Author + information
- Received July 31, 1997
- Revision received March 31, 1998
- Accepted May 13, 1998
- Published online September 1, 1998.
- KristinE Ellison, MDa,
- PeterL Friedman, MD, PhD, FACCa,
- LeonardI Ganz, MD, FACCa and
- WilliamG Stevenson, MD, FACCa,* ()
- ↵*Address for correspondence: Dr. William G. Stevenson, Cardiovascular Division, Brigham and Women’s Hospital, 75 Francis Street, Boston, MA 02115
Objectives. The purpose of this study was to determine if entrainment mapping techniques and predictors of successful ablation sites previously tested in coronary artery disease can be applied to ventricular tachycardia (VT) in arrhythmogenic right ventricular dysplasia (ARVD).
Background. VT in ARVD has not been well characterized. Reentry circuits in areas of abnormal myocardium are the likely cause, but these circuits have not been well defined.
Methods. Mapping of 19 VTs in 5 patients with ARVD was performed. At 58 sites pacing entrained VT and radiofrequency current (RF) was applied to assess acute termination of VT.
Results. Sites classified as exits, central/proximal, inner loop, outer loop, remote bystander and adjacent bystander were identified by entrainment criteria. The reentrant circuit sites were clustered predominantly around the tricuspid annulus and in the right ventricular outflow tract (RVOT). RF ablation acutely terminated VT at 13 sites or 22% of the applications. Of the 19 VTs, eight were rendered noninducible and three were modified to a longer cycle length. In 2 patients ablation at a single site abolished two VTs.
Conclusion. VT in ARVD shows many of the characteristics of VT due to myocardial infarction. Entrainment mapping techniques can be used to characterize reentry circuits in ARVD. The use of entrainment mapping to guide ablation is feasible.
Sustained monomorphic ventricular tachycardia (VT) originating in regions of infarction or scarring are due to reentry circuits that are difficult to define with point-by-point activation sequence mapping (1–5). Entrainment has been useful for characterizing reentry circuits and regions of abnormal conduction due to myocardial infarction (1,2). Arrhythmogenic right ventricular dysplasia (ARVD) is a disease of unknown etiology characterized by ventricular arrhythmias and fibrofatty atrophy of the right ventricular myocardium (5–9). Reentry circuits in areas of abnormal myocardium are the likely cause of VT; however, the reentry circuits have not been well characterized. Entrainment mapping has been used to study reentry circuits causing VT after myocardial infarction (1,2). Entrainment can provide an indication of whether a site is within or outside a reentry circuit and whether it is in a region of abnormal conduction that may be critical to reentry. The purpose of this study is to test the feasibility of using entrainment to identify reentry circuits and guide catheter ablation.
Mapping with entrainment and radiofrequency ablation was performed in 5 patients (4 males, 1 female; ages 30 to 68 years) with spontaneous episodes of sustained monomorphic VT without cardiac arrest. Four patients had spontaneous VT despite trials of 1, 2, 3, or 4 antiarrhythmic medications, respectively (including beta blockers). One had a history of palpitations for years before presenting with an episode of sustained VT. The patients had the following abnormalities consistent with ARVD: 1) incomplete right bundle branch block or T wave inversion in the anterior precordial leads of sinus rhythm ECG (7); 2) right ventricular enlargement and/or hypokinesis on echocardiogram, (7,8); 3) VT with a left bundle branch block morphology; and 4) abnormal, low amplitude or fractioned electrograms recorded from one or more areas of the RV. In patients over 30 years of age, coronary angiography had excluded coronary artery disease.
Endocardial mapping and catheter ablation was performed following our methods previously described in patients with prior myocardial infarction (1,2). Mapping was performed with a steerable 7 French catheter with a 4 mm distal electrode. Initial mapping in sinus rhythm was performed to locate areas of abnormal electrograms. VT was then initiated by programmed electrical stimulation. Entrainment was performed by unipolar pacing from the mapping catheter distal electrode at a cycle length 10 to 50 ms shorter than the tachycardia cycle length. If the location was determined to be an exit, central, or proximal site in the reentry circuit (Fig. 1), radiofrequency (RF) current was applied. If the RF application terminated VT the lesion was expanded during sinus rhythm. If the site was not in the reentry circuit, and if RF current was applied it did not terminate VT, then the catheter was moved to a new site. If exit, central, or proximal sites were not identified, ablation was attempted at outer loop or adjacent bystander sites (Fig. 1)or sites with abnormal electrograms although entrainment criteria were not met. This sequence of events was continued until there were no inducible VTs or no desirable target sites were found. Data are presented in detail (Table 1)for the 58 sites where pacing entrained VT and RF current was then applied during VT to assess termination.
Entrainment with QRS fusion (ENT): entrainment with a change in QRS configuration in comparison to the VT morphology. Entrainment with concealed fusion (ECF): entrainment with no change in the QRS morphology. Post-pacing interval (PPI): the interval from the last stimulus that entrained VT to the subsequent electrogram at the pacing site.
VT termination at different types of reentry circuit sites was compared using logistic regression, adjusted for correlated outcomes, using the generalized estimating equations approach, implemented in the GENMOD procedure in the SAS statistical package (10). We assumed equal correlation between any two sites in the same patient, and independence between patients. The p value comparing all six different types of sites was based on a likelihood ratio test with 5° of freedom. In an alternative analysis, the different types of site were divided into two groups (exit, central and proximal vs all others). To assure the robustness of the results, we also adjusted for correlation within different VTs, rather than patients and the p-values obtained were qualitatively similar.
There were 19 different sustained monomorphic VTs induced; all 5 patients having multiple morphologies of VT. At 58 sites VT was entrained and RF was applied to the site during VT. RF terminated VT at 13 of the 58 sites or in 22% of the applications (Table 1) (Figure 2). ⇓A variety of different reentry circuit sites were seen in all patients (Table 1). Of the 58 sites where pacing and RF ablation were performed, entrainment classified 16 as exits (Figure 2), 2 as central/proximal, 24 as outer loop sites (Figure 3), 2 as inner loop sites, 8 as adjacent bystander sites and 6 as remote bystander sites. Of the 16 exit sites, RF terminated VT in 4 cases (Figure 2)or 25% of the applications. Ablation terminated VT at one of the two central/proximal sites, at six of the 24 outer loop sites, and at two of the eight adjacent bystander sites. No termination occurred at the two inner loop and six remote bystander sites. Logistic regression, adjusted for within-patient correlation, showed no difference in the incidence of VT termination between the six different types of sites (p = 0.41), nor between the two combined groups of exit, central and proximal compared to all other sites (p = 0.32). The lack of significance could easily be attributable to the small sample sizes.
Locations of various reentry circuit sites and sites where RF terminated VT are shown in Figure 4. These reentry circuits sites tended to cluster around the tricuspid annulus and the right ventricular outflow tract, which are the typical areas of fibrofatty infiltration in ARVD (6).
Of the 19 VTs, ablation rendered eight no longer inducible. Three VTs that remained inducible were modified to longer cycle lengths. For these 11 VTs, reentry circuit exits and central/proximal were identified near the tricuspid annulus in seven and in the right ventricular outflow tract (RVOT) in three. None of the VTs with circuits remote from these regions, such as in the inferoapical RV, was successfully ablated. In 2 patients RF ablation at a single site (at the RVOT in one and tricuspid annulus in the other) abolished two VTs.
There were no complications related to the ablation procedure. Follow-up ranges from 11 to 24 months (mean 17 months). In 1 patient with VTs originating only in the RVOT, no VTs were inducible after RF ablation; he has remained symptom free without antiarrhythmic drug therapy. One patient had only a new faster VT inducible at the end of the procedure. He was maintained on the same drug therapy as prior to ablation and has not had clinical recurrences. One patient who underwent ablation in hopes of discontinuing amiodarone remained inducible and was continued on amiodarone without symptoms. The remaining two patients also had inducible VT at the end of the procedure; one received an implantable defibrillator and has had no spontaneous episodes of VT. Amiodarone therapy was initiated in the other with no episodes of spontaneous VT during follow-up.
Entrainment has been useful in the characterization of reentrant circuits due to myocardial infarction (1,2). These circuits can be large and a variety of different types of reentry circuit sites have been defined. In this study, we have further characterized the reentrant circuits in ARVD. These circuits have many of the features observed in post-infarct VT patients. The circuits were comprised of zones of abnormal conduction, characterized by low amplitude abnormal electrograms, with identifiable exit regions to the surrounding myocardium. Outer loops, which may be broad portions of the reentry circuit in communication with the surrounding myocardium, were also observed. Targets for ablation previously identified in coronary VT may also be useful for targeting VT in ARVD. Termination of VT was more frequent at exits and central/proximal sites than at bystander sites. In this study, several terminations also occurred at outer loop sites; however, the majority of these terminations occurred in one patient. Complete ventricular mapping was not performed prior to RF application; therefore, not all the reentry circuit sites were identified. Thus, we can not ascertain which portion of the reentry circuit yields the greatest likelihood for successful ablation.
In our patients, reentrant circuit sites clustered around the RVOT and the inferolateral tricuspid annulus, which are typical areas of fibrous and fatty infiltration in ARVD (6). Interestingly, VT from these locations appeared to be more susceptible to ablation. In contrast, VTs originating from the body of the RV were not successfully ablation. It is tempting to speculate that the tricuspid annulus or pulmonary valve can serve as anatomic obstacles, defining a border of an isthmus in the reentry circuit that can sometimes be interrupted by ablation (9,11). Varied pathophysiologic variants of ARVD have been described (6,8). The disease can be focal or have more diffuse involvement. It is interesting to speculate that ablation of VT in cases of focal involvement may more likely be acutely successful than ablation of VTs when there is diffuse involvement. RF ablation of VT in ARVD has variable efficacy and is generally reserved for those patients who are intolerant of antiarrhythmic drugs (7). In our referral population, patients were either refractory to pharmacologic interventions or desired VT ablation to avoid long-term use of antiarrhythmic with potential side effects. Improved drug control of spontaneous VT, despite continued inducibility of VT, after ablation has also been reported by Marcus and Fontaine (7). ARVD may be a progressive disease; new VTs may emerge during long-term follow-up (7). The number of patients in the present study is not sufficient to comment on the long-term efficacy or the risk of perforation, which is of concern in view of the RV thinning present in ARVD.
VT in patients with ARVD shares many of the features observed in the post-myocardial infarction population. Multiple morphologies of inducible VT are common. A variety of different reentry circuit sites are identifiable with entrainment mapping. A single region can give rise to multiple VT morphologies. Entrainment mapping techniques can be used to characterize reentry circuits in ARVD and potentially to guide ablation. However, ablation can be difficult and should be viewed as a potential palliative procedure in selected patients.
- arrhythmogenic right ventricular dysplasia
- entrainment with concealed fusion
- entrainment with QRS fusion
- post-pacing interval
- right ventricle
- right ventricular outflow tract
- ventricular tachycardia
- Received July 31, 1997.
- Revision received March 31, 1998.
- Accepted May 13, 1998.
- American College of Cardiology
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