Radiofrequency Catheter Ablation of Postinfarction Ventricular Tachycardia
Long-term Success and the Significance of Inducible Nonclinical Arrhythmias
Background Radiofrequency (RF) catheter ablation is effective therapy for monomorphic ventricular tachycardia (VT) in patients without structural heart disease. In patients with postinfarction VT; however, this procedure has been used predominantly as adjunctive therapy, targeting only the patient’s clinically documented arrhythmia. By targeting all inducible, sustained VT morphologies, we sought to determine the utility of RF catheter ablation as a primary cure in patients who present with hemodynamically tolerated VT.
Methods and Results RF ablation was attempted in 35 patients with a previous myocardial infarction and recurrent, hemodynamically tolerated VT. A mean of 3.9±2.7 VTs were induced per patient (range, 1 to 10). The clinically documented arrhythmia was successfully ablated in 30 of 35 patients (86%), and on follow-up electrophysiological testing, 11 patients had no inducible VT and were discharged without other therapy. Nineteen patients had inducible “nonclinical” arrhythmias on follow-up testing, and the majority underwent cardiac defibrillator implantation. Freedom from recurrent arrhythmias, including sudden death, was 91% in patients without inducible VT and 53% in patients with persistently inducible “nonclinical” arrhythmias (P<.05; mean follow-up, 17±12 and 12±11 months, respectively).
Conclusions In patients with well-tolerated VT, RF catheter ablation may be useful as a primary cure if no other ventricular arrhythmias are inducible on follow-up testing. Ablation of all hemodynamically tolerated arrhythmias should be attempted in patients with multiple inducible VT morphologies because of the high rate of recurrence of unablated VTs in these patients.
Radiofrequency catheter ablation has been used for the treatment of postinfarction VT with varying success rates reported. Several studies have demonstrated the efficacy of this technique as an adjunctive treatment in selected patient populations with recurrent, drug-resistant VT.1–4 These studies, however, were limited by either a small patient population, the study of patients with only a single VT morphology, or targeting of only the “clinical” arrhythmia (electrocardiographically documented spontaneous episode). The usefulness of this technique in patients with multiple ECG morphologies of inducible VT (which includes the majority of postinfarction patients with VT)5–7 is not known. The purposes of this study were to determine the efficacy of RF catheter ablation in a more generalized population of postinfarction patients and as a definitive cure of hemodynamically tolerated, recurrent postinfarction VT. We also sought to determine both the long-term effects of RF catheter ablation on the inducibility of VT and the significance of persistently inducible rapid ventricular arrhythmias that were not clinically apparent before the ablative procedure and not amenable to catheter ablation.
RF catheter ablation was considered a therapy option in any patient with recurrent, hemodynamically tolerated, postinfarction VT at the time of presentation. The VT was considered hemodynamically tolerated if the patient’s systolic blood pressure was >80 mm Hg and there were no symptoms of inadequate cerebral or cardiac perfusion. A total of 42 patients were brought to the electrophysiology laboratory over a 36-month period who met these criteria, and RF catheter ablation was attempted in 35 of these patients. Reasons for not attempting RF catheter ablation included 6 patients in whom the inducible VT was not sufficiently well tolerated to allow extensive mapping and 1 patient in whom left ventricular mapping could not be performed due to severe peripheral vascular and aortic disease.
The mean age of patients undergoing attempted RF ablation was 62±13 years, and all except 2 patients were male. Seventeen of the patients had had a previous anterior wall myocardial infarction, 17 patients had had a previous inferior myocardial infarction, and 1 patient had multiple sites of infarction. The mean ejection fraction was 24±8%. VT first occurred 6.9±9.4 years after the myocardial infarction and had a frequency (mean±1 SD) of 4.2±8.4 episodes per month after its index occurrence (range, 1 episode per year to 40 episodes per month). Sixteen of the 35 patients had recurrent VT despite chronic treatment with antiarrhythmia agents. Of these patients, only 5 had been treated with amiodarone for their VT; in 1 patient, the amiodarone was discontinued 6 months before the electrophysiology study due to toxicity. An additional patient was being treated with a “low” dose of amiodarone (200 mg/d) for atrial fibrillation when the VT occurred
The study protocol was approved by the Temple University Institutional Review Board, and informed consent was obtained from all patients. Patients were brought to the electrophysiology laboratory in the fasting, drug-free state (except patients previously treated with amiodarone). Three or four 6F quadripolar electrode catheters were advanced from the femoral veins to the high right atrium (in patients without atrial fibrillation), atrioventricular junction (His-bundle recording), right ventricular apex, and right ventricular outflow tract. Programmed ventricular stimulation was performed at twice the diastolic threshold with a 1-ms pulse width using a programmable stimulator (Bloom Stimulator, Fischer Imaging Corp) with one, two, and three extrastimuli from both RV sites at two drive CLs (usually 600 and 400 ms). Left ventricular stimulation was also performed in 1 patient; in 10 patients, programmed stimulation was performed during three drive trains, including normal sinus rhythm. All 12 standard ECG leads were recorded continuously along with the intracardiac ECGs through the use of a digital recording system and optical storage (Arrhythmia Research Technologies). In 10 patients in whom the induced VT was only marginally tolerated (hypotensive without syncope), intravenous procainamide was infused with a maximum loading dose of 15 mg/kg at a rate of 50 mg/min followed by a continuous infusion at a maximum rate of 0.11 mg · kg−1 · min−1; attempts at mapping and ablation were then resumed.
Left ventricular mapping was performed with a 7F deflectable quadripolar catheter advanced from a femoral artery and retrogradely across the aortic valve to the left ventricular cavity. The deflectable catheter had a 4-mm distal tip electrode and 2- to 5-mm interelectrode spacing (Mansfield-Webster, EPT Technologies, or Medtronic CardioRhythm). A unipolar electrogram was recorded between the distal tip and a large skin electrode, and bipolar electrograms (filtered 30 to 500 Hz) were recorded between adjacent electrode pairs. The local endocardial activation time was measured from the onset of the diastolic electrogram in the distal bipolar recording to the onset of the QRS during VT. Sites with a diastolic local activation time were targeted for RF ablation when participation of the electrogram in the VT circuit could be inferred by one or more of the following criteria: (1) constant electrogram morphology and timing relationship with the return cycle onset after entrainment from a remote RV site with bipolar pacing at a CL of 30 to 50 ms shorter than the VT CL,8,9 (2) concealed entrainment by pacing from the target site at a CL of 30 to 50 ms shorter than the VT CL and producing an exact morphological ECG match to the VT (Fig 1⇓),2,10,11 and (3) left ventricular pace mapping during normal sinus rhythm that produced an exact morphologic ECG match to the VT.12 Unipolar pace mapping, between the distal electrode and a large skin electrode/grounding pad, was performed with an output just above threshold. Bipolar pace mapping, between the two distal electrodes, was performed in 6 patients when unipolar pacing with the catheter ablation system was not technically feasible. A “perfect” pace map was defined as an exact, superimposable morphological ECG match to the VT QRS in all 12 standard ECG leads, and a “good” pace map was defined as a nearly identical morphological match in all 12 standard ECG leads, when the ECGs of the induced VT and pacing were compared on a side-by-side basis.
RF catheter ablation was attempted of all inducible and hemodynamically tolerated VT morphologies. In 27 patients, RF energy was delivered as a continuous, unmodulated sine wave at 500 kHz (Radionics model RFG-3C) with an average power delivery of 30 to 50 W. In 8 patients, RF energy was applied using a temperature-controlled system (Medtronic Atakr; EPT Technologies model 1000) with a temperature set point of 70°C. Power was generally delivered during VT and continued for 60 to 90 seconds during applications, which resulted in the termination of VT. A second RF application was typically given at successful target sites if VT could not immediately be reinitiated and the catheter had not moved fluoroscopically. The complete protocol of programmed stimulation was performed until all hemodynamically tolerated VTs were successfully ablated. The full stimulation protocol was again repeated after a 30-minute waiting period, and the study was concluded if no hemodynamically tolerated VTs could be induced.
A predischarge electrophysiology study was performed a mean of 5±3 days after the ablative procedure. Programmed stimulation with one, two, and three ventricular extrastimuli from the right ventricular apex and right ventricular outflow tract at two paced CLs was performed, along with burst ventricular pacing, with patients in the drug-free state as previously described. Patients with no inducible sustained ventricular arrhythmias were discharged without antiarrhythmic therapy. Patients with persistently inducible sustained, rapid monomorphic ventricular arrhythmias were advised to undergo implantation of an ICD despite the successful ablation of their “clinical” VT. An ICD with electrogram storage capabilities (Ventritex Cadence) was implanted, when possible, in these patients. The induction of ventricular flutter with CL of ≤200 ms or ventricular fibrillation/polymorphic VT with triple extrastimuli was considered a nonspecific finding and was not treated in the absence of prior clinical episodes of a similar arrhythmia.
A late follow-up electrophysiology study (3 to 4 months after ablation) was performed in 8 of 11 patients in whom no sustained VT could be induced at the time of their predischarge study. Programmed stimulation was performed as above to assess the long-term efficacy of the ablative procedure. A follow-up study was also performed in 7 of 12 patients who had successful RF catheter ablation of their clinical arrhythmia but persistent inducibility of a rapid monomorphic VT with no recurrent symptoms.
Patients were seen in follow-up by either their referring cardiologist or one of the authors every 3 to 4 months. In patients who underwent implantation of a cardiac defibrillator, the electrograms of all recurrent events were retrieved from the ICD and recorded on an ink-jet recording system (Mingograf 7, Siemens-Elema). The CLs of the recurrent ventricular arrhythmias were compared with the VT CL of the patient’s spontaneous VT before catheter ablation. Recurrence of the patient’s initial spontaneous VT was thought to occur if either (1) a 12-lead ECG demonstrated the same VT morphology as the initial VT or (2) the VT CL as recorded from the ICD was within 20 ms of the initial VT CL.
The “clinical VT” was defined as an inducible VT that matched the morphology of the patient’s documented, spontaneously occurring, monomorphic VT. “Nonclinical VTs” were defined as inducible monomorphic VTs that were not previously known to have occurred spontaneously. The induction of “polymorphic VT” was considered a nonspecific finding. “Multiple VT morphologies” were defined as two or more inducible VTs having contralateral bundle-branch block patterns, frontal plane axis of ≥90° divergent, or marked differences in individual ECG leads recorded from the same electrode locations.
“Complete success” of the ablation procedure was defined as having no inducible, sustained monomorphic VT on predischarge follow-up testing. The patients in whom the “clinical” arrhythmia could no longer be induced at the predischarge follow-up study but had sustained, nonclinical VT induced with programmed stimulation were defined as having “partial success.” “Failure” was defined as the inability to ablate the clinical VT, recurrence of the clinical VT before follow-up testing, or inducibility of the clinical VT at the time of the predischarge follow-up study. “Sudden cardiac death” was defined as a death from a presumed arrhythmic cause occurring within 1 hour of the onset of symptoms.
All values are summarized as the mean±1 SD. Continuous variables were compared using the Student’s t test for unpaired data, and categorical data were compared by χ2 analysis. A Kaplan-Meier analysis and Mantel-Cox log-rank test was used to compare the freedom from recurrent arrhythmias between groups. Values of P<.05 were considered significant.
A total of 140 distinct VTs were induced in the 35 patients studied. Of these VTs, 79 (56%) were successfully ablated. Characteristics of the inducible arrhythmias in each group are shown in Table 1⇓. A mean of 3.9±2.7 VT morphologies per patient were induced with only one VT morphology inducible in 6 of the 35 patients. There was no difference in the number of inducible VTs in patients with an anterior infarction (4.5±3.1 VTs per patient) versus an inferior infarction (3.2±2.2 VTs per patient; P=.17). The mean VT CL was 345±74 ms. There also was no significant difference in the VT CL (342±48 versus 369±68 ms for anterior versus inferior infarction, respectively). The CL of the successfully ablated VTs (370±68 ms) was significantly longer than the CL of VTs that remained inducible (313±69 ms; P<.0001).
Target sites for ablation were usually identified by activation mapping during the VT and confirmed, as described above, with entrainment techniques, pace mapping, or both. Approximately 62% of the successful target sites were confirmed by entrainment, and 77% had a “good” or “perfect” pace map; evidence of concealed entrainment was observed at 37% of the target sites. Of the 61 VTs not amenable to catheter ablation, 27 were not sufficiently well tolerated to allow adequate mapping and ablation, 19 could not be terminated with RF energy delivery despite extensive mapping, and during 15 VTs, no adequate target sites could be identified. A total of 324 applications of RF energy were delivered at potential target sites (9±8 RF applications per patient; range, 1 to 27).
Successful ablation of at least the clinical arrhythmia was achieved in 31 of 35 patients (89%) (Fig 2⇓). In 4 patients in whom the clinical VT could not be successfully ablated, the procedure was considered an ablation failure. A follow-up electrophysiology study was performed before discharge in 27 of the 31 patients with initial success. No sustained monomorphic VT could be induced in 10 patients who were subsequently considered complete successes. In 16 patients, only nonclinical monomorphic VTs could be induced with programmed stimulation, and they were considered partial successes. The ablation procedure was considered a failure in 1 patient with persistent inducibility of his clinical arrhythmia on follow-up testing. The total procedure time was 311±164 minutes per patient, with a fluoroscopy time of 67±49 minutes. Nine patients required two ablation procedures (the second procedure performed 3 to 9 days after the first procedure) to achieve clinical success.
Of the 4 patients who did not undergo a predischarge electrophysiology study, two refused the follow-up study but had persistently inducible nonclinical VTs at the time of the initial procedure and were grouped as partial successes. A third patient underwent a follow-up study several weeks after ablation by his referring cardiologist and was found to have persistent inducibility of only nonclinical VTs, which were not ablated; this patient was also considered a partial success. One patient with frequently recurring (two or three times daily) but self-terminating sustained VT had a single inducible morphology of VT that was successfully ablated, and the procedure was considered a complete success. A follow-up study, however, was not performed because the patient remained hospitalized awaiting orthotopic heart transplantation while on intravenous inotropic agents for severe left ventricular dysfunction.
Complete success was achieved in 11 patients (31%). A mean of 2.3±1.2 VTs per patient were induced and ablated in this group (range, 1 to 4). The mean VT CL in this group was 385±63 ms. Before the ablation procedure, 4 of these patients had recurrent VT despite treatment with antiarrhythmic agents (none had received amiodarone). On follow-up testing before discharge, no patient had inducible sustained, monomorphic VT. Two patients did have inducible ventricular flutter with closely coupled triple extrastimuli, and 4 patients had inducible nonsustained VT (4 to 14 beats in duration). Ten of the 11 patients were discharged without either antiarrhythmic therapy or implantation of a cardiac defibrillator. One patient underwent implantation of a defibrillator at the request of the referring physician due to the rapidity of his presenting VT (CL of 260 ms, associated with marked lightheadedness).
Long-term follow-up studies were performed in 8 of these 11 patients at 4.2±2.3 months after the initial ablative procedure. Of those not undergoing long-term follow-up stimulation, 1 patient had undergone his initial electrophysiology study before implementation of the long-term follow-up in our protocol, 1 patient refused a follow-up study, and the third patient underwent orthotopic heart transplantation 2 months after the ablative procedure. Six of the 8 patients had no inducible sustained arrhythmias at the time of the follow-up study, and 1 patient had inducible polymorphic VT with a CL of 150 ms. A monomorphic VT with a CL of 220 ms was induced with closely coupled triple extrastimuli in the eighth patient; this patient’s clinical VT had a CL of 330 ms. Nonsustained ventricular arrhythmias of <18 beats in duration were induced in 4 of the remaining patients. There were no documented recurrences of VT in this group over a mean follow-up of 17±12 months (range, 2 to 34 months). One patient died suddenly 18 months after the ablative procedure; this patient had multiple recurrences of a well-tolerated VT before the ablative procedure and only rapid polymorphic VT induced at the time of his long-term follow-up study.
Nineteen patients had successful ablation of their clinical VT but persistent inducibility of nonclinical VTs with programmed stimulation before discharge. The mean number of inducible VTs per patient in this group was 5.3±2.7, with a mean CL of 344±57 ms. There were 2.7±2.2 VTs per patient successfully ablated and not reinducible on the predischarge follow-up study. These VTs had a mean CL of 376±51 ms and included the clinical VT. Inducible VTs that could not be successfully ablated had a mean CL of 300±64 ms; this was significantly shorter than the ablated VTs (P<.0001). The number of inducible VTs was significantly greater in the partial success group than in the complete success group (P<.005).
Four of the 19 patients who had partial success were discharged without a cardiac defibrillator or antiarrhythmic therapy. Two of these patients had only rapid, sustained monomorphic VT (CL <230 ms) induced with programmed stimulation. The other 2 patients had persistently inducible VT with CLs ranging from 280 to 310 ms and refused implantation of a cardiac defibrillator. Thirteen patients underwent implantation or had a cardiac defibrillator previously implanted, and 2 of these patients also required antiarrhythmic medication for suppression of atrial fibrillation; 1 was continued on amiodarone, which he was receiving when he presented with VT, and a second was maintained on procainamide. Two of the 19 patients were placed on medical therapy alone for treatment of the inducible nonclinical arrhythmias; 1 received amiodarone empirically, and the second was placed on oral procainamide, which suppressed his nonclinical arrhythmias.
A late follow-up study at 2.5±0.5 months after the ablative procedure was performed in 7 of 12 patients who had no recurrent spontaneous episodes within 2 to 3 months of the ablative procedure. Three of these patients no longer had any inducible arrhythmias (rapid VTs, with CLs of <260 ms, were induced at the time of their predischarge follow-up study). The other 4 patients had persistently inducible sustained monomorphic VT, but none of the previously ablated VT morphologies were induced. One of these patients had previously received no concurrent treatment and was subsequently treated with empiric amiodarone after refusing to undergo implantation of cardiac defibrillator.
Nine of the 19 patients with successful ablation of their clinical VT had a spontaneous VT recurrence during follow-up (Table 2⇓). Five of the 9 patients had recurrence of a VT not previously seen clinically but compatible with an inducible VT that was not ablated. The recurrent VTs in these patients had a CL that was markedly shorter than their clinical arrhythmia. A sixth patient had ICD electrogram documentation of multiple VT CLs before ablation, and although the recurrent VT was of a different CL than the ablated VTs, not all of his clinical VTs could be definitively known. Two patients developed a possible “new” arrhythmia during follow-up. One presented with a bundle-branch reentrant VT 2 months after ablation. This patient had been treated with amiodarone that was discontinued at the time of ablation procedure; no bundle-branch reentrant VT was induced at the ablative procedure or a follow-up study performed 5 weeks later. The second patient died suddenly 3 months after the ablation procedure; this patient had frequent recurrences of a well-tolerated VT before ablation and only rapid monomorphic VT, with a CL of 280 ms, induced at follow-up. His clinical VTs had a CL of 420 and 520 ms, and the patient refused implantation of a cardiac defibrillator. This patient also developed a new anginal syndrome before his death. Documented recurrence of the clinical, ablated VT occurred in 1 additional patient; this was the only definitive recurrence of a “successfully” ablated VT observed in our study.
Patients with a VT recurrence during follow-up had a greater number of VT morphologies that remained inducible after the ablative procedure (3.7±2.4 versus 1.9±0.8, P=.05). There also was a trend toward a longer CL of the persistently inducible VTs in patients who had VT recurrence (326±79 ms in patients with recurrent VT versus 275±33 ms in patients with no recurrent event, P=.09). A comparison between patients with and without a recurrent event is shown in Table 3⇓. One of the 19 patients with partial success who did not undergo a complete stimulation protocol was not included in this analysis. This patient had heparin-induced thrombocytopenia, and the ablation procedure was terminated after successful ablation of the clinical VT; although no further tachyarrhythmias were induced, the patient’s follow-up study was performed via a previously implanted cardiac defibrillator with up to triple extrastimuli from a single site. The clinical VT occurred both spontaneously and in response to single extrastimuli before ablation.
In 4 of the initial 35 patients, the clinical VT could not be not be successfully ablated. Reasons for unsuccessful ablation included difficulty mapping secondary to marginal hemodynamic tolerance and frequent, spontaneous terminations of the targeted VT in 2 patients, and the inability to ablate the targeted VT despite apparently adequate mapping in a 1 patient. In a fourth patient, the electrophysiology study was discontinued prematurely secondary to the development of abdominal pain, which was thought to be caused by peripheral embolization of an aortic atherosclerotic plaque. Initial clinical success was achieved during the ablative procedure in a fifth patient, but the clinical VT was again inducible at the time of his follow-up study. Because of marginal hemodynamic tolerance, the VT was not amenable to repeat ablation.
The mean number of VTs induced in this group was 2.8±2.4 VTs per patient, with successful ablation of 0.6±0.5 nonclinical VT per patient. The mean VT CL in this group was 325±33 ms. Four of the patients in this group were treated with an implantable defibrillator—3 in combination with an antiarrhythmic agent. The fifth patient underwent a subendocardial resection with no inducible arrhythmias at a follow-up study before discharge. Spontaneous recurrences occurred in 2 of the 5 patients; both had a recurrence of their clinical VT. The 1 patient with initial clinical success but persistent inducibility of the clinical VT on predischarge testing was treated with an ICD only and has had no spontaneous recurrences.
Overall, the clinical VT was ablated in 30 of 35 patients (86%), with 31% of all patients having no additional inducible ventricular arrhythmias. The freedom from recurrent arrhythmias and sudden death at 24 months was 91% in the complete success group and 53% in the partial success group (P<.05) (Fig 3⇓). The freedom from recurrent arrhythmias at 24 months was 60% in the failure group, with most of these patients being treated with antiarrhythmic medications or surgical therapy. Six patients in the study group died during the follow-up period. As previously noted, 2 patients died suddenly—1 in the partial success group and 1 in the complete success group. Three other patients in the partial success group died of congestive heart failure. One patient in the failure group died of sepsis secondary to ischemic bowel disease.
A total of 94 electrophysiology studies were performed in the 35 patients, not including cardiac defibrillator implants or their follow-ups. Procedure-related complications occurred in 8 of the 35 patients. Three patients developed a hematoma at the arterial access site. In 2 patients, the hematoma was minor, and in the third patient, a blood transfusion was given because of hypotension; surgical intervention was not required. Heart block occurred in 4 patients and was catheter-induced in 3; 1 patient developed transient right bundle-branch block, and 2 patients with a preexisting right bundle-branch block developed complete heart block during left ventricular mapping that remained permanent. A third patient developed transient complete heart block after the infusion of intravenous procainamide. As discussed above, 1 patient developed severe abdominal pain during the procedure. Although no definitive etiology was determined, the patient’s symptoms were thought to be best explained by a possible embolic event. In addition to the above, in 1 patient in whom RF ablation was unsuccessful, ICD implantation was undertaken and complicated by an infection at the generator pocket. This required explantation of the device and lead, intravenous antibiotic administration, and subsequent reimplantation of the defibrillator and lead system.
The usefulness of RF catheter ablation in the successful treatment of monomorphic VT has been proven in patients without structural heart disease. Success rates of >95%13–16 have been achieved with no recurrence on long-term follow-up. This high success rate may be due to the relatively focal point of VT origin and the relatively large lesion size (up to several millimeters in diameter) that can be achieved with the application of RF energy in normal myocardium.17,18 In the postinfarction patient, successful termination of a specific, targeted VT has also been demonstrated, although the long-term efficacy of this technique has remained in question. These VTs involve reentrant circuits that can be large, encompassing an area of up to several centimeters in length,19,20 and may not be entirely subendocardial in location.21 The successful ablation of such VTs therefore depends on the localization of a relatively narrow area of the circuit, critical for continuation of VT, that can be affected by the application of RF energy.
Success of VT Ablation
The reported success rates of RF catheter ablation in the postinfarction patient have varied widely, due, in part, to differing definitions of “success.” In our series, the spontaneously occurring VT was successfully ablated in 86% of patients. More importantly, however, almost one third of patients undergoing RF ablation had all of their VTs rendered noninducible on follow-up study and were discharged without further treatment. These results were achieved despite an average of 2.3 VT morphologies induced per patient. This group had no recurrence of a documented VT over a mean follow-up of 17 months. In contrast, 9 of 19 patients with persistently inducible nonclinical monomorphic VTs had a spontaneous VT recurrence on follow-up. Most of these recurrences were of a VT not previously observed to have occurred spontaneously. Overall, a total of 140 distinct monomorphic VTs were induced in the 35 patients, 56% of which were rendered noninducible with RF catheter ablation. Our study also demonstrates, for the first time, that once monomorphic VTs are ablated, they remain noninducible on long-term follow-up with programmed stimulation.
Previous reports of postinfarction VT ablation have demonstrated similar “clinical success” results. Morady et al1 reported successful RF ablation in 11 of 15 patients with postinfarction VT in whom ablation was performed as an adjunctive therapy. In this series, 16 of 20 spontaneously occurring VTs were successfully ablated. These 11 patients had no clinical recurrences of the ablated VT, although most were treated with some adjunctive therapy. The incidence of “nonclinical” VT recurrences in this series was not reported. Similar success rates were also reported in studies by Kim et al3 and Stevenson et al.2 In the study of Kim et al, 9 of 20 patients had recurrent VT, including all 4 patients with an initial unsuccessful result. Of the 16 patients with initial clinical success, 1 patient had a recurrence of their previous spontaneous VT and 4 patients had a recurrence of a VT morphology that was induced, but not ablated, at the initial electrophysiological study. In the study of Stevenson et al, ablation of all inducible VTs was attempted in 15 patients; on follow-up study, 6 patients had no inducible monomorphic VT, whereas 4 patients had only a “new” VT morphology induced. None of these patients had recurrent VT, but of the 5 patients with persistently inducible VT, 3 had recurrences. Compared with the present study, the lower incidence of “nonclinical” VT recurrences reported in these series might be explained by the use of adjunctive antiarrhythmic therapy. The majority of patients in the series of Kim et al who had persistently inducible VT were treated with antiarrhythmic agents, and in the study of Stevenson et al, most patients had been on amiodarone before the ablation procedure, with 4 patients continuing to receive antiarrhythmic therapy after ablation. In our study, most patients were initially treated with only an ICD, and the use of amiodarone before the ablation procedure was minimal.
Significance of Other Arrhythmias
Our study clearly demonstrates a risk of recurrent ventricular arrhythmias in patients with persistently inducible VTs even though these arrhythmias were not previously documented clinically. These results are not surprising in light of past experiences with surgical treatment of ventricular arrhythmias. Several studies have shown an excellent prognosis for patients without inducible VT on their postsurgical follow-up study, with >90% remaining free from recurrent arrhythmias and sudden death for up to 5 years, despite many patients initially presenting with hemodynamically unstable ventricular arrhythmias and sudden cardiac death.6,22–24 In contrast, up to 64% of patients with postoperative inducible VT have had recurrent ventricular arrhythmias on follow-up, despite concurrent antiarrhythmic treatment,5,6,25–27 and the recurrence rate was even higher (77%) in patients with postoperative inducible VTs with a CL equal to or longer than any clinically or preoperatively manifested VT.28 In the present study, patients with recurrent ventricular arrhythmias tended to have a greater number of inducible nonclinical arrhythmias with a longer CL after ablation compared with patients without clinical recurrences. This is consistent with data in unselected post–myocardial infarction patients where patients with rapid, inducible ventricular arrhythmias (CL <230 ms) had a lower risk of recurrent ventricular arrhythmias than patients with a slower inducible VT.29
Role of VT Ablation
The role of RF catheter ablation in the management of postinfarction VT continues to be refined. In patients with an ICD and frequent recurrences of VT unresponsive to medical therapy, catheter ablation can result in a marked decrease in the number of VT recurrences.30 Few would argue with the use of RF ablation in this patient population, but there has been little experience in the use of this technique as a primary treatment of postinfarction VT. Several factors have been given as contraindications to attempting VT ablation,3,31 including (1) multiple inducible VT morphologies, (2) inability to ablate large areas of scar, and (3) inability to document the clinical VT.
The significance of multiple inducible ventricular arrhythmias cannot be underestimated, and many authors will not attempt catheter ablation on patients with more than one inducible morphology.32 In the present series, patients with persistently inducible arrhythmias did have a significantly higher number of inducible arrhythmias at the initial study. Complete success, however, was achieved in several patients with as many as four distinct VT morphologies induced. One reason for success in these patients may be the ablation of tissue essential for perpetuation of two or more VT morphologies. This phenomenon has been well characterized in previous studies,1,33–35 and up to 20% of inducible morphologies may be terminated by the ablation of different VT morphologies.36
In postinfarction VT, a critical portion of the reentrant circuit has been shown to involve the peri-infarction subendocardium.37,38 This location lends itself to possible RF catheter ablation because RF energy can result in lesions of >5 mm in diameter and up to 3 mm in depth,39 although studies characterizing the morphology of such lesions in the postinfarction heart have been lacking. Our study demonstrates that the effects of such lesions tend to be stable over time, since previously ablated VTs could not be reinitiated on long-term follow-up, verifying the low rate of recurrence of ablated VTs seen in other studies.1–3 Not all inducible, hemodynamically tolerated VTs, however, can be successfully ablated despite extensive endocardial mapping. Possible reasons for unsuccessful ablation include relatively wide zones of critical conducting tissue, poor penetration of scar tissue with RF energy, and inadequate catheter contact. In addition, up to one third of inducible VTs may involve a reentrant circuit with a critical zone of conduction located in the deeper subepicardium.21
Although this was one of the larger studies of RF catheter ablation of postinfarction VT, the number of patients limits the ability of the analysis to distinguish in detail factors associated with both short- and long-term success. This study, however, was designed to select a population with an increased frequency of recurrences by excluding patients with only a single episode of VT. The small study size is particularly limiting in determining any characteristics that may predict subsequent events in patients with successful ablation of only their clinical VT. The 1 patient in our complete success group who died suddenly 18 months after ablation does raise the concern of possible proarrhythmic effects of RF catheter ablation as well as the significance of the patient’s inducible polymorphic VT on long-term follow-up. Larger studies will be necessary to determine whether patients whose VTs are rendered completely noninducible with RF ablation are at an increased risk of subsequent cardiac events compared with other postinfarction patients. The rate of sudden cardiac death that we observed, however (5.7% over 14±11 months of follow-up), is similar to that reported previously with surgical and pharmacological treatment.40
RF catheter ablation of postinfarction VT can be performed with a high degree of success when targeted against specific, inducible VTs and is associated with a low likelihood of recurrence of the successfully ablated VT. These VTs remain noninducible with chronic programmed stimulation, demonstrating long-term stability of the RF lesion. Therefore, in patients with well-tolerated VT, adjunctive therapy may not be warranted if the patient has no inducible VTs on follow-up study. The high rate of recurrent VT in patients with persistently inducible “nonclinical” tachyarrhythmias, however, suggests that all inducible VTs should be treated with either antiarrhythmic drug therapy, ICD implantation (ideally with antitachycardia pacing) or RF catheter ablation of the nonclinical VTs. Ablation of all inducible, hemodynamically tolerated ventricular arrhythmias may help avoid the morbidity associated with recurrent ICD discharges and antiarrhythmic therapy but can be expected to result in long, arduous procedures requiring extensive fluoroscopy time and operator expertise. In consideration of this and the limitations of current technology, catheter ablation procedures for postinfarction VT should probably be limited to centers willing to make the necessary investments to afford the highest chances of success.
Selected Abbreviations and Acronyms
Reprint requests to Steven A. Rothman, MD, Temple University Hospital, 908 Parkinson Pavilion, 3401 N Broad St, Philadelphia, PA 19140.
- Received May 29, 1997.
- Revision received July 18, 1997.
- Accepted August 1, 1997.
- Copyright © 1997 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 ventricular tachycardia late after myocardial infarction. Circulation. 1993;88(pt 1):1647–1670.
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