Incidence and significance of pleomorphism in patients with postmyocardial infarction ventricular tachycardia

Acute and long-term outcome of radiofrequency catheter ablation

Paolo Della Bellaa,*, Stefania Rivaa, Gaetano Fassinia, Francesco Giraldia, Marco Bertia, Catherine Klersyb and Nicola Trevisia

a Arrhythmia Department, Centro Cardiologico Monzino, Institute of Cardiology, University of Milan, Via Parea 4, Milan 20138, Italy
b Biometry and Clinical Epidemiology, Research Department, IRCCS San Matteo Hospital, University of Pavia, Pavia, Italy

* Corresponding author. Tel.: +39-2-580021/58002340/58002275; fax: +39-2-504-667
E-mail address: pdellabella{at}cardiologicomonzino.it

Received 14 February 2003; revised 15 January 2004; accepted 22 January 2004

Abstract

Aims The prognostic significance of multiple ventricular tachycardia (VT) morphologies, whether spontaneous or induced, was investigated in patients who underwent radiofrequency catheter ablation (RFCA) for postinfarction ventricular tachycardia.

Methods and results We studied 137 patients with postinfarction ventricular tachycardia. Catheter ablation of all induced ventricular tachycardias was attempted.

A single ventricular tachycardia morphology was documented in 102/137 patients (MONO group); 35 patients had spontaneous pleomorphism (PLEO group). Multiple VT morphologies were induced in 58/102 (57%) MONO patients and in all PLEO patients. A higher rate of arrhythmia suppression was obtained in MONO as compared to PLEO patients (162/212 [76%] vs. 43/110 [39%]). Clinical presentation (VT pleomorphism) (OR: 0.22, CI: 0.08–0.62) and the induced VT cycle (mean PLEO/MONO: 338/385 ms, OR: 1.06) were independent predictors of acute RFCA success. Among MONO patients, the procedure was successful in 75% of the patients with a single induced ventricular tachycardia compared to 64% of those with multiple tachycardias. The acute success rate was lower in PLEO patients (23%). PLEO patients had a significantly higher 3- and 5-year arrhythmia recurrence rate than MONO patients. RFCA acute success was the only independent predictor of long-term outcome in multivariate analysis.

Conclusions Spontaneous, but not induced, VT pleomorphism in patients with prior myocardial infarction adversely affects the acute and long-term success rate of RFCA.

Key Words: Ventricular tachycardia • Catheter ablation

Introduction

Multiple morphologies of sustained monomorphic ventricular tachycardia (VT) may occur spontaneously or by induction during electrophysiological testing at different times in the same patient. This phenomenon, defined as pleomorphism,1,2 is frequently observed following a myocardial infarction. The presence of multiple exit sites from a single or multiple re-entry circuits is one possible explanation and this feature is potentially present in all patients with a prior myocardial infarction.3–9

Previous studies have demonstrated the relation between VT pleomorphism and multiple infarctions, compromised ventricular function, and the extent of coronary artery disease.1,2 The number of documented VT morphologies is influenced by clinical variables, such as the number of VT occurrences and the number of antiarrhythmic drug treatments.2

A reduced efficacy of antiarrhythmic drugs has been described in patients with multiple VT morphologies10,11; likewise, multiple VT configurations are less likely to be cured by surgery, particularly when various sites of origin can be demonstrated in intraoperative mapping.3,12,13

The creation of a line of blockade between the mitral annulus and posterior rim of infarcted myocardial areas resulted in the ablation of dual VT morphologies in a selected series of patients with previous inferior myocardial infarction.14 Aside from this series of patients with a very distinct arrhythmia pattern, the relation between the occurrence of multiple clinical VTs and the results of catheter ablation has not been investigated.

This issue was addressed in the present study, where the occurrence of multiple VT morphologies, both spontaneous and induced, was related to the acute and long-term outcome of catheter ablation in a consecutive series of patients suffering from recurrent ventricular tachycardia following myocardial infarction.

Methods

Population
The clinical and electrophysiological data of 177 consecutive patients who underwent catheter ablation for recurrent sustained monomorphic VT following a myocardial infarction from April 1993 to November 2000 were retrospectively analysed.

The inclusion criteria were:

  1. Availability of complete clinical data, including 12-lead ECG recordings of spontaneous and all induced VTs.
  2. A complete electrophysiological study and catheter ablation protocol available for analysis.
  3. Reliable follow-up data, including documentation of recurrent arrhythmias by 12-lead ECG or ICD interrogation.
  4. An electrophysiological procedure performed at least 6 months before enrolment in the present study.

The final population included 137 patients (91 males) with a mean age of 67±6 years.

An ethics committee approved the study and all patients gave written consent to the procedure.

Electrophysiological mapping and ablation data
Under local anaesthesia, multiple electrode catheters were introduced percutaneously and advanced to the right atrium, His bundle region, and right ventricular apex. A 4-mm tip 7 F steerable catheter was introduced into the left ventricle by a retrograde transaortic or a transseptal approach. Patients were kept mildly sedated by intravenous boluses of morphine and/or midazolam while blood pressure and oxygen saturation were continuously monitored invasively. Anticoagulation with heparin infusion, titrated to achieve an ACT value near 200–250 s, was instituted before the procedure. Programmed stimulation with up to three extrastimuli at multiple drives (600–500–430 ms) from the right and the left ventricle was performed to induce clinical arrhythmia or other sustained VTs. Computerised multichannel recordings of all 12 standard ECG leads and bipolar intracardiac tracings were obtained.

Sustained VTs causing a persistent systolic blood pressure reduction to 50 mm Hg 30 s after induction and requiring termination by overdrive pacing or external DC shock were considered hemodynamically intolerable and were not targeted unless non-conventional mapping techniques had been instituted (see below).

Catheter ablation was guided by conventional activation mapping and entrainment techniques, as previously described,15–21 and was performed under temperature (up to 60 °C) and impedance control. All the VTs considered in this study were ablated in the left ventricle. VT ablation was considered effective if VT interruption occurred within 10 seconds of the onset of delivery of radiofrequency energy, without any ventricular premature beat.

Thereafter, a repeated stimulation protocol was undertaken to assess the inducibility of the target or any other sustained monomorphic VT.

In 12 patients (9 with multiple clinical VT morphologies), non-contact mapping (10 patients)22–25 or electroanatomical mapping (2 patients)26 were used to guide catheter ablation.

Definitions
Spontaneous pleomorphism
Multiple clinical VT configurations were defined by ECGs recorded at different times showing different bundle-branch-block patterns in V1 or a QRS axis on the frontal plane differing by 45° or more.2 The same criteria were also used to define multiple VT morphologies induced by electrophysiological study. Minor changes in VT cycle length (50 ms) were not considered to define different VT morphologies.

Acute result
The procedure was defined as successful (Class A) any sustained monomorphic VT was interrupted and inducibility was prevented.27

Effective ablation of clinical VT and/or other VT morphologies with persistent inducibility of one or more non-clinical sustained VTs was defined as a partial success (Class B).

Failure to interrupt even clinical VT was defined as a Class C result.

In patients without an ICD implanted before the procedure, the device was implanted following a Class B or C ablation result.

In patients presenting with intolerable VT, an ICD was implanted even after a completely successful procedure.

Ablation site
When two distinct VT morphologies were ablated at the same site, a single slow conduction isthmus was judged to be shared by the VTs.

Electrophysiological confirmation of this definition was provided:

by proving concealed entrainment of both morphologies at the same site.
by producing an accurate 12-lead pacemap of both VTs during sinus rhythm.28

Multiple isthmuses and/or exit sites were considered to be present when ablation had to be performed at clearly different sites (spaced at least 2 cm apart as judged by fluoroscopy). In 12 patients either non-contact mapping (ESI) for intolerable VT or electroanatomical mapping (CARTO) for tolerated VT was undertaken to define the endocardial activation pattern during VT or the scar contour during SR. In patients undergoing a non-contact mapping procedure, the following definitions were used22,23,25:

  1. Exit point. The site where a QS unipolar virtual electrogram is recorded on the map, which corresponds to the site of earliest activation followed by a rapid activation front, spreading to the surrounding healthy endocardium.
  2. Diastolic pathway. A defined region of endocardium, usually bordered by scar tissue, where the diastolic electrical activity preceding the exit point is recorded over a variable amount of the diastolic interval.

For any induced VT, both the exit point and the part of the diastolic pathway that could be reliably tracked were marked on the same ventricle as defined by virtual geometry.

Activation mapping during multiple morphologies of hemodynamically tolerated VTs was obtained by electroanatomical mapping by the CARTO system; the landmarks of the ablation sites for different VTs were superimposed typically on the sinus rhythm voltage map to visually relate the ablation site to defined areas of the infarction.

In these cases, a precise estimate of the distance between ablation sites was made and used to confirm findings derived from fluoroscopic observations.

Follow-up
All patients, in the absence of major side effects, were discharged with amiodarone therapy (200 mg/day), which was continued during follow-up unless contraindicated.

Follow-up after hospital discharge was carried out by visits to the outpatient clinic at 2-month intervals and by ICD interrogation every 4 months or whenever an arrhythmic event occurred.

The endpoints were recurrence of any VT, documented either by 12-lead ECG and/or by ICD interrogation, sudden death (defined as death after sudden cardiocirculatory collapse occurring within an hour of the onset of symptoms)29, and cardiac death.

Statistical analysis
Descriptive statistics were computed as the mean and standard deviation (SD) for continuous variables, median and quartiles (IQR) for skewed distributions, and absolute frequencies and percentage for categorical variables. Clinical and electrophysiological characteristics were compared between patients with monomorphic or pleomorphic clinical VT by means of the unpaired t test, Mann–Whitney U test for continuous variables, or the Fisher exact test for categorical variables, or by logistic modelling with robust standard errors to account for intrapatient correlation when evaluating the characteristics of single VTs.

Multiple logistic regression analysis with a robust standard error was used to assess the association between VT pleomorphism and the acute catheter ablation result, controlled for clinically meaningful potential confounders (site of previous myocardial infarction, left ventricular ejection fraction, induction of multiple VTs, and induced VT cycle). All covariates considered were included in the multivariate model after checking for co-linearity. The goodness of fit, calibration, and discrimination of the model were assessed.

Both VT-free survival and survival after the procedure were evaluated by means of Kaplan–Meier estimation. To evaluate the prognostic value of VT pleomorphism while controlling for clinically meaningful confounding factors (site of previous myocardial infarction, left ventricular ejection fraction, induction of multiple VTs, and acute ablation results), a multivariate Cox model was used. Hazard ratios (HR) and 95% confidence intervals (95%CI) were calculated. The event rates per 100 person-years were computed. All covariates considered were included in the multivariate model after checking for co-linearity. The proportional hazard assumption was tested by means of Shoenfeld residuals. Model validation was performed by calculating explained variation and by evaluating calibration and discrimination.

No selection technique was used in any of the multivariate models.

Stata 8 (StataCorp, College Station, TC) was used for computation. A P value0.05 was retained for statistical significance.

Results

A single VT morphology was documented in 102/137 (74%) patients (MONO Group); the remaining 35 (26%) patients with spontaneous pleomorphism constituted PLEO Group.

As shown in Table 1, there were no differences in the clinical variables between groups, except for a lower left ventricular ejection fraction in patients with clinical pleomorphism, where the proportion of patients with impaired LVEF (30%) was higher, although not significantly so.


View this table:
[in this window]
[in a new window]
 
Table 1 Population characteristics according to clinical VT presentation

 
Although syncope or hemodynamically intolerable VT occurred in a similar proportion in both groups, an ICD had been previously implanted more frequently in patients with VT pleomorphism, which suggested a higher number of VT occurrences among the latter patients.

At electrophysiological evaluation, 322 episodes of sustained monomorphic VT were induced and targeted for ablation. Among patients presenting with a single VT morphology, multiple configurations (2–7) were induced by programmed electrical stimulation in 58 patients (57%). Two or more VTs were induced in all the PLEO group patients.

A significantly higher median number of sustained VTs were induced in patients with clinical pleomorphism (2 vs. 3 VTs/patient), with a significantly shorter average cycle length (338 vs. 385 ms) (Table 1). The proportion of intolerable VTs induced was higher in patients with pleomorphism (49/110 vs. 23/212). Finally, a higher percentage of VT suppression was obtained in patients presenting with a single VT as compared to those with VT pleomorphism (162/212 vs. 43/110).

Determinants of the acute result of the ablation procedure
The ablation procedure was successful in 78 patients (57%), partially successful in 28 patients (20%), and a failure in 31 (23%); RFCA was successful in 70/102 patients (69%) in the MONO group and in only 8/35 patients (23%) in the PLEO group. Partial success was achieved in 14/102 (13%) patients in the MONO group and 14/35 (40%) patients in the PLEO group, while the procedure was a complete failure in 18/102 (18%) MONO group and 13/35 (37%) PLEO group patients.

The distribution of acute results differed significantly between PLEO and MONO patients (): of 78 patients in whom all induced VTs (Class A) were prevented, 70 patients (90%) had a single clinical VT as compared to 8 with clinical pleomorphism. Conversely, partial success (Class B result) or failure (Class C result) occurred more frequently in the patients with clinical pleomorphism, in whom hemodynamically intolerable and, therefore, unmappable VTs were induced more frequently (14/28 [50%] and 13/31 [42%], for both Class B and C vs. Class A post hoc comparisons). The odds of success (Class A result) for patients with pleomorphic VTs was 5 times lower than for patients with monomorphic VTs, after accounting for possible confounders (Table 2). The only other independent predictor was the induced VT cycle length, which was about 15% longer when the ablation procedure was fully successful. Particularly, inducing a single VT morphology or 2 or more VT morphologies was irrelevant in determining RFCA success in MONO patients (33/44 [75%] and 37/58 [64%], respectively, ).


View this table:
[in this window]
[in a new window]
 
Table 2 Determinants of acute success of the ablation procedure at multivariate logistic model

 
Multiple induced VTs: relation of acute procedure result to the presence or absence of a shared isthmus
Among 93 patients with multiple VT morphologies induced by electrophysiological stimulation, 35 had clinical pleomorphism while the remaining 58 presented with a single VT morphology. In 30 patients (33%), a single isthmus was shared by two VT morphologies based upon the aforementioned criteria. In 20/30 (67%) of these patients, ablation of dual VT morphologies was accomplished by a series of RF lesions delivered to the same area. In an additional 16% of cases, only the clinically documented VT could be ablated.

At variance with this, successful abolition of all induced VTs was achieved in only 39% of patients with multiple isthmuses or areas of slow conduction. In an additional 34%, only clinical VTs could be ablated and persistent inducible non-clinical morphologies remained (Fig. 1).



View larger version (24K):
[in this window]
[in a new window]
 
Fig. 1 Acute procedure result in patients with multiple induced VTs in relation to the presence or absence of a shared isthmus.

 
Results improved when non-conventional mapping techniques had been implemented to guide catheter ablation. Prevention of all induced VTs could be achieved in 9/12 patients (75%), all of them displaying different exit sites or diastolic pathways during different VTs; all these patients had pleomorphic VT at clinical presentation.

Non-contact mapping
In 10 patients (8 presenting with clinical pleomorphism), non-contact mapping of the left ventricle was undertaken to guide catheter ablation of at least one form of hemodynamically intolerable VT. Twenty-six episodes of VT were induced and mapped (2–3 per patient). Details are shown in Table 3.


View this table:
[in this window]
[in a new window]
 
Table 3 Noncontact mapping (pts # 1–# 10) and electroanatomical mapping (pts # 11–# 12) guided VT RFCA

 
In all these patients different VTs had clearly different exit sites; on the other hand, in 6/10 patients at least part of the diastolic pathway of one morphology could be tracked within the same area of at least one of the other morphologies (Figs. 2–5).



View larger version (62K):
[in this window]
[in a new window]
 
Fig. 2 Simultaneous recording of a left ventricular isopotential activation map and selected unipolar non-contact electrograms from the apical region (virtual 10–15, in green) and the posterior–inferior left ventricular wall (virtual 19–23, in yellow). The different colours of the isopotential map show the different voltages recorded at selected times during sinus rhythm, at any given location; the voltage scale is shown on the left side of each panel. The figure shows that in a patient with a previous posterior–inferior myocardial infarction, lower voltages are recorded in the infarcted area. Please note the extent of fragmentation displayed on the virtual electrograms recorded from the infarcted area.

 


View larger version (42K):
[in this window]
[in a new window]
 
Fig. 3 A 12-lead ECG of the first VT induced in the patient (cycle length: 367 ms) (A). (B–G) The pattern of endocardial activation at various times during VT. Diastolic activity is observed in the posterolateral wall, which shifts upward (C) and exits at the anterolateral wall (F–G) The rapid spread of endocardial activity at the exit is indicated by the large high-voltage area and sharp QS pattern of the virtual electrogram recorded at sites 11–15.

 


View larger version (42K):
[in this window]
[in a new window]
 
Fig. 4 A second type of VT induced (cycle length: 370 ms) in the same patient shows a RBBB pattern with a shift to a superior axis (A). Part of the diastolic pathway is shared with the previous VT (posterior wall, panels B and C), but in the later phase of diastolic activation advances to the inferior wall, with the exit site located on the infero-septal wall (F,G).

 


View larger version (40K):
[in this window]
[in a new window]
 
Fig. 5 Third VT (cycle length: 419 ms) in the same patient (A). Early diastolic activity is evident on the posteroinferior wall (B,C), then activation proceeds toward the inferoapical wall where the exit site is shown (D,E). Although the overall direction of diastolic activation is different, part of the diastolic activity can be observed at sites where mid-late diastolic activity was tracked during VT2. This observation is consistent with the QS pattern observed in V5–V6. In panel F, the complete set of RF lesions is displayed. No VT remained inducible after ablation.

 
In two patients who underwent electroanatomical mapping, all the different induced VTs were ablated at different sites (Fig. 6).



View larger version (32K):
[in this window]
[in a new window]
 
Fig. 6 Sinus rhythm voltage map of a patient with prior inferosposterior MI. The score scale is shown in the right upper panel. Three different VT morphologies were induced and successful ablation was performed at the sites marked by arrows for each VT. In all cases, areas of slow conduction where VT was interrupted were located at the border between the scar and the surrounding healthy myocardium.

 
Long-term outcome of catheter ablation
Follow-up data on arrhythmia recurrence and cardiac and sudden death were obtained for all patients included in the study over a median follow-up of 36 months (IQR 18–60 months). During this observation period, 67 patients had a recurrence of VT, with a 3 and 5-year cumulative TV-free survival of 54% (95%CI 45–62) and 46% (95%CI 36–57), respectively, as illustrated in Fig. 7(a). Of them, 51 had a recurrence of clinical VT. The 3 and 5-year cumulative clinical VT-free survival was 64% (95%CI 55–72) and 58% (95%CI 48–67). Twelve patients died, 10 of them from heart failure; cumulative survival was 93% (95%CI 87–97) at 3 years and 90% (95%CI 81–95) at 5 years.



View larger version (20K):
[in this window]
[in a new window]
 
Fig. 7 Unadjusted Kaplan–Meier estimate of arrhythmic event-free survival in the overall population (a) and event-free survival according to number of clinical VTs (b), acute RFCA result (c), and number of induced VTs (d).

 
Determinants of long-term VT recurrence
Table 4 summarises the role of potential risk factors in determining the occurrence of VT recurrences. Although clinical presentation appeared to be associated with VT recurrence (HR 2.5, 95%CI 1.5–4.15, ) in univariate analysis, its prognostic value was not maintained when possible confounders were accounted for in the Cox multivariate model (HR 1.63, 95%CI: 0.84–3.19). Similarly, the induction of multiple VT morphologies did not affect VT recurrence rate.


View this table:
[in this window]
[in a new window]
 
Table 4 Determinants of long-term VT free survival (any VT) at multivariate Cox model (model ; Likelihood based explained variation=0.27; shrinkage (calibration)=0.83; graphical discrimination=2 risk groups identified (survival curves for 1st and 2nd quartiles of predictive index separate from 3rd and 4th))

 
Actually, the only independent prognostic factor was the acute RFCA result, partial success and failure significantly increased the risk of recurrence (3 and 5-fold, respectively) with respect to complete success. Clinical presentation acquired prognostic value only when information about the RFCA procedure was eliminated from the model, at the cost of a lower explained variation, higher shrinkage, and poorer discriminative value (data not shown). VT-free survival curves are shown in Fig. 7(b)–(d) for clinical presentation, acute results, and the number of induced morphologies, respectively, all adjusted for variables in the multivariate model.

Sudden death and cardiac death
Of 12 deaths, two were sudden. They were observed in patients with a single VT presentation, reduced LVEF, and fully successful RFCA procedure. The remaining 10 patients died from heart failure, with a 3 and 5-year cumulative survival of 93% (95%CI: 87–97%) and 90% (95%CI: 81–95%), respectively. Table 5 presents the univariate survival analysis for the potential risk factor considered. Due to the low number of deaths, no multivariate model could be fitted. A low ejection fraction was the only predictor of death and the risk increased with decreasing LVEF.


View this table:
[in this window]
[in a new window]
 
Table 5 Determinants of survival at univariate Cox analysis (no multivariate model fitted due to the low number of death)

 
Discussion

The spontaneous occurrence of multiple distinct morphologies has been reported in 23–64.2%1,10,17 of patients suffering from recurrent sustained VT following myocardial infarction. The incidence of clinical pleomorphism recorded in the present series was low (25%), which may be related to one or more of the following factors:

  1. Almost all our patients had been treated with oral amiodarone alone since VT first occurred. Multiple antiarrhythmic drug treatments may increase the number of VT configurations recorded at the time of arrhythmia recurrence,10 as demonstrated in an earlier series published when the use of serial drug testing was more widespread.
  2. A referral bias cannot be completely ruled out since many patients were referred and considered eligible for catheter ablation if they had a simpler arrhythmia pattern, i.e., a single VT morphology that was hemodynamically tolerated.

In spite of this, the average rate of induction of multiple VTs increased to 65% of patients, including more than 50% of those who presented with a single VT morphology.

This finding indicates that the arrhythmia substrate can support multiple re-entry circuits or different exit sites from a given circuit in the majority of patients with prior infarction.5–9 Yet the clinical arrhythmia history is different in patients presenting with VT pleomorphism since the likelihood of effective antiarrhythmic drug therapy is lower in these patients10; likewise, the presence of multiple VT configurations and various sites of origin of VT has been described as a predictor of failure of surgical arrhythmia treatment.12,13

The complexity of the arrhythmia substrate is probably the most important limitation to more extensive use of catheter ablation in treating postmyocardial infarction VT. It is a widespread concern that selective interruption of the diastolic pathway resulting in effective ablation of the target arrhythmia may not be sufficient to prevent further recurrences due to the possible onset, in the subsequent period, of functional re-entry circuits related to the scar tissue.

The induction of multiple VT morphologies has been seen as a relative contraindication to catheter ablation by some authors17–19 since the persistent inducibility of non-clinical VT after catheter ablation is associated with an increased likelihood of arrhythmia recurrence.20,21,27

On the other hand, in patients presenting with hemodynamically tolerated VTs, the long-term outcome is primarily related to the acute result of catheter ablation and is unaffected by the number of presenting or induced VT morphologies.27

The question of whether the occurrence of spontaneous pleomorphism carries the same adverse prognostic significance as the induction of multiple VTs has never been addressed. Furthermore, it remains unclear whether the induction of multiple VTs in a patient with only a single clinically documented morphology carries the same adverse prognostic significance as the spontaneous occurrence of multiple VTs.

Clinical vs. induced VTs
In our study, the induction of multiple VT morphologies was the rule among patients with clinical pleomorphism but it also occurred in more than 55% of those who had had only one VT morphology, as has also been described in other series.20,21

Prevention of the target arrhythmia (fully successful and partially successful RFCA) was achieved in 75% of patients in whom a single VT was induced compared to 86% of those with 2 or more induced morphologies; overall prevention of any inducible VT was obtained in 64% of patients who had suffered only one VT but in whom multiple VTs could be induced at electrophysiological study. It appears, therefore, that in patients with a single clinical VT morphology the induction of multiple VT morphologies did not affect the acute success of catheter ablation.

At variance with this, acute results were much poorer among patients with clinically documented VT pleomorphism, in whom a fully successful procedure could be achieved in only 23%; a partial result (i.e., prevention of single clinical VT, with persistent inducibility of other VTs) was achieved in an additional 40% of these patients. The most frequent cause for the impossibility to achieve a complete success in this group of patients was hemodynamic intolerance of the induced VTs, that could be demonstrated in a significantly higher percentage of patients with VT pleomorphism. This may result from the more advanced degree of left ventricular dysfunction in this group of patients and the shorter cycle length of the induced VTs, both features that have already been recognised in other series20 describing the electrophysiological properties of patients with multiple VTs.

The possibility of demonstrating multiple separate sites of origin of arrhythmias adversely affects the outcome of the acute procedure. On the one hand, detailed experimental mapping studies in a canine post-MI VT model5 have shown that in a substantial number of cases different surface VT morphologies are related to different patterns of endocardial activation that, however, spread from the same single site of breakthrough (probably a shared isthmus).

The non-contact mapping data in the small subgroup of this patient population support this view. A shared part of the diastolic pathway followed by different patterns of endocardial activation in a later phase of diastole and clearly separate exit points was a frequent finding in pleomorphic VTs. Usually, in spite of these findings, distinct ablation lines crossing the diastolic pathways were required to prevent further induction of the different VTs. It follows that information on the activation pattern of any induced VT should probably be part of the mapping procedure for patients undergoing catheter ablation of pleomorphic VT. The use of non-contact mapping techniques offers a significant advantage in this setting, since it can be also applied to hemodynamically intolerable arrhythmia.

Determinants of long-term outcome
While clinical presentation with multiple VT morphologies adversely affected long-term arrhythmia-free survival, the induction of different VTs in the pre-ablation electrophysiological study did not confer a worse prognosis, provided that complete arrhythmia suppression could be achieved by the catheter ablation procedure. The data of our study, however, stress the importance of so-called non-clinical VT induced after ablation in predicting arrhythmia recurrence. The target of a VT-ablation procedure should be the complete prevention of any induced VT.

The relevance of the extent of arrhythmia suppression is further supported by the finding at multivariate analysis that the only factor associated to enhanced arrhythmia-free survival was a fully successful procedure; partially successful results, i.e., prevention of clinical VT with persistent inducibility of other forms of sustained ventricular arrhythmias, are in fact equivalent to complete failure.

Conclusions

Caution is advised before considering documented morphology as the only relevant target in patients with recurrent VTs following myocardial infarction.20,21,27

Treatment with different antiarrhythmic drugs may affect the functional properties of the arrhythmia substrate, originating a different QRS configuration.5 The extent of abnormal myocardial tissue and number of arrhythmia recurrences are factors facilitating the onset of multiple VT morphologies,2 and it may well be that the ultimate fate of patients with VT following myocardial infarction is the occurrence of multiple arrhythmia morphologies.

However, patients who present a single VT morphology seem to be more favourably suited to a catheter ablation procedure, even if multiple VT morphologies are demonstrated in the electrophysiological study.

As shown in a recent study,27 catheter ablation and antiarrhythmic drug treatment are a reasonable strategy in patients presenting with hemodynamically tolerated postmyocardial infarction ventricular tachycardias refractory to pharmacological treatment. The number of previously induced VTs did not affect arrhythmia recurrence, while prevention of any induced arrhythmia following the procedure was a significantly favourable prognostic factor.

A second relevant point is the poorer result of catheter ablation in patients presenting with multiple VT morphologies, where the higher occurrence of intolerable arrhythmias poses major limitations.

More advanced mapping techniques allowing the analysis of endocardial activation during fast VTs, such as non-contact mapping23–25 or electroanatomical location and isolation of the scar tissue,26 should probably be used to guide catheter ablation when the treatment of a patient with spontaneous multiple VTs is considered, since the result of the procedure rather than the clinical presentation is what affects long-term outcome.

References

  1. Josephson ME, Horowitz LN, Farshidi A et al. Recurrent sustained ventricular tachycardia. 4. Pleomorphism. Circulation. 1979;59(3):459–468.[Abstract]
  2. Wilber DJ, Davis MJ, Rosenbaum M et al. Incidence and determinants of multiple morphologically distinct sustained ventricular tachycardias. J. Am. Coll. Cardiol. 1987;10(3):583–591.[Medline]
  3. Miller JM, Kienzle MG, Harken AH et al. Morphologically distinct sustained ventricular tachycardias in coronary artery disease: significance and surgical result. J. Am. Coll. Cardiol. 1984;4(6):1073–1079.[Medline]
  4. Stevenson W. Ventricular tachycardia after myocardial infarction: from arrhythmia surgery to catheter ablation. J. Cardiovasc. Electrophysiol. 1995;6:942–950.[Medline]
  5. Osswald S, Wilber DJ, Lin JL et al. Mechanism underlying different surface ECG morphologies of recurrent monomorphic ventricular tachycardia and their modification by procamide. J. Cardiovasc. Electrophysiol. 1997;8(1):11–23.[Medline]
  6. De Baaker JMT, van Capelle FJL, Janse MJ et al. Reentry as a cause of ventricular tachycardia in patients with chronic ischemic heart disease: electrophysiologic and anatomic correlation. Circulation. 1988;77(3):589–606.[Abstract]
  7. Costeas C, Peters NS, Waldecker B et al. Mechanism causing sustained ventricular tachycardia with multiple QRS morphologies: result of mapping studies in the infarcted canine heart. Circulation. 1997;96(10):3721–3731.[Abstract/Free Full Text]
  8. Downar E, Kimber S, Harris L et al. Endocardial mapping of ventricular tachycardia in the intact human ventricle. II. Evidence of multiuse reentry in a functional sheet of surviving myocardium. J. Am. Coll. Cardiol. 1992;20(4):869–878.[Medline]
  9. Downar E, Saito J, Doig C et al. Endocardial mapping of ventricular tachycardia in the intact human ventricle. III. Evidence of multiuse reentry with spontaneous and induced block in portions of reentrant path complex. J. Am. Coll. Cardiol. 1995;25(7):1591–1600.[CrossRef][ISI][Medline]
  10. Mitrani RD, Biblo RA, Carlson MD et al. Multiple monomorphic ventricular tachycardia configurations predict failure of antiarrhythmic drug therapy guided by electrophysiologic study. J. Am. Coll. Cardiol. 1993;22(4):1117–1122.[Medline]
  11. Trappe HJ, Brugada P, Talajic M et al. Value of induction of pleomorphic ventricular tachycardia during programmed stimulation. Eur. Heart J. 1989;10(2):133–141.[Abstract]
  12. Kron IL, Lerman BB, Nolan SP et al. Sequential endocardial resection for the surgical treatment of refractory ventricular tachycardia. J. Thorac Cardiovasc. Surg. 1987;94(6):843–847.[Abstract]
  13. Miller JM, Kienzle MG, Harken AH et al. Subendocardial resection for ventricular tachycardia: predictors of surgical success. Circulation. 1984;70(4):624–631.[Abstract]
  14. Wilber DJ, Kopp DE, Glascock DN et al. Catheter ablation of the mitral isthmus for ventricular tachycardia associated with inferior infarction. Circulation. 1995;92(12):3481–3489.[Abstract/Free Full Text]
  15. Morady F, Kadish A, Rosenheck S et al. Concealed entrainment as a guide for catheter ablation of ventricular tachycardia in patients with prior myocardial infarction. J. Am. Coll. Cardiol. 1991;17(3):678–689.[ISI][Medline]
  16. Aizawa Y, Chinushi M, Naitoh N et al. Catheter ablation of ventricular tachycardia with radiofrequency currents, with special reference to the termination and minor morphologic change of reinduced ventricular tachycardia. Am. J. Cardiol. 1995;76:574–579.[CrossRef][Medline]
  17. Morady F, Harvey M, Kalbfeisch SJ et al. Radiofrequency catheter ablation of ventricular tachycardia in patients with coronary artery disease. Circulation. 1993;87(2):363–372.[Abstract]
  18. Kim YH, Sosa-Suarez G, Trouton TG et al. Treatment of ventricular tachycardia by transcatheter radiofrequency ablation in patients with ischemic heart disease. Circulation. 1994;89(3):1094–1102.[Abstract]
  19. Gonska BD, Cao K, Schaumann A et al. Catheter ablation of ventricular tachycardia in 136 patients with coronary artery disease: result and long-term follow-up. J. Am. Coll. Cardiol. 1994;24(6):1506–1514.[ISI][Medline]
  20. Rothman SA, Hsia HH, Cossù SF et al. Radiofrequency catheter ablation of post-infarction ventricular tachycardia. Long-term success and the significance of inducible nonclinical arrhythmias. Circulation. 1997;96(10):3499–3508.[Abstract/Free Full Text]
  21. Stevenson WG, Friedman PL, Kocovic D et al. Radiofrequency catheter ablation of ventricular tachycardia after myocardial infarction. Circulation. 1998;98(28):308–314.[Abstract/Free Full Text]
  22. Schilling RJ, Peters NS, Davies DW. Feasibility of a non-contact catheter for endocardial mapping of human ventricular tachycardia. Circulation. 1999;99:2543–2552.[Abstract/Free Full Text]
  23. Schilling RJ, Peters NS, Davies DW. Mapping and ablation of ventricular tachycardia with the aid of a non-contact mapping system. Heart. 1999;81(6):570–575.[Abstract/Free Full Text]
  24. Strickberger SA, Knight BP, Michaud GF et al. Mapping and ablation of ventricular tachycardia guided by virtual electrograms using a noncontact, computerized mapping system. J. Am. Coll. Cardiol. 2000;35(2):414–421.[CrossRef][Medline]
  25. Della Bella P, Pappalardo A, Riva S et al. Non contact mapping to guide catheter ablation of untolerated ventricular tachycardia. Eur. Heart J. 2002;23:742–752.[Abstract/Free Full Text]
  26. Marchlinski FE, Callans DJ, Gottlieb CD et al. Linear ablation lesions for control of unmappable ventricular tachycardia in patients with ischemic and nonischemic cardiomyopathy. Circulation. 2000;101(11):1288–1296.[Abstract/Free Full Text]
  27. Della Bella P, De Ponti R, Uriarte JAS et al. Catheter ablation and antiarrhythmic drugs for hemodynamically tolerated ventricular tachycardia. Eur. Heart J. 2002;23:414–424.[Abstract/Free Full Text]
  28. Bogun F, Li YG, Groenefeld G et al. Prevalence of a shared isthmus in postinfarction patients with pleiomorphic, hemodynamically tolerated ventricular tachycardias. J. Cardiovasc. Electrophysiol. 2002;13(3):237–241.[CrossRef][Medline]
  29. Poole JE, Bardy GH. Sudden Cardiac Death. Zipes DP, Jalife J. Cardiac Electrophysiology - From Cell to Bedside. second ed. : WB Saunders; 1995. p. 812–832.




This Article
Abstract
Full Text (PDF)
Alert me when this article is cited
Alert me if a correction is posted
Services
Email this article to a friend
Similar articles in this journal
Similar articles in ISI Web of Science
Similar articles in PubMed
Alert me to new issues of the journal
Add to My Personal Archive
Download to citation manager
Search for citing articles in:
ISI Web of Science (2)
Request Permissions
Google Scholar
Articles by Della Bella, P.
Articles by Trevisi, N.
PubMed
PubMed Citation
Articles by Della Bella, P.
Articles by Trevisi, N.