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Predictors for Successful Ablation of Right- and Left-Sided Idiopathic Ventricular Tachycardia
Predictors for Successful Ablation of Right- and Left-Sided Idiopathic Ventricular Tachycardia Luz-Maria Rodriguez,
MD,
Joep L.R.M. Smeets, MD, Carl Timmermans, and Hein J.J. Wellens, MD
MD,
This study reports on predictors for successful radiofrequency (RF) ablation of idiopathic ventricular tachycardia (VT) in 48 patients—35 with right ventricular (RV) outflow tract and 13 with left ventricular VT. In RV outflow tract idiopathic VT, RF ablation was successful in 29 of 35 patients (83%). The following information allowed differentiation between patients with and without a successful RF ablation: ú1 induced VT morphology (0 vs 3); presence of delta wave–like beginning of the QRS (2 vs 3) and ¢11 of 12 leads showing a ‘‘match’’ between the clinical VT and the pacemap (28 vs 1). Endocardial activation times were not different between both groups (015 { 18 vs 04 { 5 ms). In left ventricle idiopathic VT, RF ablation was successful in 12 of 13 patients (92%). In patients who underwent successful ablation, 1 VT morphology was induced and no delta wave–like beginning of the QRS was present; a correlation between clinical VT and the pacemap ¢11 of 12 leads was found and the endocardial activation time preceded the QRS (range of 05 to 058 ms [mean 030 { 14]). Purkinje
activity was observed in 5 of 7 patients with an idiopathic VT originating from the inferoposterior region but not from the inferoapical region of the left ventricle. Four patients (14%) with RV outflow tract idiopathic VT had recurrence during a mean follow-up of 2 to 50 months (mean 30 { 12). Thus, (1) in RV outflow tract idiopathic VT a good pacemap was more important than an early endocardial activation time; (2) an optimal pacemap as well as an early endocardial activation time were important predictors for successful ablation of the left ventricle idiopathic VT; (3) Purkinje activity was recorded in VTs arising in the inferoposterior region of the left ventricle; and (4) factors for unsuccessful ablation for idiopathic VT were ú1 induced VT morphology, a delta wave–like beginning of the QRS, and a VT/pacemap correlation õ11 of 12 leads. Idiopathic VT can be successfully ablated with both immediate and long-term success. Q1997 by Excerpta Medica, Inc. (Am J Cardiol 1997;79:309–314)
adiofrequency (RF) catheter ablation in idiopathic ventricular tachycardia (VT) has shown R excellent initial results, but less is known about
clinical VT was available in all patients. Electrocardiograms during VT were analyzed for: morphology, QRS axis, QRS width, and the presence of a slow (delta wave – like) beginning of the QRS. Thirty-five patients (16 women, aged 7 to 61 years [mean 40 { 12]) had idiopathic VT originating in the RV outflow tract, and 13 patients (5 women, aged 12 to 60 years [mean 31 { 14]) had this VT in the left ventricle. All patients had been treated before RF ablation by various antiarrhythmic drugs including a b blocker, a class IC drug (flecainide, propafenone), a class III drug (sotalol, amiodarone), and a calcium antagonist (verapamil, diltiazem). These antiarrhythmic drugs, except amiodarone, were discontinued for at least 5 half-lives before electrophysiologic examination. Electrophysiologic study protocol: After written informed consent, each patient was studied in the fasting state without sedation. Under local anesthesia, via the femoral route, a quadripolar 6Fr electrode catheter (USCI) with 1 cm interelectrode spacing was positioned in the right atrium and the RV apex. A 4Fr bipolar catheter (Cordis, Europa NV, Roden, The Netherlands) was placed in the His bundle region. Programmed electrical stimulation was performed as previously described,6 first in the right atrium and then in the right ventricle using up to 3 extrastimuli. When sustained VT could not be induced, the stimulation protocol was repeated under isoproterenol infusion at a rate of 1 to 3 mg/min.
1–5
the long-term results. Several parameters to predict successful RF ablation of idiopathic VT have been described by other investigators.2 – 5 These parameters included: presence of Purkinje activity in idiopathic VT originating in the left ventricle,2 – 5 and an excellent correlation between spontaneous VT and the pacemap4 in idiopathic VT originating in the right ventricular (RV) outflow tract. This study describes our experience with predictors of successful ablation in 48 patients with symptomatic idiopathic VT. Study group: From March 1992 to March 1996, 48 patients with idiopathic monomorphic VT were treated by RF ablation in our institution. The diagnosis of idiopathic VT was made after an extensive workup including clinical history, physical examination, 12-lead electrocardiogram, exercise testing, signal-averaged electrocardiogram (8 patients), 24hour Holter, and an echo-Doppler investigation. On indication a coronary angiography was performed (2 patients). A 12-lead electrocardiogram of the From The Department of Cardiology, Academic Hospital Maastricht, Maastricht, The Netherlands. Manuscript received May 7, 1996; revised manuscript received and accepted August 14, 1996. Address for reprints: Luz-Maria Rodriguez, MD, Academic Hospital, P.O. Box 5800, Maastricht, The Netherlands. Q1997 by Excerpta Medica, Inc.
0002-9149/97/$17.00 PII S0002-9149(96)00753-9
All rights reserved.
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FIGURE 1. Panel A, 12-lead electrocardiogram during sinus rhythm. Panel B, shows an example of the 12-lead electrocardiogram during ventricular tachycardia with left bundle branch block morphology and right axis deviation. Note the slow (delta wave–like) beginning of the QRS complex.
Also, rapid ventricular pacing was performed using cycle lengths of 430, 400, 350, and 300 ms giving 10, 20, 35, and 50 stimuli. Mapping procedure: After the baseline study, a 7Fr quadripolar deflectable ablation catheter with a 4 mm tip electrode and an interelectrode distance of 2 mm (Webster) was introduced into the right or left ventricle. Endocardial activation mapping was performed during VT. Pacemapping was done by using bipolar pacing between the distal pair of the electrodes with a stimulus pulse width of 2 ms. Two methods were used during pacemapping: (1) pacemapping during VT at a cycle length 20 ms shorter than the tachycardia cycle length using a stimulus strength limited to 1 mA greater than required for capture of the tachycardia, or (2) pacemapping during sinus rhythm by pacing at the same rate as the clinical VT to obtain an identical QRS-VT morphology. An optimal pacemap was defined as a 12-lead electrocardiogram showing all 12 leads during pacing with an identical QRS complex as during spontaneous VT. In all patients, we carefully searched for Purkinje activity preceding the QRS complex. Radiofrequency catheter ablation procedure: Radiofrequency current was delivered from a 500 kHz generator (HAT 200; Dr. Osypka, Wyhlen, Germany) at 30 W between the large-tip (4 mm) electrode of the ablation catheter and an adhesive electrosurgical dispersion pad applied to the left posterior chest. The current was delivered during VT or in sinus rhythm for 30 to 60 seconds or until a sudden increase in impedance occurred. After each 310
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FIGURE 2. A, an example of an optimal match between the clinically recorded 12-lead electrocardiogram of an idiopathic left bundle branch block–shaped ventricular tachycardia and B, the electrocardiogram recorded during pacing on the septal site of the right ventricular outflow tract.
FIGURE 3. Number of ventricular tachycardias (black dots) ablated in A (the septum) and B (the free wall) of the RV outflow tract. LA Å left atrium; LV Å left ventricle; PV Å pulmonary valve; RA Å right atrium; RV Å right ventricle; TV Å tricuspid valve.
application of energy, programmed ventricular stimulation was repeated, if necessary with isoproterenol to see if VT was still inducible. The procedure was terminated when VT could not be induced for a period of at least 30 minutes after ablation. Intravenous heparin in a bolus dose of 10,000 U initially and additional boluses of 5,000 U every hour were administered during the procedure. FEBRUARY 1, 1997
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FIGURE 4. Panel A, 12-lead electrocardiogram of an idiopathic ventricular tachycardia originating in the inferoposterior region of the left ventricle. Panel B illustrates the optimal pacemap in this patient. Note the identical paced QRS in 12 of 12 leads compared with the clinical ventricular tachycardia.
Postablation management: All patients had 24-hour Holter monitoring immediately after the ablation procedure. Patients were also maintained under telemetry surveillance in an intermediate-care unit for 24 hours after ablation. Exercise testing was performed on the second or third day after ablation. Patients were discharged from the hospital after 72 hours on oral aspirin, 80 mg/day for 3 months. Follow-up: Every patient was seen in our outpatient clinic 6 weeks after the RF ablation procedure, and patients living in the Maastricht area were seen afterward at intervals of 6 months. For patients living out of this area (in The Netherlands or another country), information (clinical and electrocardiograms) was obtained through the general practitioner or cardiologist. Definitions: Successful procedure: if VT could not be induced under isoproterenol. Early recurrences: recurrent VT observed within the hospital stay. Late recurrences: Recurrent VT occurring after hospital discharge.
RESULTS Idiopathic ventricular tachycardia arising from the right ventricular outflow tract: ELECTROCARDIOGRAPHIC CHARACTERISTICS: Most of the clinically occurring monomorphic VTs were sustained. VT originating from the septum showed a right frontal plane axis,
FIGURE 5. The 12-lead electrocardiogram during idiopathic left ventricular tachycardia with a right bundle branch block–like morphology and left axis deviation. Note a very sharp high-frequency potential preceding the QRS in the endocardial recording from the radiofrequency ablation catheter. CS d Å a recording from the distal coronary sinus electrode; HBE Å His bundle electrogram.
whereas the axis was intermediate in VTs arising from the free wall of the RV outflow tract. The width of the QRS during VT was similar in both locations (septal Å 143 { 13 vs free wall Å 147 { 12 ms; p Å NS). Twenty-nine of 35 patients (83%) were successfully ablated. Five VTs (2 successfully and 3 unsuccessfully ablated patients) showed a delta wave–like beginning of the QRS complex (Figure 1). ELECTROPHYSIOLOGIC CHARACTERISTICS: Ventricular tachycardia could be induced in the basal state or during isoproterenol infusion in 28 of 35 patients (80%). Four patients had incessant VT and 3 were not inducible. Fourteen patients were induced by extrastimulus testing and 14 patients by rapid ventricular pacing. Two different VT morphologies were induced in 2 and 3 VT morphologies in 1 patient. In all, 39 VTs were induced in 35 patients. RADIOFREQUENCY CATHETER ABLATION: Pacemapping endocardial activation time at the successful ablation site: All patients in whom RF ablation succeeded had only 1 morphology of VT induced, similar to the one clinically documented. A match of 12 of 12 leads between the clinical VT and the pacemap (Figure 2) was obtained in 20 patients; 11 of 12 leads in 8 patients and 10 of 12 leads in the remaining patients were similar. Endocardial activation time during VT in 29 VTs ranged from 0 to 060 ms (mean 015 { 18). VT could not be ablated in 6 patients. In these patients, 10 VTs were induced (3
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FIGURE 8. Location of ventricular tachycardias ablated in the inferoposterior and apical region of the left ventricle. LA Å left atrium.
Site of origin: Twenty-nine of 39 VTs were successfully ablated. Nineteen VTs originated from the septum in the outflow tract, 3 from a lower location in the direction of the midseptum and 7 from the free wall of the RV outflow tract (Figures 3A and 3B). Ten VTs could not be ablated; therefore, the exact site of origin could not be established. The electrocardiographic pattern of these VTs corresponded to VTs originating in the septum (6 VTs), closer to the midseptum (1 VT), and in the free wall (3 VTs) of the RV outflow tract. Purkinje activity, fractionated potentials, or a zone of slow conduction was not observed in any patient with RV idiopathic VT. Recurrences: During a follow-up of 2 to 50 months (mean 30 { 15), 4 recurrences occurred (14%). In 3 patients the recurrences were early (in 2 patients the VT showed a delta wave–like beginning of the QRS) and only 1 patient had a late recurrence (3 months after RF ablation). In 3 of the 4 patients with a recurrence, a new RF ablation was attempted. In 1 patient the RF ablation succeeded and in the 2 other patients the procedure failed. These unsuccessfully ablated patients are currently treated with sotalol 40 mg twice daily. The patient in whom no second ablation was performed has less complaints and is without antiarrhythmic drug treatment.
FIGURE 6. Panel A, 12-lead electrocardiogram during sinus rhythm before radiofrequency ablation in a patient with idiopathic ventricular tachycardia originating from the inferoposterior region of the left ventricle. Panel B, 12-lead electrocardiogram of the clinical ventricular tachycardia with a right bundle branch block–like morphology and left-axis deviation. Panel C, 12-lead electrocardiogram after radiofrequency ablation. Note the presence of a left posterior hemiblock.
Idiopathic ventricular tachycardia arising from the left ventricle: ELECTROCARDIOGRAPHIC CHARACTERISTICS:
FIGURE 7. Same patient as in Figure 6 showing a 12-lead electrocardiogram 14 months after radiofrequency (RF) ablation with persistence of left posterior hemiblock.
patients with 1, 2 patients with 2, and 1 patient with 3 VT morphologies). Only 1 of those patients had an optimal pacemap (12 of 12 leads). The endocardial activation time ranged from 0 to 010 ms (mean 04 { 5) (obtained in 6 VTs). The endocardial activation times during VT were not different between successful and unsuccessful ablation (015 { 18 vs 04 { 5 ms); p Å NS. 312
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Twelve of 13 patients had sustained monomorphic VT. A left axis was observed in 7 and a northwest axis in the remaining 6 patients. The width of the QRS during VT was wider in VTs showing a northwest axis (150 { 12 ms) compared with those a left axis (121 { 10 ms); p õ0.001. Twelve of the 13 patients were successful ablated (92%). A delta wave–like beginning of the QRS during VT was observed in the patient in whom RF ablation failed. ELECTROPHYSIOLOGIC CHARACTERISTICS: Induction of VT by programmed electrical stimulation during the basal state or with isoproterenol was possible in 10 of 13 patients (77%). One patient had an incessant VT and 2 patients were not inducible. Nine FEBRUARY 1, 1997
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patients were induced by extrastimulus testing, and 1 with rapid ventricular pacing. In only 1 patient were 2 different VT morphologies induced. In total, 14 VTs were induced in 13 patients. RADIOFREQUENCY CATHETER ABLATION: Pacemapping and endocardial activation times at the successful ablation site. All patients with successful ablation had only 1 morphology of VT induced (similar to the one clinically documented). Eleven patients were ablated during VT and 2 during sinus rhythm. A match of 12 of 12 lead QRS between the clinical VT and during the pacemap was obtained in 11 patients (Figure 4): 11 of 12 leads in 2 patients. The endocardial activation time ranged from 05 to 058 ms (mean 030 { 14) (11 patients). Purkinje activity was recorded in 5 VTs. These sharp potentials preceded the beginning of the QRS during VT by 20 to 30 ms and were recorded in idiopathic VT showing a left axis (Figure 5), whereas no Purkinje activity was recorded in those with a northwest axis. After ablation, 2 patients in whom Purkinje activity had been recorded had electrocardiographic changes suggestive of a left posterior hemiblock. This pattern was still present after 26 and 14 months, respectively (Figures 6 and 7). Site of origin: The origin of the VT was the inferoposterior region of the left ventricle in 7 and the inferoapical area in 6 patients (Figure 8). The patient in whom RF ablation failed had 2 VT morphologies. The pacemap showed a match of 11 of 12 leads; the earliest endocardial activation during VT was 0 ms and the VT showed a delta wave–like beginning of the QRS. The electrocardiographic pattern of this VT suggested an origin in the inferoposterior region of the left ventricle. Recurrences: After a mean follow-up of 1 to 48 months (mean 36 { 12), no recurrences were observed in these 12 patients. The patient in whom RF ablation failed is treated with verapamil.
DISCUSSION RV outflow tract idiopathic VT can originate from 3 different sites: the septum, somewhat lower in the midseptum, and in the free wall, giving characteristic electrocardiographic patterns.7,8 The successfully ablated patients had only 1 VT morphology induced. In these patients the pacemap showed at least a match of 11 of 12 leads with the QRS of the clinical VT. The earliest endocardial activation time ranged from 0 to 060 ms and was not different from patients in whom VT could not be ablated. In the unsuccessfully ablated patients, ú1 VT morphology could be induced. In these patients, a nonoptimal pacemap (10 of 12 leads) and a delta wave–like beginning of the QRS during VT was observed. This slow beginning of the QRS may indicate a possible intramural or subepicardial origin of the VT. No Purkinje activity, fractionated potentials, or zone of slow conduction were observed. These findings are in agreement with a data by Coggins et al.4 In 83% of the patients, a definitive cure was obtained without complications. The initial success rate in our popu-
lation is comparable with previous data.4 Recurrences were observed in 4 of 35 patients (14%). In 3 patients, recurrent VT occurred during hospital stay (early recurrences); 2 of them had VT showing a delta wave–like beginning of the QRS. The remaining patient had a recurrence 3 months after RF ablation. Left-sided idiopathic VT can originate from 2 different sites in the left ventricle: the inferoposterior or inferoapical region. The 12-lead electrocardiogram of these idiopathic VTs showed typical features7,9: a right bundle branch block – like morphology with a left or northwest axis. The width of the QRS was wider in VTs originating in the inferoapical area compared with VTs arising in the inferoposterior region of the left ventricle. The successfully ablated patients had only 1 VT morphology. In contrast to a previous report,5 optimal pacemapping was observed in all but 1 patient. The endocardial activation time always preceded the QRS complex during VT. Purkinje activity was recorded in 5 of 7 VTs arising in the inferoposterior region of the left ventricle but was absent in all VTs originating from the apical region, suggesting that in the apical region the VT originates distant from the Purkinje network. In patients without Purkinje activity, pacemapping alone was sufficient to target the site of RF ablation. Therefore, the presence of Purkinje activity at the site of successful ablation apparently is not a requisite for ablation of left-sided VTs as postulated by other investigators.3,5 Contrary to another report,10 fractionated potentials or a zone of slow conduction were not observed. As in unsuccessfully ablated RV outflow tract idiopathic VT, the patient in whom the RF ablation failed also had ú1 VT morphology induced, showed a delta wave – like beginning of the QRS, did not have an optimal pacemap, and the endocardial activation time did not precede the beginning of the QRS complex. The immediate and late success rate was 92% and no recurrences were observed during a mean follow-up of 36 { 12 months. The immediate success in our population is comparable with a publication by Wen et al.5 Our observations suggest (as supported by findings after the long follow-up) that the best predictor for successful RF ablation of idiopathic VT originating from both regions in the left ventricle is an optimal pacemap rather than the presence of Purkinje activity.
1. Klein LS, Shih HT, Hackett K, Zipes DP, Miles WM. Radiofrequency cath-
eter ablation of ventricular tachycardia in patients with structural heart disease. Circulation 1992;85:1666–1674. 2. Wilber DM, Baerman J, Olshansky B, Kall J, Kopp D. Adenosine sensitive ventricular tachycardia: clinical characteristics and response to catheter ablation. Circulation 1993;97:126–134. 3. Nakagawa H, Beckman KJ, McClelland JH, Wang X, Arruda M, Santoro I, Hazlitt HA, Abdalla I, Singh A, Gossinger H, Sweidan R, Hirao K, Widman L, Pirha JV, Lazzara R, Jackman WM. Radiofrequency catheter ablation of idiopathic left ventricular tachycardia guided by a Purkinje potential. Circulation 1993:88:2607–2617. 4. Coggins DL, Lee RJ, Sweeney J, Chein WW, VanHare G, Epstein L, Gonzalez R, Griffin JC, Lesh MD, Scheinman MM. Radiofrequency catheter abla-
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tion as a cure for idiopathic tachycardia of both left and right ventricular origin. J Am Coll Cardiol 1994;23:1333–1341. 5. Wen MS, Yeh SJ, Wang CC, Lin FC, Chen JC, Wu D. Radiofrequency therapy in idiopathic left ventricular tachycardia with no obvious structural heart disease. Circulation 1994;89:1690–1696. 6. Wellens HJJ, Farre´ J, Brugada P, F Ba¨r: The method of programmed electrical stimulation in the study of ventricular tachycardia. In: Josephson ME, ed. Ventricular Tachycardia. Mount Kisco, NY: Futura, 1982:237–283. 7. Wellens HJJ, Rodriguez LM, Smeets JLRM. Ventricular tachycardia in structurally normal hearts. In: Zipes DP, Jalife J, eds. Cardiac Electrophysiology. From Cell to Bedside. 2nd ed. Philadelphia: WB Saunders, 1995:780–788.
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8. Jadonath RL, Schwartzman DS, Preminger NW, Gottlieb CD, Marchlinski FE. Utility of the 12-lead electrocardiogram in localizing the origin of right ventricular outflow tract tachycardia. Am Heart J 1995;130:1107–1113. 9. Rosas F, Eslami M, Elias J, Kinoshita O, Nakazato Y, Marcus FI, Frank R, Tonet J, Fontaine G. Diagnostic clues from the surface ECG to identify idiopathic (fascicular) ventricular tachycardia: correlation with electrophysiologic findings. J Cardiovasc Electrophysiol 1996;7:2–8. 10. Kottkamp H, Chen X, Hindricks G, Willems S, Haverkamp W, Wichter T, Breithardt G, Borgreffe M. Idiopathic left ventricular tachycardia: new insights into electrophysiologics and radiofrequency catheter ablation. PACE 1995;18:1285–1297.
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MD,
Joep L.R.M. Smeets, MD, Carl Timmermans, and Hein J.J. Wellens, MD
MD,
This study reports on predictors for successful radiofrequency (RF) ablation of idiopathic ventricular tachycardia (VT) in 48 patients—35 with right ventricular (RV) outflow tract and 13 with left ventricular VT. In RV outflow tract idiopathic VT, RF ablation was successful in 29 of 35 patients (83%). The following information allowed differentiation between patients with and without a successful RF ablation: ú1 induced VT morphology (0 vs 3); presence of delta wave–like beginning of the QRS (2 vs 3) and ¢11 of 12 leads showing a ‘‘match’’ between the clinical VT and the pacemap (28 vs 1). Endocardial activation times were not different between both groups (015 { 18 vs 04 { 5 ms). In left ventricle idiopathic VT, RF ablation was successful in 12 of 13 patients (92%). In patients who underwent successful ablation, 1 VT morphology was induced and no delta wave–like beginning of the QRS was present; a correlation between clinical VT and the pacemap ¢11 of 12 leads was found and the endocardial activation time preceded the QRS (range of 05 to 058 ms [mean 030 { 14]). Purkinje
activity was observed in 5 of 7 patients with an idiopathic VT originating from the inferoposterior region but not from the inferoapical region of the left ventricle. Four patients (14%) with RV outflow tract idiopathic VT had recurrence during a mean follow-up of 2 to 50 months (mean 30 { 12). Thus, (1) in RV outflow tract idiopathic VT a good pacemap was more important than an early endocardial activation time; (2) an optimal pacemap as well as an early endocardial activation time were important predictors for successful ablation of the left ventricle idiopathic VT; (3) Purkinje activity was recorded in VTs arising in the inferoposterior region of the left ventricle; and (4) factors for unsuccessful ablation for idiopathic VT were ú1 induced VT morphology, a delta wave–like beginning of the QRS, and a VT/pacemap correlation õ11 of 12 leads. Idiopathic VT can be successfully ablated with both immediate and long-term success. Q1997 by Excerpta Medica, Inc. (Am J Cardiol 1997;79:309–314)
adiofrequency (RF) catheter ablation in idiopathic ventricular tachycardia (VT) has shown R excellent initial results, but less is known about
clinical VT was available in all patients. Electrocardiograms during VT were analyzed for: morphology, QRS axis, QRS width, and the presence of a slow (delta wave – like) beginning of the QRS. Thirty-five patients (16 women, aged 7 to 61 years [mean 40 { 12]) had idiopathic VT originating in the RV outflow tract, and 13 patients (5 women, aged 12 to 60 years [mean 31 { 14]) had this VT in the left ventricle. All patients had been treated before RF ablation by various antiarrhythmic drugs including a b blocker, a class IC drug (flecainide, propafenone), a class III drug (sotalol, amiodarone), and a calcium antagonist (verapamil, diltiazem). These antiarrhythmic drugs, except amiodarone, were discontinued for at least 5 half-lives before electrophysiologic examination. Electrophysiologic study protocol: After written informed consent, each patient was studied in the fasting state without sedation. Under local anesthesia, via the femoral route, a quadripolar 6Fr electrode catheter (USCI) with 1 cm interelectrode spacing was positioned in the right atrium and the RV apex. A 4Fr bipolar catheter (Cordis, Europa NV, Roden, The Netherlands) was placed in the His bundle region. Programmed electrical stimulation was performed as previously described,6 first in the right atrium and then in the right ventricle using up to 3 extrastimuli. When sustained VT could not be induced, the stimulation protocol was repeated under isoproterenol infusion at a rate of 1 to 3 mg/min.
1–5
the long-term results. Several parameters to predict successful RF ablation of idiopathic VT have been described by other investigators.2 – 5 These parameters included: presence of Purkinje activity in idiopathic VT originating in the left ventricle,2 – 5 and an excellent correlation between spontaneous VT and the pacemap4 in idiopathic VT originating in the right ventricular (RV) outflow tract. This study describes our experience with predictors of successful ablation in 48 patients with symptomatic idiopathic VT. Study group: From March 1992 to March 1996, 48 patients with idiopathic monomorphic VT were treated by RF ablation in our institution. The diagnosis of idiopathic VT was made after an extensive workup including clinical history, physical examination, 12-lead electrocardiogram, exercise testing, signal-averaged electrocardiogram (8 patients), 24hour Holter, and an echo-Doppler investigation. On indication a coronary angiography was performed (2 patients). A 12-lead electrocardiogram of the From The Department of Cardiology, Academic Hospital Maastricht, Maastricht, The Netherlands. Manuscript received May 7, 1996; revised manuscript received and accepted August 14, 1996. Address for reprints: Luz-Maria Rodriguez, MD, Academic Hospital, P.O. Box 5800, Maastricht, The Netherlands. Q1997 by Excerpta Medica, Inc.
0002-9149/97/$17.00 PII S0002-9149(96)00753-9
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FIGURE 1. Panel A, 12-lead electrocardiogram during sinus rhythm. Panel B, shows an example of the 12-lead electrocardiogram during ventricular tachycardia with left bundle branch block morphology and right axis deviation. Note the slow (delta wave–like) beginning of the QRS complex.
Also, rapid ventricular pacing was performed using cycle lengths of 430, 400, 350, and 300 ms giving 10, 20, 35, and 50 stimuli. Mapping procedure: After the baseline study, a 7Fr quadripolar deflectable ablation catheter with a 4 mm tip electrode and an interelectrode distance of 2 mm (Webster) was introduced into the right or left ventricle. Endocardial activation mapping was performed during VT. Pacemapping was done by using bipolar pacing between the distal pair of the electrodes with a stimulus pulse width of 2 ms. Two methods were used during pacemapping: (1) pacemapping during VT at a cycle length 20 ms shorter than the tachycardia cycle length using a stimulus strength limited to 1 mA greater than required for capture of the tachycardia, or (2) pacemapping during sinus rhythm by pacing at the same rate as the clinical VT to obtain an identical QRS-VT morphology. An optimal pacemap was defined as a 12-lead electrocardiogram showing all 12 leads during pacing with an identical QRS complex as during spontaneous VT. In all patients, we carefully searched for Purkinje activity preceding the QRS complex. Radiofrequency catheter ablation procedure: Radiofrequency current was delivered from a 500 kHz generator (HAT 200; Dr. Osypka, Wyhlen, Germany) at 30 W between the large-tip (4 mm) electrode of the ablation catheter and an adhesive electrosurgical dispersion pad applied to the left posterior chest. The current was delivered during VT or in sinus rhythm for 30 to 60 seconds or until a sudden increase in impedance occurred. After each 310
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FIGURE 2. A, an example of an optimal match between the clinically recorded 12-lead electrocardiogram of an idiopathic left bundle branch block–shaped ventricular tachycardia and B, the electrocardiogram recorded during pacing on the septal site of the right ventricular outflow tract.
FIGURE 3. Number of ventricular tachycardias (black dots) ablated in A (the septum) and B (the free wall) of the RV outflow tract. LA Å left atrium; LV Å left ventricle; PV Å pulmonary valve; RA Å right atrium; RV Å right ventricle; TV Å tricuspid valve.
application of energy, programmed ventricular stimulation was repeated, if necessary with isoproterenol to see if VT was still inducible. The procedure was terminated when VT could not be induced for a period of at least 30 minutes after ablation. Intravenous heparin in a bolus dose of 10,000 U initially and additional boluses of 5,000 U every hour were administered during the procedure. FEBRUARY 1, 1997
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FIGURE 4. Panel A, 12-lead electrocardiogram of an idiopathic ventricular tachycardia originating in the inferoposterior region of the left ventricle. Panel B illustrates the optimal pacemap in this patient. Note the identical paced QRS in 12 of 12 leads compared with the clinical ventricular tachycardia.
Postablation management: All patients had 24-hour Holter monitoring immediately after the ablation procedure. Patients were also maintained under telemetry surveillance in an intermediate-care unit for 24 hours after ablation. Exercise testing was performed on the second or third day after ablation. Patients were discharged from the hospital after 72 hours on oral aspirin, 80 mg/day for 3 months. Follow-up: Every patient was seen in our outpatient clinic 6 weeks after the RF ablation procedure, and patients living in the Maastricht area were seen afterward at intervals of 6 months. For patients living out of this area (in The Netherlands or another country), information (clinical and electrocardiograms) was obtained through the general practitioner or cardiologist. Definitions: Successful procedure: if VT could not be induced under isoproterenol. Early recurrences: recurrent VT observed within the hospital stay. Late recurrences: Recurrent VT occurring after hospital discharge.
RESULTS Idiopathic ventricular tachycardia arising from the right ventricular outflow tract: ELECTROCARDIOGRAPHIC CHARACTERISTICS: Most of the clinically occurring monomorphic VTs were sustained. VT originating from the septum showed a right frontal plane axis,
FIGURE 5. The 12-lead electrocardiogram during idiopathic left ventricular tachycardia with a right bundle branch block–like morphology and left axis deviation. Note a very sharp high-frequency potential preceding the QRS in the endocardial recording from the radiofrequency ablation catheter. CS d Å a recording from the distal coronary sinus electrode; HBE Å His bundle electrogram.
whereas the axis was intermediate in VTs arising from the free wall of the RV outflow tract. The width of the QRS during VT was similar in both locations (septal Å 143 { 13 vs free wall Å 147 { 12 ms; p Å NS). Twenty-nine of 35 patients (83%) were successfully ablated. Five VTs (2 successfully and 3 unsuccessfully ablated patients) showed a delta wave–like beginning of the QRS complex (Figure 1). ELECTROPHYSIOLOGIC CHARACTERISTICS: Ventricular tachycardia could be induced in the basal state or during isoproterenol infusion in 28 of 35 patients (80%). Four patients had incessant VT and 3 were not inducible. Fourteen patients were induced by extrastimulus testing and 14 patients by rapid ventricular pacing. Two different VT morphologies were induced in 2 and 3 VT morphologies in 1 patient. In all, 39 VTs were induced in 35 patients. RADIOFREQUENCY CATHETER ABLATION: Pacemapping endocardial activation time at the successful ablation site: All patients in whom RF ablation succeeded had only 1 morphology of VT induced, similar to the one clinically documented. A match of 12 of 12 leads between the clinical VT and the pacemap (Figure 2) was obtained in 20 patients; 11 of 12 leads in 8 patients and 10 of 12 leads in the remaining patients were similar. Endocardial activation time during VT in 29 VTs ranged from 0 to 060 ms (mean 015 { 18). VT could not be ablated in 6 patients. In these patients, 10 VTs were induced (3
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FIGURE 8. Location of ventricular tachycardias ablated in the inferoposterior and apical region of the left ventricle. LA Å left atrium.
Site of origin: Twenty-nine of 39 VTs were successfully ablated. Nineteen VTs originated from the septum in the outflow tract, 3 from a lower location in the direction of the midseptum and 7 from the free wall of the RV outflow tract (Figures 3A and 3B). Ten VTs could not be ablated; therefore, the exact site of origin could not be established. The electrocardiographic pattern of these VTs corresponded to VTs originating in the septum (6 VTs), closer to the midseptum (1 VT), and in the free wall (3 VTs) of the RV outflow tract. Purkinje activity, fractionated potentials, or a zone of slow conduction was not observed in any patient with RV idiopathic VT. Recurrences: During a follow-up of 2 to 50 months (mean 30 { 15), 4 recurrences occurred (14%). In 3 patients the recurrences were early (in 2 patients the VT showed a delta wave–like beginning of the QRS) and only 1 patient had a late recurrence (3 months after RF ablation). In 3 of the 4 patients with a recurrence, a new RF ablation was attempted. In 1 patient the RF ablation succeeded and in the 2 other patients the procedure failed. These unsuccessfully ablated patients are currently treated with sotalol 40 mg twice daily. The patient in whom no second ablation was performed has less complaints and is without antiarrhythmic drug treatment.
FIGURE 6. Panel A, 12-lead electrocardiogram during sinus rhythm before radiofrequency ablation in a patient with idiopathic ventricular tachycardia originating from the inferoposterior region of the left ventricle. Panel B, 12-lead electrocardiogram of the clinical ventricular tachycardia with a right bundle branch block–like morphology and left-axis deviation. Panel C, 12-lead electrocardiogram after radiofrequency ablation. Note the presence of a left posterior hemiblock.
Idiopathic ventricular tachycardia arising from the left ventricle: ELECTROCARDIOGRAPHIC CHARACTERISTICS:
FIGURE 7. Same patient as in Figure 6 showing a 12-lead electrocardiogram 14 months after radiofrequency (RF) ablation with persistence of left posterior hemiblock.
patients with 1, 2 patients with 2, and 1 patient with 3 VT morphologies). Only 1 of those patients had an optimal pacemap (12 of 12 leads). The endocardial activation time ranged from 0 to 010 ms (mean 04 { 5) (obtained in 6 VTs). The endocardial activation times during VT were not different between successful and unsuccessful ablation (015 { 18 vs 04 { 5 ms); p Å NS. 312
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Twelve of 13 patients had sustained monomorphic VT. A left axis was observed in 7 and a northwest axis in the remaining 6 patients. The width of the QRS during VT was wider in VTs showing a northwest axis (150 { 12 ms) compared with those a left axis (121 { 10 ms); p õ0.001. Twelve of the 13 patients were successful ablated (92%). A delta wave–like beginning of the QRS during VT was observed in the patient in whom RF ablation failed. ELECTROPHYSIOLOGIC CHARACTERISTICS: Induction of VT by programmed electrical stimulation during the basal state or with isoproterenol was possible in 10 of 13 patients (77%). One patient had an incessant VT and 2 patients were not inducible. Nine FEBRUARY 1, 1997
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patients were induced by extrastimulus testing, and 1 with rapid ventricular pacing. In only 1 patient were 2 different VT morphologies induced. In total, 14 VTs were induced in 13 patients. RADIOFREQUENCY CATHETER ABLATION: Pacemapping and endocardial activation times at the successful ablation site. All patients with successful ablation had only 1 morphology of VT induced (similar to the one clinically documented). Eleven patients were ablated during VT and 2 during sinus rhythm. A match of 12 of 12 lead QRS between the clinical VT and during the pacemap was obtained in 11 patients (Figure 4): 11 of 12 leads in 2 patients. The endocardial activation time ranged from 05 to 058 ms (mean 030 { 14) (11 patients). Purkinje activity was recorded in 5 VTs. These sharp potentials preceded the beginning of the QRS during VT by 20 to 30 ms and were recorded in idiopathic VT showing a left axis (Figure 5), whereas no Purkinje activity was recorded in those with a northwest axis. After ablation, 2 patients in whom Purkinje activity had been recorded had electrocardiographic changes suggestive of a left posterior hemiblock. This pattern was still present after 26 and 14 months, respectively (Figures 6 and 7). Site of origin: The origin of the VT was the inferoposterior region of the left ventricle in 7 and the inferoapical area in 6 patients (Figure 8). The patient in whom RF ablation failed had 2 VT morphologies. The pacemap showed a match of 11 of 12 leads; the earliest endocardial activation during VT was 0 ms and the VT showed a delta wave–like beginning of the QRS. The electrocardiographic pattern of this VT suggested an origin in the inferoposterior region of the left ventricle. Recurrences: After a mean follow-up of 1 to 48 months (mean 36 { 12), no recurrences were observed in these 12 patients. The patient in whom RF ablation failed is treated with verapamil.
DISCUSSION RV outflow tract idiopathic VT can originate from 3 different sites: the septum, somewhat lower in the midseptum, and in the free wall, giving characteristic electrocardiographic patterns.7,8 The successfully ablated patients had only 1 VT morphology induced. In these patients the pacemap showed at least a match of 11 of 12 leads with the QRS of the clinical VT. The earliest endocardial activation time ranged from 0 to 060 ms and was not different from patients in whom VT could not be ablated. In the unsuccessfully ablated patients, ú1 VT morphology could be induced. In these patients, a nonoptimal pacemap (10 of 12 leads) and a delta wave–like beginning of the QRS during VT was observed. This slow beginning of the QRS may indicate a possible intramural or subepicardial origin of the VT. No Purkinje activity, fractionated potentials, or zone of slow conduction were observed. These findings are in agreement with a data by Coggins et al.4 In 83% of the patients, a definitive cure was obtained without complications. The initial success rate in our popu-
lation is comparable with previous data.4 Recurrences were observed in 4 of 35 patients (14%). In 3 patients, recurrent VT occurred during hospital stay (early recurrences); 2 of them had VT showing a delta wave–like beginning of the QRS. The remaining patient had a recurrence 3 months after RF ablation. Left-sided idiopathic VT can originate from 2 different sites in the left ventricle: the inferoposterior or inferoapical region. The 12-lead electrocardiogram of these idiopathic VTs showed typical features7,9: a right bundle branch block – like morphology with a left or northwest axis. The width of the QRS was wider in VTs originating in the inferoapical area compared with VTs arising in the inferoposterior region of the left ventricle. The successfully ablated patients had only 1 VT morphology. In contrast to a previous report,5 optimal pacemapping was observed in all but 1 patient. The endocardial activation time always preceded the QRS complex during VT. Purkinje activity was recorded in 5 of 7 VTs arising in the inferoposterior region of the left ventricle but was absent in all VTs originating from the apical region, suggesting that in the apical region the VT originates distant from the Purkinje network. In patients without Purkinje activity, pacemapping alone was sufficient to target the site of RF ablation. Therefore, the presence of Purkinje activity at the site of successful ablation apparently is not a requisite for ablation of left-sided VTs as postulated by other investigators.3,5 Contrary to another report,10 fractionated potentials or a zone of slow conduction were not observed. As in unsuccessfully ablated RV outflow tract idiopathic VT, the patient in whom the RF ablation failed also had ú1 VT morphology induced, showed a delta wave – like beginning of the QRS, did not have an optimal pacemap, and the endocardial activation time did not precede the beginning of the QRS complex. The immediate and late success rate was 92% and no recurrences were observed during a mean follow-up of 36 { 12 months. The immediate success in our population is comparable with a publication by Wen et al.5 Our observations suggest (as supported by findings after the long follow-up) that the best predictor for successful RF ablation of idiopathic VT originating from both regions in the left ventricle is an optimal pacemap rather than the presence of Purkinje activity.
1. Klein LS, Shih HT, Hackett K, Zipes DP, Miles WM. Radiofrequency cath-
eter ablation of ventricular tachycardia in patients with structural heart disease. Circulation 1992;85:1666–1674. 2. Wilber DM, Baerman J, Olshansky B, Kall J, Kopp D. Adenosine sensitive ventricular tachycardia: clinical characteristics and response to catheter ablation. Circulation 1993;97:126–134. 3. Nakagawa H, Beckman KJ, McClelland JH, Wang X, Arruda M, Santoro I, Hazlitt HA, Abdalla I, Singh A, Gossinger H, Sweidan R, Hirao K, Widman L, Pirha JV, Lazzara R, Jackman WM. Radiofrequency catheter ablation of idiopathic left ventricular tachycardia guided by a Purkinje potential. Circulation 1993:88:2607–2617. 4. Coggins DL, Lee RJ, Sweeney J, Chein WW, VanHare G, Epstein L, Gonzalez R, Griffin JC, Lesh MD, Scheinman MM. Radiofrequency catheter abla-
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tion as a cure for idiopathic tachycardia of both left and right ventricular origin. J Am Coll Cardiol 1994;23:1333–1341. 5. Wen MS, Yeh SJ, Wang CC, Lin FC, Chen JC, Wu D. Radiofrequency therapy in idiopathic left ventricular tachycardia with no obvious structural heart disease. Circulation 1994;89:1690–1696. 6. Wellens HJJ, Farre´ J, Brugada P, F Ba¨r: The method of programmed electrical stimulation in the study of ventricular tachycardia. In: Josephson ME, ed. Ventricular Tachycardia. Mount Kisco, NY: Futura, 1982:237–283. 7. Wellens HJJ, Rodriguez LM, Smeets JLRM. Ventricular tachycardia in structurally normal hearts. In: Zipes DP, Jalife J, eds. Cardiac Electrophysiology. From Cell to Bedside. 2nd ed. Philadelphia: WB Saunders, 1995:780–788.
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8. Jadonath RL, Schwartzman DS, Preminger NW, Gottlieb CD, Marchlinski FE. Utility of the 12-lead electrocardiogram in localizing the origin of right ventricular outflow tract tachycardia. Am Heart J 1995;130:1107–1113. 9. Rosas F, Eslami M, Elias J, Kinoshita O, Nakazato Y, Marcus FI, Frank R, Tonet J, Fontaine G. Diagnostic clues from the surface ECG to identify idiopathic (fascicular) ventricular tachycardia: correlation with electrophysiologic findings. J Cardiovasc Electrophysiol 1996;7:2–8. 10. Kottkamp H, Chen X, Hindricks G, Willems S, Haverkamp W, Wichter T, Breithardt G, Borgreffe M. Idiopathic left ventricular tachycardia: new insights into electrophysiologics and radiofrequency catheter ablation. PACE 1995;18:1285–1297.
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