, especially since there was no statistical difference between groups.
Comparing VT mapping and substrate mapping may be criticized because there is some heterogeneity from non-systematic variation in lesion strategy (focal/linear), ablation delivery (conventional/cooled-tip), using limited VT induction and entrainment criteria in the substrate-mapping group and not targeting VTs faster than the clinical VT. However, since focal and linear ablations, as well as irrigated ablations, were used in both groups to the same extent with identical endpoints, a subgroup analysis seems possible. This is especially so since haemodynamic instability during the ongoing VT and mechanical block of the clinical VT by catheter ablation is clinically relevant. For the treating physician, it is important to realize that even if the VT cannot be mapped with CARTO, the outcome was the same, which may actually lead to the assumption that a complete three-dimensional VT map is not necessary in any patient undergoing VT ablation.
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Conclusion |
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When using a CARTO-guided approach for VT ablation in patients with coronary artery disease, the freedom from any ventricular arrhythmia is high (75%). However, the patient has a residual 23% risk of developing fast VT/VF during follow-up. Mapping during sinus rhythm or pacing is as successful as mapping during VT.
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The authors would like to thank Sigrid Boczor for the biometric calculations and Detlef Hennig for technical assistance.
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[1] Della Bella P, De Ponti R, Uriarte JA, Tondo C, Klersy C, Carbucicchio C, et al. Catheter ablation and antiarrhythmic drugs for haemodynamically tolerated post-infarction ventricular tachycardia; long-term outcome in relation to acute electrophysiological findings. Eur Heart J 2002; 23: 414–24.
[2] Kim YH, Sosa-Suarez G, Trouton TG, O'Nunain SS, Osswald S, Mc Govern BA, et al. Treatment of ventricular tachycardia by transcatheter radiofrequency ablation in patients with ischemic heart disease. Circulation 1994; 89: 1094–102.
[3] Marchlinski FE, Callans DJ, Gottlieb CD, Zado E. Linear ablation lesions for control of unmappable ventricular tachycardia in patients with ischemic and nonischemic cardiomyopathy. Circulation 2000; 101: 1288–96.
[4] Sra J, Bhatia A, Dhala A, Blanck Z, Deshpande S, Cooley R, et al. Electroanatomical guided catheter ablation of ventricular tachycardias causing multiple defibrillator shocks. Pacing Clin Electrophysiol 2001; 24: 1645–52.[CrossRef][Medline]
[5] Soejima K, Suzuki M, Maisel WH, Brunckhorst CB, Delacretaz E, Blier L, et al. Catheter ablation in patients with multiple and unstable ventricular tachycardias after myocardial infarction. Circulation 2001; 104: 664–9.
[6] Stevenson WG, Khan H, Sager P, Saxon LA, Middlekauff HR, Natterson PD, et al. Identification of reentry circuit sites during catheter mapping and radiofrequency ablation of VT late after myocardial infarction. Circulation 1993; 88: 1647–70.
[7] Stevenson WG, Sager PT, Natterson PD, Saxon LA, Middlekauff HR, Wiener I. Relation of pace mapping QRS configuration and conduction delay to ventricular tachycardia reentry circuits in human infarct scars. J Am Coll Cardiol 1995; 26: 481–8.[Abstract]
[8] Kuck K-H, Schlüter M, Geiger M, Siebels J. Successful catheter ablation of human ventricular tachycardia with radiofrequency current guided by an endocardial map of the area of slow conduction. Pacing Clin Electrophysiol 1991; 14: 1060–71.[CrossRef][Medline]
[9] Stevenson WG, Friedman PL, Sager PT, Saxon LA, Kocovic D, Harada T, et al. Exploring postinfarction reentrant ventricular tachycardia with entrainment mapping. J Am Coll Cardiol 1997; 19: 1180–89.
[10] Chillou C, Lacroix D, Klug D, Magnin-Poull I, Marquié C, Messier M, et al. Isthmus characteristics of reentrant ventricular tachycardia after myocardial infarction. Circulation 2002; 105: 726–31.
[11] Wilber DJ, Kopp DE, Glaskock DN, Kinder CA, Kall JG. Catheter ablation of the mitral isthmus for ventricular tachycardia associated with inferior infarction. Circulation 1995; 92: 3481–89.
[12] Hadjis TA, Stevenson WG, Harada T, Friedman PL, Sager P, Saxon LA. Preferential locations for critical reentry circuit sites causing ventricular tachycardia after inferior wall myocardial infarction. J Cardiovasc Electrophysiol 1997; 8: 363–70.[ISI][Medline]
[13] Reddy VY, Neuzil P, Taborsky M, Ruskin JN. Short-term results of substrate mapping and radiofrequency ablation of ischemic ventricular tachycardia using a saline-irrigated catheter. J Am Coll Cardiol 2003; 41: 2228–36.
[14] Borger van der Burg AE, de Groot NM, van Erven L, Bootsma M, van der Wall EE, Schalij MJ. Long-term follow-up after radiofrequency catheter ablation of ventricular tachycardia: a successful approach? J Cardiovasc Electrophysiol 2002; 13: 417–23.[CrossRef][ISI][Medline]
[15] Zado ES, Gottlieb CD, Callans DJ, Coyne RF, Man DC, Sarter BH, et al. Successful ventricular tachycardia catheter ablation: an argument for having defibrillator backup. (Abstract). Circulation 1997; 96: 319.
[16] Watanable I, Masaki R, Min N, Oshikawa N, Okubo K, Sugimura H, et al. Cooled-tip ablation results in increased radiofrequency power delivery and lesion size in canine heart: importance of catheter-tip temperature monitoring for prevention of popping and impedance rise. J Interv Card Electrophysiol 2002; 6: 9–16.[CrossRef][ISI][Medline]
[17] Soejima K, Delacretaz E, Suzuki M, Brunckhorst CB, Maisel WH, Friedman PL, et al. Saline-cooled versus standard radiofrequency catheter ablation for infarct-related ventricular tachycardia. Circulation 2001; 103: 1858–62.
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  J. Almendral and M. E. Josephson All Patients With Hemodynamically Tolerated Postinfarction Ventricular Tachycardia Do Not Require an Implantable Cardioverter-Defibrillator Circulation, September 4, 2007; 116(10): 1204 - 1212. [Full Text] [PDF]
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